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What to Buy: Ventolin or Symbicort? Best Asthma Inhalers Available Online

Ventolin (Albuterol) and Symbicort are used to treat or prevent breathing problems in patients who have asthma or other other lung diseases.

You should understand the difference between Symbicort and Ventolin. Here is a comparative analysis which may shed light on your asthma medications:

Ventolin Inhaler

Ventolin (Salbutamol) is a selective antagonist of beta2-adrenoreceptors. In therapeutic doses, the medication acts on beta2-adrenergic receptors of the smooth muscles of the bronchi. The drug produces a bronchodilator effect, prevents and arrests bronchospasm, increases the vital capacity of the lungs, prevents secretion of histamine, causes a slight positive chrono and inotropic effect, dilates the coronary arteries and practically does not reduce blood pressure. Ventolin has a tocolytic effect: the medication lowers the tone and contractile activity of the myometrium. The drug has a number of metabolic effects: reduces the potassium content in the plasma, affects glycogenolysis and insulin secretion, has hyperglycemic (especially in patients with bronchial asthma) and lipolytic effect, increases the risk of acidosis. Nowadays, you can buy Ventolin Inhaler online over the counter.

Symbicort Inhaler

Symbicort (official site) is a combined preparation for treatment of bronchial asthma. The medication contains Formoterol and Budesonide, which have different mechanisms of action and show an additive effect in reducing the frequency of bronchial asthma exacerbations. The specific properties of Budesonide and Formoterol allow to use their combination as maintenance therapy and relief of asthma seizures, or as a supporting therapy for bronchial asthma. See how to use Symbicort inhaler correctly to get the maximum effect.

Difference between Ventolin and Symbicort

Comparative unit Ventolin Inhaler Symbicort Inhaler Visual appearance Components Albuterol + auxiliary components Micronized budesonide + formoterol fumarate dihydrate + auxiliary components Indications for use Prevention and relief of bronchial asthma, chronic obstructive pulmonary disease (COPD), chronic bronchitis, emphysema Bronchial asthma (when inhaled glucocorticosteroids (GCS) and short-acting beta2-adrenomimetics do not work), maintenance therapy and relief of seizures, COPD, recurrent asthma exacerbations Minimum price per unit $25.95 $65.90 Package type Inhaler Inhaler Dosages available 100mcg/100mcg 400/12mcg; 200/6mcg; 100/6mcg Min/max dosage 100mcg/100mcg 100/6mcg / 400/12mcg Maximum dosage per day 100mcg 6 times a day 8 inhalatins a day (the dosage can be increased up to 12 inhalation aday with a physician’s permission) Onset of action Starts action in 5 minutes (75% of cases) Starts action within 20 minutes Duration of action Lasts up to 6 hours Lasts up to 24 hours Possible side effects Tremor of fingers; headache; dizziness; increased excitability; anxiety; sleep disturbance; insomnia; expansion of peripheral vessels (congestion of the facial skin); pain in the chest; arthralgia; angioedema; hives; nasal congestion; bronchospasm; muscle cramps; nausea, vomiting; dyspepsia; cough; increase of activity in children; arrhythmia Headache; anxiety; nausea; dizziness; sleep disorders; depression; behavioral disorders (mainly in children); taste violation; tachycardia; atrial fibrillation; stenocardia pectoris; fluctuations of blood pressure; tremor Contraindications Rhythm disturbances (paroxysmal tachycardia, polytopic ventricular extrasystole); myocarditis; heart defects; aortic stenosis; cardiac ischemia; tachyarrhythmia; thyrotoxicosis; decompensated diabetes mellitus; glaucoma; epileptic seizures; pyloroduodenal constriction; renal or hepatic insufficiency; hypersensitivity to any component of the drug Children under the age of 6 (for all medicinal forms); children under the age of 12; hypersensitivity to Budesonide, Formoterol or inhaled lactose Alcohol interaction There may be a negative interaction between Ventolin and alcohol There may be a negative interaction between Symbicort and alcohol Food interaction No food restrictions No food restrictions Use in children Children aged from 2 to 12 use Ventolin to prevent attacks of bronchial asthma Contraindicated in children under the age of 6 (all medicinal forms)

Conclusion: There is a big difference between Ventolin and Symbicort inhalers. Symbicort is an inhaled corticosteroid that dilates the lungs and airways. It works in two ways: reduces inflammation (one of the leading causes of asthma attacks), and also helps to open the airways, improving the airflow quality in a patient. Ventolin is used only as a rescue inhaler for asthmatic patients. It works by relaxing the muscles in the airways and spasms that are a side effect of an asthma attack. Ventolin is not used to prevent asthma attacks; it only works effectively when treating an asthma attack. Therefore, it should be used on an “as needed basis.” Symbicort is a preventative and maintenance inhaler for asthmatic patients. The best option is to consult your doctor before buying asthma inhalers online.

