A closer look at the Bradykinin hypothesis
Very long, very wonky, very scary article.
You should read it anyway, and make your “COVID’s no big deal” friends read it too.
You really, really do not want to catch this virus.
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A closer look at the Bradykinin hypothesis
Very long, very wonky, very scary article.
You should read it anyway, and make your “COVID’s no big deal” friends read it too.
You really, really do not want to catch this virus.
The Scientific Research Notes Of S. Sunkavally (years: 2002-2011).
1902.
Angioedema
Angioedema with pruritus and urticaria is caused by mast cell activation (type I hypersensitivity). Opioids can directly activate mast cells.
Angioedema without pruritus and urticaria is due to excess bradykinin. ACE inhibitors and C1 inhibitor deficiency can cause excess bradykinin.
Angioedema is a rare and serious adverse effect of ACE inhibitor therapy. ACE inhibition increases bradykinin levels, which increase vascular permeability and lead to angioedema. Symptoms include tongue, lips, or eyelid swelling and, less frequently, laryngeal oedema and difficulty breathing. ACE inhibitors should be discontinued in affected patients.
ARBs do not cause excess bradykinin.
We are finally unravelling the mystery of what causes severe covid-19
We are finally unravelling the mystery of what causes severe covid-19
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By Mark Anderson
A computer graphic representation of the molecular structure of bradykinin
HANK MORGAN/SCIENCE PHOTO LIBRARY
An out-of-control human peptide called bradykinin could be responsible for some of the varied and sometimes deadly symptoms seen in people who have contracted the coronavirus. We already have drugs to control bradykinin, which are being tested as…
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https://www.the-scientist.com/news-opinion/is-a-bradykinin-storm-brewing-in-covid-19--67876
Lord, please let this be it. Please let bradykinin inhibitors be a good drug for COVID 😭😭
Excess of the inflammatory molecule bradykinin may explain the fluid build-up in the lungs of patients with coronavirus infections. Clinical
A closer look at the Bradykinin hypothesis
Responses of neurons in rostral ventrolateral medulla to activation of cardiac receptors in rats
De-pei li and Hui-lin pan
The aim of this study is to determine the afferent pathways underlying the activation of barosensitive neurons in the RVLM on stimulation of cardiac receptors in rats.
Epicardial application of bradykinin (BK) activated the cardiac receptors and thereby stimulated the barosensitive neurons in the RVLM. To determine the mechanism underlying this, cervical vagotomy and blockade of stellate ganglia was done.
Epicardial application of BK after cervical vagotomy did not alter the response of barosensitive neurons in the RVLM. But the bilateral blockade of stellate ganglia which is the major sympathetic afferent pathway by local infiltration of lidocaine eliminated the response of RVLM vasomotor neurons to the epicardial application of BK.
Based on these results it can be stated that epicardial application of BK stimulated majority of the barosensitive neurons in the RVLM and for this stimulation of neurons cardiac sympathetic afferents are essential.
This study demonstrates that sympathetic afferent pathway selectively excites the barosensitive neurons in the RVLM on stimulation of cardiac receptors.
Mahesh Kumar Sivasubramanian
Source: https://www.physiology.org/doi/full/10.1152/ajpheart.2000.279.5.H2549
Preconditioning Your Way to Better Stem Cells
Preconditioning Your Way to Better Stem Cells
When stem cells are implanted into injured tissues, they often face a hostile environment that is inimical to their survival. A stroke, for example, can produce brain tissue without ample blood flow, low oxygen levels, and lots of cell debris and inflammation. The same can be said for the heart after a heart attack. If stem cells are going to help anyone we have to find a way for them to survive.
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