Treatment of Shock- Vasopressin Question

[PrePharmStu2009]

Hi I am a student and I kind of have been stuck on a concept and having a hard time making it clear, so hopefully some medical students or doctors can help me. My question is during shock such as sepsis shock or any type of shock, the body loses a lot of blood internally or externally. So through my research Vasopressin is used to " increase peripheral vascular resistance, which in turn increases arterial blood pressure "

So if we increase peripheral vascular resistance, does it mean the body is actually causing coronary artery, arteries to the brain, kidney to DILATE since they are vital organs? Then How does the Vasopressin only cause peripheral vasoconstriction (to skin ?) and not cause constriction of coronary artery or arteries to brain ? My thought is if during shock vasopressin is given, it will causes ALL arteries and veins to constrict which will make it harder to supply blood to heart and all organs causing person to die. This is obviously a wrong thought but I am just trying to understand exactly what is happening when we use drugs such as Vasopressin or epinephrine, Dobutrex to increase blood pressure.

And if coronary artery for example is dilated, then wouldn't the blood have harder time flowing through the artery. Yes, it will be easier for blood to fit, but from understanding the constrictions of smooth vessels is needed to propel blood through the artery otherwise blood will stay stagnant such as in orthostatic hypotension, where arteries are not constricted enough to propel the blood to organs above the heart such as the brain, and blood pools toward the legs? So these are two contradictory statements on what actually is occurring during treatment of shock. Thank you your help.

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[leviathan]

You do not have vasoconstriction to coronary vessels in shock. It has to do with which specific adrenergic receptors are present on which blood vessels, and what those receptors do in response to hormones. The coronary vessels are actually rich in beta receptors but weak in alpha receptors, so the presence of non receptor-specific catecholamines like epinephrine or even norepinephrine will lead to vasodilation of these arteries (which is a beta effect), and not vasoconstriction (which is an alpha effect).

In a shock state, or when adding a pressor agent, you get constriction of arterioles to non-vital organs, and this blood is then redirected to organs like the heart where you don't get that constriction, or in some cases you may get dilation. Blood, like any fluid, or even electrical current, flows through the path of least resistance. So in this case it will be flowing to the heart and other vital organs.

 

[Paseo Del Norte]

Vasopressin is a bit different from say norepinephrine activating an alpha receptor in a blood vessel. Vasopressin has it's own receptors; however, I believe they are G protein coupled like the adrenergic receptors. As I understand vasopressin does cause constriction in some vascular beds and dilation in others. I am not sure this is completely understood but I believe it is related to the release of nitric oxide in certain vascular beds.

Also, dobutamine actually consists of two isomers that have opposing alpha 1 effects, so blood pressure may not change like you may thing. Additionally, I believe dobutamine has mild vasodilation like effects. It's more of a contractility agent than a true pressor that you would expect to increase SVR.

Not sure if this post adds anything significant to the conversation, but I hope it helps in any event.