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Ventolin Inhalers: Medication for Treatment Asthma

Enhancement of bronchial reactivity has been observed by many investigators following the late asthmatic response induced by allergen in sensitized human subjects. Cockcroft et al first discovered that nonallergic airway reactivity was increased in only those individuals who developed either a definite or “equivocal” late asthmatic response. Postallergenic reactivity status was assessed between eight hours and seven days after antigenic challenge in these asthmatic subjects. More recently, Cartier and colleagues have published a comparable study where reactivity status was evaluated eight or more hours after the antigen. They concluded that the allergen-induced late asthmatic response was associated with the increase in airway reactivity observed. Because of reports such as these, it has generally been thought that the increased bronchial reactivity after inhalation of allergen is associated with the late response, but not with the immediate asthmatic response.

We have wondered whether reactivity status in man may, in fact, change during or soon after the immediate asthmatic response. Although some experimental investigations in animals may pertain to this question, information derived from clinical investigation is needed, in that naturally occurring asthma is a disorder unique to humans. To our knowledge, all relevant clinical studies in the literature are based on evaluations of bronchomotor tone done six or more hours following exposure to antigen.

Consequently, we assessed histamine reactivity before and after an allergenic challenge that precipitated a dual response in bluegrass allergic asthmatics. To obviate the possible effects that changes in airway caliber could have on reactivity testing, we waited to evaluate these subjects after allergen until the increase in their specific airway resistance (SRaw) during the immediate asthmatic response had resolved. It has previously been shown in hyperreactive subjects that as many as four serial, cumulative histamine challenge tests at 30-minute to 40-minute intervals can be done reproducibly. This suggests that upon such repeated testing, no change in sensitivity to ventolin inhaled histamine per se occurs.

Materials and Methods

Subjects

Seven atopic asthmatic adults (four women and three men between 20 and 50 years of age) who were known to develop dual asthmatic responses upon inhalation of Kentucky bluegrass antigen participated in this study at least ten weeks after the bluegrass pollen season had ended. All individuals had clinical histories characterized by recurrent wheezing, dyspnea, or chest tightness and allergic rhinitis that worsened during the bluegrass pollen season. All had reversible bronchoconstriction and positive prick and intradermal sldn tests to bluegrass antigen documented by physicians. At the time of study, each subjects condition was clinically stable, with respiratory symptoms being mild and well controlled with minimal or no medication. Initial values for SRaw and forced expiratory volume in one second (FEV1 were within normal ranges (Table 1 and Fig 1). Respiratory infection and exposure to allergens to which the subjects were sensitive had not occurred for at least six weeks prior to the study. This study was performed with the approval of the University Human Research Committee and with the informed consent of the participants. Asthma is a disease making the breathing difficult. Such attacks are dangerous while it may lead to death. To read more about asthma and its ways of treatment due to ventolin inhalers you may on buy-asthma-inhalers-online.com.

Design of Study

In all subjects, the FEV1 SRaw, and airway reactivity to histamine were determined on each of the two days prior to ventolin inhalation of allergen, on the day of allergenic exposure (after resolution of the immediate asthmatic response), and on a day at least seven days thereafter. Prior to reactivity testing, medication was withheld as follows: slow-release theophylline compound, 48 hours; and 0-adrenergic agonists, eight hours. None of the subjects was being treated with corticosteroids or cromolyn sodium for their asthma.

On the day of allergenic challenge, a dose of antigen was used that was sufficient to induce a significant immediate asthmatic response (see procedures) defined by a decrease in FE of at least 20 percent below baseline for longer than 20 minutes. After the immediate asthmatic response had manifested, the FEVt and SRaw were measured frequently until each parameter had returned to within 6 percent of the values before challenge. At that time, reactivity to histamine was reassessed within five minutes. The occurrence of late asthmatic responses after allergenic exposure was confirmed by the recurrence of bronchospasm. Seven or more days after the allergen, SRaw and histamine reactivity were remeasured in all subjects.

