Q: In anaphylaxis, why does the bronchial constrict and capillaries dilate?

Q: It seems counter intuitive that in anaphylaxis, the systemic capillaries dilate and the bronchial constrict. Histamine signals dilation (relaxation of the smooth muscles) of blood vessels, and increased permeability of capillaries, causing edema / inflammation. The bronchial tree also has smooth muscle around it, why would it constrict and the other relax?  Can the tissue around the body swell without causing the constriction of the blood vessels? And the lungs can’t do that?

A: You are not alone in your confusion.  One of the beauties (in a mysterious way) and perils of medicine is that logic does not always work or at least it becomes complicated and convoluted.

There are different kinds of receptors for specific chemicals; their locations vary by end organs.  In turn, not all end organs have the same distribution of these sites.  Although histamine is the quintessential mediator, there are a variety of others that either act directly or stimulate the release of other mediators resulting in organ responses and/or inflammation.  Responses are therefore dependent on the mediators and the location of the receptors.

As I understand it, vascular dilation and change in permeability is at the capillary bed level and is direct, perhaps related to nitric acid.  This is not a smooth muscle issue.  On the other hand, bronchoconstriction is based on muscular spasm and swelling the occurs as a result of fluid accumulation from leaky, dilated vessels in the bronchial capillary beds.

Epinephrine has its major effects directly via vascular constriction and bronchial dilation and indirectly by halting vascular leakage.  Epinephrine also helps to stabilize the mast cells from which histamine and other mediators are released.  The effects of antihistamines is more local and slower.

Bottom line: Don’t lose the forest for the trees.  Epinephrine works.




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