The effects of norepinephrine on active hyperemia in the canine gracilis muscle

S. F. Flaim, W. Crede, A. Beech, S. H. Nellis, R. Zelis

Research output: Contribution to journalArticle

10 Scopus citations

Abstract

We studied the effects of intra-arterial norepinephrine (NE) on skeletal muscle blood flow (BF), oxygen consumption (VO2), and arteriovenous oxygen difference (A-VO2) at rest and during exercise in an autoperfused canine gracilis muscle preparation. Static continuous exercise at a fixed level of maximal developed tension (P(0)) was induced by gracilis nerve stimulation; developed tension was monitored and used to control stimulation voltage. In one group of dogs (n = 10), data were collected before (rest) and at the end of each of a series of four 2-minute periods of exercise (10% P(0)) in each preparation. During both the rest and the exercise phases, continuous intra-arterial infusions of isotonic saline alone (control) and saline plus NE (0.11, 0.22, and 0.44 μg/min) were made. Control resting data were: BF= 5.90 ml/min; A-VO2 = 5.30 vol %; VO2= 0.31 ml/min. NE during rest reduced BF by 39-69%, increased A-VO2 by 79-91%, and reduced VO2 by an average of 41.9%. Control exercise data were: BF = 17.2 ml/min; A-VO2 = 11.2 vol %; VO2 = 1.96 ml/min. NE during exercise attenuated BF by 7-65% and widened A-VO2 by 22-35%. VO2 was maintained at control exercise levels during lower NE infusion levels but was attenuated by 56% at the highest NE level. In the second group of dogs (n = 8), data were collected at rest and at four times during a 10-minute exercise period (2.5% P(0)). NE (0.089, 0.17, and 0.34 μg/min) or saline (control saline) was infused for 2 minutes each during the final 7 minutes of exercise. At the lower NE doses, no significant difference was observed relative to the control-saline experiment. At the highest NE dose BF and VO2 were attenuated (BF: -22%, VO2: -20%), and A-VO2 was unchanged compared to control. The NE-induced attenuation in BF and VO2 during exercise may in part result from a mechanism similar to that which occurs in congestive heart failure in which an exaggerated sympathoadrenal response during exercise and an attenuated exercise-induced rise in forearm VO2 occurs.

Original languageEnglish (US)
Pages (from-to)660-666
Number of pages7
JournalUnknown Journal
Volume44
Issue number5
DOIs
StatePublished - Jan 1 1979

    Fingerprint

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this