Procedures

The FEV1 was measured using a 14-L water spirometer (Collins Instruments). The FEV, on each occasion was derived from the average of three measurements. The SRaw was measured using a constant-volume whole-body plethysmograph and the quiet breathing technique previously described by Krell and associates that we have found useful for testing in animals as well. Briefly, airflow was measured with a heated pneumotachygraph (Fleisch No. 3) connected to a differential pressure transducer (Validyne MP 45); box pressures were also measured with a pressure transducer (Validyne MP 45). Electrical outputs from both of these tranducers, via carrier demodulators (Validyne CD15), were amplified by a dual trace amplifier (Tektronix 5A18N) and displayed simultaneously on a X-Y storage oscilloscope (Tektronix 5113) so that the angle described during the initial rapid phase of inspiration could be measured and SRaw calculated from it. So that the inspiratory limb was sharply defined on the oscilloscope screen for measurement, each subject breathed slightly fester than their usual respiratory rate in time to a metronome that was set at the same rate on eaph testing.

Serial dilutions of histamine (16 to 0.03 mg/ml) were prepared at 14-day intervals from a stock supply of histamine (32 mg/ml) stored in aliquots at 4°C. All dilutions were made using physiologic saline solution. Bronchial reactivity was assessed by measuring SRaw as a function of the concentration of aerosol histamine inhaled. Aerosol (with a particle size of 1.2)1. aerodynamic mass median diameter) was generated using a nebulizer (DeVilbiss 646) (filled with a 2-ml aliquot of histamine) and equipped with a modified Rosenthal French dosimeter triggered by the onset of tidal inspirations. This dosimeter delivered a stream of compressed air to the nebulizer at 25 psi for 0.6 second per inspiration. Dose-response curves were constructed by having the subjects inhale ten consecutive breaths of histamine solution in doubling concentrations at six-minute intervals, until at least a doubling of SRaw occurred. The first concentration of histamine chosen for each subject on initial reactivity testing varied according to their past respiratory history and medication. All subsequent testing began with this same concentration of histamine. Baseline values of SRaw and values after each dose of histamine were derived from the means of measurements made of three consecutive breaths at 60-second intervals for four minutes. The provocative concentration of histamine producing a doubling of baseline SRaw (PCwHis) was determined by interpolation from log dose-response curves plotted on semilogarithmic paper.

Allergenic challenge testing was performed using a powder extract of Kentucky bluegrass antigen dissolved in physiologic saline solution and stored in aliquots at 4°C. Prior to allergenic challenge, threefold dilutions were made with physiologic saline solution and were stored at 4°C. The initial concentration of allergen inhaled was based upon the results of intradermal skin testing using the serial dilutions of bluegrass antigen (Hollister-Stier Laboratories) injected in 0.02-ml volumes. These dilutions were also used for the bronchial challenges. The concentration of antigen producing a wheal at least 5 mm greater than the saline control was used as the starting dose for bronchial challenge in that subject. Response to aerosol allergen was quantitated by measuring SRaw and FEV1 (as described previously) ten minutes after inhalation. Aerosols were generated by a second nebulizer (DeVilbiss 646) that was connected and used for testing essentially in the same manner as described previously for the histamine challenges. To identify dual asthmatic responders for inclusion in the study and to ascertain the concentration of allergen sufficient to cause a dual response, the allergen was inhaled in threefold increasing concentrations until an immediate asthmatic response occurred (as characterized previously). The concentration of allergen so determined was subsequently used as the initial concentration for the protocol.

Changes in the groups SRaw and in the Δ log PC200 His Δ log PC200His on the first day before allegen minus Δ log PC200His on the subsequent occasion) on the second day before allergen or at a time after allergen were compared using Students t-test. In all cases, differences were considered significant for p values less than 0.05.

