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Coronary vascular smooth muscle function in E. coli endotoxemia in dogs
J L Parker1, R S Keller, D V DeFily
1John M. Dalton Research Center, University of Missouri, Columbia 65211.
The American Journal of Physiology
|March 1, 1991
Summary
Acute endotoxemia impairs acetylcholine-mediated relaxation in canine coronary arteries, indicating altered endothelial-dependent vasodilation. This effect was not linked to oxygen free radicals or improved by antioxidant therapy.
Area of Science:
- Cardiovascular Physiology
- Endotoxic Shock
- Vascular Pharmacology
Background:
- Gram-negative endotoxemia causes systemic hypotension and cardiovascular depression.
- Coronary artery function may be altered during endotoxemia, impacting myocardial blood flow.
Purpose of the Study:
- To investigate if intrinsic contraction-relaxation properties of coronary arteries change during acute gram-negative endotoxemia.
- To assess the impact of endotoxemia on vascular smooth muscle responses to various stimuli.
Main Methods:
- Isolated canine coronary artery rings (large and small) from control and endotoxin-treated dogs were studied in vitro.
- Vascular smooth muscle responses were measured using isometric tension recordings after stimulation with K+, prostaglandin F2 alpha, nitroprusside, and acetylcholine.
Main Results:
- Endotoxemia did not alter length-active tension, vessel compliance, or responses to K+, prostaglandin F2 alpha, and nitroprusside.
- Relaxation responses to acetylcholine, an endothelial-dependent vasodilator, were significantly reduced in endotoxin-treated vessels.
- Antioxidant therapy did not improve the impaired acetylcholine-mediated relaxation.
Conclusions:
- Coronary arteries maintain normal contractile and basal vasodilator mechanisms during acute endotoxemia.
- Endotoxemia impairs endothelial-dependent vasodilation mediated by acetylcholine in coronary arteries.
- The impairment of acetylcholine-mediated relaxation is not caused by oxygen free radicals.