Paul J. Marks

Abstract

Although much is known about the factors involved in the control of blood flow, the cellular mechanisms of their action are poorly understood. This study investigated the mechanisms of norepinephrine, epinephrine, isoproterenol, and acetylcholine.

First, in a constant pressure/variable flow preparation we characterized the sheep brachial artery blood flow response to, and recovery from, 10-min infusions of each of these drugs. Then we used a computer model to simulate changes in blood flow in response to altered ion permeabilities or pump speeds (the mechanisms). We tried to produce responses like those to the drug infusions so that we could infer that the mechanisms invoked by the model were the ones involved in producing the experimental response.

Norepinephrine produces a rapid vasoconstriction and decrease in flow. There is a slight recovery during the infusion. The recovery takes several minutes and it is without overshoot. The response to epinephrine is diphasic. During the first minute there is a vasodilation and subsequent intense vasoconstriction which continues throughout the infusion. When the infusion is stopped there is a rapid recovery and an overshoot in flow. Isoproterenol results in an initial peak increase in flow during the first minute, hut recovers about one third of the increase and then steadily increases to the level of the original peak during the remainder of the infusion. There is a slow recovery. Acetylcholine also produces an extreme peak increase in flow, but about half of the increase is recovered in the first minute or two, and there is a slight decline during the remainder of the infusion. Flow recovers very rapidly when the infusion is stopped.

On the basis of our simulations our hypotheses are: (1) increased PNA is the major mechanism of norepinephrine action (alpha receptor); (2) stimulated Na-L ATPase is a major mechanism of isoproterenol (beta receptor), but not the only one' and (3) epinephrine involves a large stimulation of the Na pump and a small increase in PNA. We have no satisfactory hypothesis to offer for the mechanism of acetylcholine action.

LLU Discipline

Physiology

Department

Physiology

School

Graduate School

First Advisor

Robert A. Brace

Second Advisor

Gordon G. Power

Third Advisor

Ramon R. Gonzalez

Degree Name

Master of Science (MS)

Year Degree Awarded

1981

Date (Title Page)

6-1981

Language

English

Library of Congress/MESH Subject Headings

Blood Flow Velocity

Type

Thesis

Page Count

vii; 74

Digital Format

PDF

Digital Publisher

Loma Linda University Libraries

Usage Rights

This title appears here courtesy of the author, who has granted Loma Linda University a limited, non-exclusive right to make this publication available to the public. The author retains all other copyrights.

Collection

Loma Linda University Electronic Theses and Dissertations

Collection Website

http://scholarsrepository.llu.edu/etd/

Repository

Loma Linda University. Del E. Webb Memorial Library. University Archives

Download

Included in

Physiology Commons

Share

COinS