Table 1—Characteristics of Subjects

Subject, Sex, Age (yr) Baseline FEVj, (percent of predicted) CurrentMedications* 1, F, 20 2.45 (80) B daily 2, F, 24 3.67 (107) None 3, M, 29 2.65 (66) B not daily 4, M, 29 3.71 (87) B, T not daily 5, F, 50 1.90 (71) B not daily 6, M, 30 3.33 (80) None 7, F, 36 2.52 (90) B nor daily

Figure 1. Dose-response curves demonstrating effect of inhalation of bluegrass allergen on bronchial reactivity to aerosol histamine in allergic asthmatic subjects. Curves were obtained on each of two days prior to allergenic challenge (open circ1es)y on day of allergen exposure within ten minutes after resolution of immediate asthmatic response (solid circles and dashed lines), and on day at least seven days thereafter (open triangles). In each case, response was measured as SRaw before and after histamine. Each subject demonstrated substantial increase in histamine reactivity soon after immediate asthmatic response had resolved.

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Ventolin Inhalers Therapy in Asthma

Clearly, the methodology of the European Audit of Asthma Therapy makes the data somewhat difficult to interpret because of the heterogeneity of the respondents. In France, these were largely pulmonary specialists or physicians involved in allergy. We need more information on the practices of general practitioners and pediatricians who diagnose and treat asthma. Surveys of randomly chosen samples of the practicing community with special examination of the nonresponders would be interesting. Nevertheless, the first European Audit of Asthma Therapy showed important differences among countries, with considerable disagreement on the choice of drugs, dosing, and mode of administration, especially between France and other European countries.

We do not know yet if the differences in the French management of asthma lead to differences in mortality, morbidity, hospital admissions and quality of life for asthmatic patients. It seems that the regional trends depend upon several considerations, such as: 1) the relative proportion in each country of general practitioners, chest physicians, allergists and pediatricians involved in treating asthma, which may depend upon demographic and economic differences in each region; 2) the official (from medical school), and non-official, (mainly from firms), postgraduate teaching programs.

These two points could lead to differences in diagnostic and therapeutic approaches to asthma. The diagnosis may differ depending upon the methods used for detecting allergy, bronchial hyperreactivity, bronchial inflammation and chronic obstructive bronchial disease. Differences in the methods used for diagnosis may influence the therapeutic approach, influencing the choice of immunotherapy and antiallergic drugs, atropine-derivatives, and doses of bronchodilators, ventolin inhalers and corticosteroids. The asthma medications inhalers – ventolin is used to arrest the asthma attacks faster that you can envision it.

In France, a population of 55 million is served by about 69,000 physicians involved in private practice. Of these, 46,000 are general practitioners, and about 700 are chest physicians, a category that is increasing disproportionately to the total number of physicians (Table 6). The number of consultations for asthma is increasing more rapidly than for other diagnoses. Consultations for asthma represent about 20 percent of the activity of chest physicians, and less than 1 percent for other physicians. If we consider sales of antiasthmatic drugs (Fig 1), theophyllines represent more than 50 percent of the total sales in France. Sales of inhaled corticosteroids are decreasing, but sales of inhaled beta-agonists are increasing rapidly. Sales of cromoglycate are stable in France and antimuscarinic agents have just appeared on the market. If total antiasthmatic drug sales are increasing in France, we do not yet know if this reflects an increase in the number of asthmatic patients treated, of the consultations per patient, or of the prescriptions per consultation.

In conclusion, possible reasons for the differences in treatment, as suggested by the Audit, are as follows: 1) more allergists are involved in the management of asthma in France than in other European countries; 2) many French physicians are still concerned about the toxicity of beta-agonists and steroids; 3) high-dose preparations of inhaled steroids are not yet available in France; 4) historic preference for rectal and oral routes of treatment.

All of these data must be confirmed by another survey conducted on the basis of a randomized distribution of questionnaires among chest physicians, allergists, pediatricians and general practitioners, in order to obtain more information on their habits in diagnosing and treating asthma. To understand the possible causes for differences between countries, we have to take into account the influence of differences in physician sampling, in the modalities of diagnosing asthma, in the graduate and postgraduate teaching of clinical pharmacology, and the availability and promotion of drugs by pharmaceutical companies. We will then be able to understand more precisely the reasons for differences in treatment and perhaps ultimately affect morbidity and mortality of asthma.

Figure 1, Sales of antiasthmatic drugs in France, 1982-1985.

