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Am J Physiol Heart Circ Physiol 264: H1118-H1123, 1993;
0363-6135/93 $5.00
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AJP - Heart and Circulatory Physiology, Vol 264, Issue 4 1118-H1123, Copyright © 1993 by American Physiological Society

ARTICLES

Arteriolar endothelium-dependent vasodilation occurs during endotoxin shock

C. H. Baker and E. T. Sutton
Department of Physiology and Biophysics, College of Medicine, University of South Florida, Tampa 33612.

Endotoxin shock has been reported to alter endothelial structure as well as function of large arteries from in vitro experiments. Cremaster muscle arteriolar dilator reactivity of pentobarbital-anesthetized rats was determined by videomicroscopy at control and 30, 90, 150, and 210 min after intravenous infusion of Escherichia coli endotoxin (6 mg/kg, 1-h period). The dilator response was tested by intra-arterial injections of 90 ng acetylcholine (ACh). At control A1, A2, and A3 arterioles dilated 45, 21, and 34%, respectively. Postendotoxin arterial pressure decreased progressively, the A1 arterioles constricted (P < 0.05), A2 diameters were unchanged and A3 diameters increased. Postendotoxin ACh dilations averaged 28, 23, and 25%. A1 dilation was significantly (P < 0.05) less than at control. Methylene blue (2.5 mg ia) attenuated the ACh response at control, but after endotoxin an intense downstream vasoconstriction resulted in stasis and reduced survival time occurred. Hydroquinone (HQ) partially blocked the responses to ACh postendotoxin. HQ significantly increased the survival time postendotoxin. It is evident postendotoxin that the endothelia of arterioles are functional and able to release nitric oxide (NO) throughout the entire survival period. The microvascular release of NO and the dilation response to ACh were substantially attenuated by methylene blue and HQ. The latter may block the more lethal effects of the inducible NO synthase.


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