[Philip Tisdall, MD]

There are 3 means of slowing down the spread of the virus:

1. Social distancing

2. Washing hands with every contact and every hour irrespective of contact.

3. Masks. There are 2 types of droplets. Big ones that are gravity-driven to surfaces where they die in minutes (outside sunlight) or days (smooth metal surfaces). Small droplets that aerosolize as fomites and get transmitted from person to to person. All masks work on the big droplets. The quality of the mask matters for the fomites.

It is not a straight forward discussion. Remember that this is a very contagious virus (not measles contagious but still up there). This means that most of us will eventually get infected. All we are trying to do is slow the rate of infection enough that we do not exceed hospital capacity and to protect those with a serious risk of death (over age 75 with a comorbid condition).

After this, it is vaccine or herd immunity.

[Philip Tisdall, MD]

<div>Hello Jay,

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<div>That is a good insight on your part. It really is a poor explanation isn’t it? Here is my explanation:

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§ Blood flow is a balance of forces. Sympathetic stimulation typically has an α₁ receptor effect greater than the β₁ receptor effect, causing vasoconstriction. Muscarinic stimulation will also cause vasoconstriction. ANS stimulation is balanced by the local endothelial cell release of NO, prostaglandins and other substances giving overall vasodilation with an increase in heart rate.

<div>§ With endothelial dysfunction, there is impaired release of local vasodilators, leading to unopposed α₁ receptor effect, or in this case muscarinic stimulation, resulting in vasoconstriction and angina.

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<div>· This is the explanation of vasospastic angina (i.e. Prinzmetal angina), which is commonly associated with non-occlusive atherosclerosis.

<div>I hope this helps, Dr T

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[Philip Tisdall, MD]

<div>M3 works through a Gq receptor when there is no endothelial NO released due to dysfunction. This means that it acts through increased intracellular calcium, leading to vasoconstriction. Some blood vessels in the body are innervated by parasympathetic cholinergic fibers (e.g., coronary vessels). These nerves release ACh, which binds to muscarinic receptors on the smooth muscle and/or endothelium. It has been shown in many arterial vessels that M3 receptors located on the vascular endothelium are coupled to the formation of nitric oxide (NO), which causes vasodilation; however, ACh causes smooth muscle contraction through a smooth muscle M3 receptors (coupled to Gq-proteins and increased IP3) and M2 receptors (coupled to Gi-proteins and decreased cAMP) when formation of NO is blocked. This latter finding has been used to assess coronary vascular dysfunction in humans in which NO production is diminished in diseased coronary arteries. In contrast to other arteries, cerebral arteries appear to have M5 muscarinic receptors that produce vasodilation in response to ACh. (Source: https://www.cvphysiology.com/Blood%20Pressure/BP011b)</div>