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Ventolin Inhaler and Bronchodilator in Asthma Treatment

Lung function prior to each drug administration was similar (Table 2). There were no significant differences for TLC, FRC, FEV,, FVC, Vmax50, Vmax25 or Rl. Both drugs resulted in bronchodilatation (Fig 2). The FE Vt and Vmax50 were significantly increased and Rl significantly decreased after both drugs. The Vmax25 was significantly increased only after fenoterol. There was no significant difference in the magnitude of change produced by either drug for any variable.

Continued bronchodilatation and ventolin inhalers did not occur during the second part of the study as the postbronchodilator FEVb measured on air before He-02 breathing, was similar to the FEVi measured on air following He-02 breathing, approximately 90 to 120 minutes after administration of the drug (4.61 L vs 4.58 L, p>0.05).

Density dependence of maximal flows and resistance were similar before each study. There were no significant changes in the density dependence of flow or resistance after either agent (Fig 3 and 4). Although only density dependence of Vmax at 50 percent VC is shown, the results at other lung volumes were similarly nonsignificant, as were the changes in density dependence of Rl at an inspiratory flow of 1 Us.

Discussion

The results of this study demonstrate that fenoterol and ipratropium bromide produce similar degrees of bronchodilatation in normal subjects. There was no systematic change in the density dependence of Vmax or Rl with either agent. Therefore, these results do not support the hypothesis that inhaled anticholinergic agents have a preferential site of action on central airways while inhaled adrenergic agents produce peripheral airway dilatation. The main component and key element of asthma treatment is ventolin inhalers for asthma. Do not forget to follow the link and you will find everything you need for asthma treatment.

The hypothesis behind localization of bronchodilatation by changes in density dependence of Vmax and/or Rl rests on the assumption that the total pulmonary resistance consists of a contribution from central airways, where turbulent flow regimens exist in series with peripheral airways where flow is more laminar. If the resistance of the more central airways, where flow is turbulent, contributes significantly to total resistance, higher flow rates and lower pulmonary resistance will be achieved when air is exchanged for a helium-oxygen mixture, owing to the lower density of the latter gas. If a drug acts predominantly on central airways, the relative contribution of a turbulent flow regimen in these airways to overall resistance will decrease and density dependence will decrease. On the other hand, if a drug acts primarily on peripheral airways where flow is laminar, the central turbulent air flow regimen would then contribute more to overall resistance and density dependence would increase.

Indeed, these were the findings of Ingram et al in seven normal subjects following inhaled atropine sulphate and isoproterenol. They measured maximal expiratory flow breathing air and helium before and after inhalation of these agents delivered by aerosol during a two-minute period of tidal breathing. They were able to show that the density dependence of maximal expiratory flow at 40 percent vital capacity decreased consistently after inhaled atropine and increased after inhaled isoproterenol despite equivalent degrees of bronchodilatation on air with both agents.

MacNee et al also measured density dependence of Vmax and were unable to confirm the findings in a study of eight normal subjects in whom ipratropium bromide and salbutamol were administered by metered dose inhaler and five minutes of tidal aerosol breathing; the combination being employed to ensure diffuse distribution of drug.

In the present study, we have re-examined the issue of drug-related site of action with a selective beta adrenergic agent, fenoterol, and the anticholinergic agent, ipratropium bromide, both administered solely by the usual metered dose inhaler. Since Lisboa et al have suggested that density dependence of maximal expiratory flow may not accurately reflect the series distribution of pulmonary resistance due to the complex factors determining maximal expiratory flow, we also measured the density dependence of pulmonary resistance.

There are several possible explanations for the difference between our results and those of Ingram et al. The first possibility involves the drugs in each study. Ingram et al used atropine and isoproterenol, while fenoterol and ipratropium bromide were given in this study. These differences are unlikely to be important; fenoterol is a specific beta-agonist like isoproterenol, although more beta selective, and ipratropium bromide has comparable anticholinergic activity to atropine. However, the feet that our results are similar to those of MacNee et al who also used ipratropium and a selective betas agonist salbutamol, makes it difficult to rule out this explanation.

The second possible source of differences relates to the site of deposition of the inhaled agents. Recent reports have stressed the importance of inhalation pattern to the distribution of the inhaled drug. Slow deep inhalations deposit aerosol within smaller more peripheral airways, whereas inhalation patterns with smaller volumes and higher inspiratory flow rates tend to deposit the drug in more central zones. Our subjects, inhaling slowly from RV to TLC, would tend to deliver more drug to the peripheral airways; on the other hand, subjects in the study of Ingram et al breathed tidally from a face mask and the smaller volumes could have resulted in more central deposition of drug. Inspiratory flow rates also contribute to the deposition pattern with fester flow rates depositing the aerosol more centrally than slower rates. These characteristics have been exploited in clinical studies to alter the effect of inhaled bronchoactive agents. Aerosol size also alters particle deposition with larger particles distributed more centrally than smaller particles. Metered dose inhalers generally produce particles of uniform size (0.5 to 2.0 μm) which penetrate more peripherally than the larger particles generated by nebulizers.

Thus, changes in the site of bronchodilatation could be influenced by changes in inhalation technique and particle size which may alter the site of drug deposition. In an attempt to circumvent this, MacNee et al used both the metered dose inhaler and tidal aerosol inhalation to deliver the drug and found results similar to the present study as regards density dependence of maximum expiratory flow.

The third potential source of discrepancy between studies relates to variation in the measurement of density dependence of Vmax. A number of studies have questioned the usefulness of the test owing to the marked variability of measurements. The coefficient of variation for AVmax may be greater than 20 percent. Part of this variability stems from the irregular shape of the flow volume curve itself and the necessity to match two curves (one air and the other He-Oa) at a constant lung volume.

Measurement of the density dependence of Vmax may not reflect the series distribution of total airway resistance, but rather may reflect the flow regimen at the site of flow limitation. Recent experimental and clinical studies have questioned the usefulness of AVmax in localizing the site of airway obstruction. Many patients with advanced airflow obstruction in whom peripheral resistance is presumably greatly increased demonstrate well preserved density dependence of Vmax presumably because flow limiting sites remain in large airways where convective acceleration and turbulent flow are important. Lisboa et al have shown that the density dependence of Vmax and Rl did not correlate in a group of asthmatic subjects, and they suggested that the density dependence of tidal resistance would better reflect the distribution of resistance in the tracheobronchial tree.

We did not observe a systematic change in ARl with either bronchodilator and thus our results with Vmax and Rl are consistent in not supporting a preferential site of action for either class of bronchodilator in these normal subjects. It is possible, of course, that a different result would be apparent in patients with asthma.

Thus, in summary, the hypothesis of preferential sites of action of beta-adrenergic agonists and anticholinergic agents is not supported by the results of the current study, at least in normal subjects. Although there is evidence to suggest that receptor densities vary throughout the bronchial tree, the insensitivity of density dependence as a measure of site of resistance and the vagaries governing inhaled drug distribution may have contributed to the negative results of this study.

Table 2—Baseline Lung Function ( ± SD)

Pre Ipratropium Bromide Pre Fenoterol TLC, L 6.40 6.60 .98 .96 FRC, L 3.17 3.35 .46 .43 FVC, L 5.25 5.34 .87 .89 FEV„ L 4.26 4.30 .77 .75 Vmax50, L/s 5.51 5.45 1.02 1.54 Vmax25, L/s 2.21 2.04 .33 .44 Rl, cmH20/L/s 1.53 1.63 .26 .63

Figure 2. Effects of fenoterol and ipratroprium bromide on pulmonary function expressed as the mean percentage change of FEVly Vmax50, Vmax25 and Rl at 1.5 US

Figure 3. Effects of fenoterol and ipratropium bromide on density dependence of Vmax50. Density dependence is defined as the ratio of maximal flow on He-O, to maximal flow on air. Values are mean and standard deviation.

Figure 4. Effects of fenoterol and ipratropium bromide on density dependence of Rl at a flow rate of 1.5 Us. Density dependence is defined as the ratio of Rl on He-Ot to Rl on air. Values are mean and standard deviation.

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Canadian Health&Care Mall In Fight with ASthma By Ventolin Inhalers

Simple immediate allergic responses do not adequately account for chronic allergic asthma. Late phase asthmatic responses (LAR) are increasingly recognized as an important factor in the pathogenesis of chronic asthma, at least in part, by inducing nonspecific bronchial hyperresponsiveness.The LAR are associated with influxes of neutrophils and eosinophils, degranulation of mast cells and eosinophils, neutrophil and eosinophil chemotactic activity, and platelet factor-4 release and thrombin generation. Pathologically, chronic asthma is characterized by inflammation, mucosal edema, and exudate which contribute to airway obstruction in conjunction with bronchospasm. Although normally a “silent zone,” small airways may be affected preferentially (compared to large airways) by cellular exudate, parenchymal inflammation, edema, and excess mucus causing increased resistance. This process could then provide the substrate for chronic asthma. Although late responses are a well-known characteristic of hypersensitivity pneumonitis and allergic bronchopulmonary aspergillosis, there is little information about LAR in patients with asthma. Therefore, we undertook this study to determine the frequency and characteristics of LAR in mild asthmatic patients with the use of spirometry and of He-02 flow volume loops for measuring airway responses. Ventolin inhalers ordered via http://buy-asthma-inhalers-online.com/ will help you to overcome such a disorder as asthma.

Methods

Subject Selection Seventeen nonsmoking allergic asthmatic subjects aged 20 to 37 years (13 male, 4 female), who were mildly symptomatic during two or more seasons or upon exposure to an animal, were studied. Each subject was informed of the risks of bronchoprovocation (BPC) and gave informed consent for the protocol which had been approved by the Human Use Committee of the University of Iowa. These subjects were part of a larger study of bronchial responses to inhaled antigen and modification of LAR by allergy immunotherapy. Prior to initiation of the study, each person received a complete history, chest x-ray, physical examination, and screening laboratory tests. They were skin-tested intracutaneously with a battery of allergens to confirm their sensitivities (positive = 5×5 mm wheal with erythema).

Bronchial Challenge

Each individual was challenged with the appropriate allergen (according to history and skin test reactivity) using a Johns Hopkins dosimeter and No. 42 DeVilbiss nebulizer. The challenge was stopped when the FE Vj had fallen 20 percent below diluent baseline or when the patient had received five breaths of 10,000 PNU/ml antigen. The BPC was performed in the early morning and the subject was then observed in the Clinical Research Center of the University of Iowa for 24 hours while pulmonary function test results were obtained throughout the night. Allergen responsiveness was quantitated for the EAR using provocative dose 20 percent FEVj (PDao). Since there is no well-accepted method for measuring LAR, we chose to use a graphic method for analysis which allowed quantitation in addition to measuring changes in the FEVi- The area (mm2) enclosed by the curve plotted as the change in FEVj over time from the highest FEV, following challenge to the FEVj recorded 24 hours after challenge was calculated with a digitizer (Fig 1).

Each subjects response to BPC was first evaluated using FEV. An EAR showed at least a 20 percent decrease from baseline. The LAR was defined here as at least a 10 percent decrease in FEVj from the lesser of diluent baseline or the new baseline established following recovery from the EAR. Using this information, each subject was classified as having an EAR, a LAR, or a dual response (both EAR and LAR). Airway responses using He-02 flow-volume measurements were then compared to those determined by changes in the FEV,.

Helium-Oxygen Flow Volume Loops

In addition to serial measurements with a Jones Pulmonor, the subjects also performed maximal exhalation maneuvers breathing both room air and a mixture of 80 percent helium and 20 percent oxygen (He-OJ during the course of each challenge day (before challenge, at peak early response, at late response [six hours postearly response] and 24 hours after challenge). Each subject performed these tests until two reproducible flow volume loops with each gas were obtained with FVCs which did not differ by more than 5 percent. The He-02 flow volume loops were obtained after three vital capacity inhalations of this gas mixture and always followed the air curves. The flow rates and volumes were measured with a Warren Collins computerized lung analyzer connected to an x-y recorder. This recorder generates flow-volume curves from computer memory using 12 counts (0.2 s) between points. Pen speed and response do not materially affect the shape or position of the curve beyond the peak flow. The response to He-02 at the middle of the vital capacity (AVmax 50 percent)910 and the volume of isoflow (VisoV) were calculated from superimposed curves aligned at their terminal ends (residual volume). For each study point, the two best air and He-02 curves (defined by the largest sum of FVC + FEVJ were used to calculate four values for AVmax 50 percent and VisoV. Then changes in AVmax 50 percent and VisoV in each subject during the challenge period were analyzed for significance using the one-way analysis of variance with replicate measures. The F values with a probability of 0.05 were considered significant, and the means were then compared using Duncans multiple comparison test to determine whether or not there were significant differences among the means during the study period. This approach corrected for the inherent variability in these tests and did not require any assumption about the magnitude of change necessary to identify a response.

We also plotted the LAR only and dual response groups separately using the percent change in FEVj and AVmax 50 percent from baseline over the 24-hour period following challenge. Since most subjects FEV, returned to a value greater than baseline one to two hours after challenge, we used this value as a new baseline with which to calculate further changes in FEV,. Similarly, for AVmax 50 percent, a new baseline value (whether it was higher or lower than the original baseline) was used for changes which occurred during the LAR (see Fig 1 for sample calculation). Comparisons of the change in FEV, and AVmax 50 percent were made using the two sample Students f-test, and p^0.05 was considered significant. Rank correlations were made using Kendalls method.

Responders and nonresponders were defined by the criteria of Despas et al. Those with a ^20 percent increase in Vmax 50 percent at the time of measurement were responders (density dependent), while those who had <20 percent increase in Vmax 50 percent were considered nonresponders (density independent).

Figure 1. Graph of data from patient 10 showing calculations of PD) (dotted line) by standard methods and the area of the late asthmatic response (2842 sq mm) (shown in diagonal lines) calculated with a Zeiss digitizer. The AVmax 50 percent is shown below the FEV, graph. The percent change in AVmax 50 percent is calculated from the baseline value at zero time for the increase observed immediately after challenge. The decrease in AVmax 50 percent at six hours and 24 hours is calculated from the value obtained after challenge as the new baseline value.

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Aerosolized Magnesium Sulfate for Acute Asthma: Introdaction

Asthma is a chronic respiratory disease that is characterized by periods of relative control and episodes of deterioration, which are referred to as exacerbations. Exacerbations range in severity from mild to severe (status asthmaticus), and can result in visits to health-care providers and emergency departments (EDs), and may at times require hospitalization. While rare, intubations, admissions to the ICU, and deaths from severe acute asthma still occur. In most people, even though the serious consequences are avoided, the prevention and treatment of asthma exacerbations are an important consideration of their disease. Due to this impact on lifestyle, the costs to the patient and the health-care system, and the potential for adverse outcomes, asthma is responsible for a significant personal and social burden.

Acute episodes of bronchoconstriction caused by airway inflammation are a hallmark of the exacerbation. These episodes generally result in increased requirements for inhaled β 2-agonist therapy. Unfortunately, in acute asthmatic episodes, this is often not enough to relieve the bronchospasm and reduce inflammation. The shortcomings of β2-agonist therapy have resulted in the use of a variety of other treatments in the management of acute asthma. For example, evidence has suggested that systemic cor-ticosteroids, anticholinergic agents delivery of β 2-agonist via metered-dose inhalers with holding chambers, and inhaled corticosteroids are effective in the short-term treatment of the disease. Other therapies, such as IV methylxanthine agents, are less effective and possibly harmful, so they are no longer recommended. In adults, evidence supporting the use of IV P2-agonists is limited, so these agents are reserved for selected patients (eg, intubated patients and those with severe disease). Finally, there are insufficient data to assess the effectiveness of antibiotic treatment in patients with acute asthma.

MgSO4 is an agent that has been proposed as a possible additive treatment in patients with acute asthma and has been shown to be effective in patients with severe acute asthma when delivered parenterally. Magnesium may be effective in acute asthma through one or more of a variety of mechanisms. Magnesium has been shown to relax the smooth muscle and may be involved with the inhibition of smooth muscle contraction. This theory has been proposed as an explanation for the effects of MgSO4 in patients with acute asthma; however, this explanation may be too simplistic. Magnesium is also involved with cellular homeostasis through its role as an enzymatic cofactor, as well as being involved in acetylcholine and histamine release, from cholinergic nerve terminals and mast cells, respectively. Investigators have proposed that the effect of MgSO4 is related to its ability to block the calcium ion influx to the smooth muscles of the respiratory system. Finally, the role of MgSO4 as an antiinflammatory has been identified in adults with asthma.

The potential clinical benefits of inhaled MgSO4 have been studied and research publications have produced conflicting results. Consequently, this agent is not currently recommended as part of the current guidelines and has not been used widely in most acute settings. Until now, there has been no attempt made to examine this effect in a systematic fashion. The few times that inhaled magnesium has been mentioned, it has been as a minor part of larger reviews. This systematic review is designed to examine this question and to provide summary estimates of the effect of aerosolized MgSO4 in the treatment of acute asthma.