Secondary Logo

Journal Logo

Myers Paul R.; Gupta, Mukesh; Rogers, Scott; Mattox, Mildred L.; Adams, H. Richard; Parker, Janet L.
Original Article: PDF Only
Free

ABSTRACT

Endotoxin acutely decreases the production of nitric oxide, leading to abnormal regulation of coronary vascular tone; however, the effects of chronic endotoxemia on vasomotion are unknown. We therefore tested the hypothesis that chronic, low-level endotoxemia inhibits endothelium-dependent vasodilation. Rabbits were continuously infused with a subclinical dose of Escherichia coli endotoxin (.6 μg/kg/24 h, intraperitoneal) or saline for 5 wk. Endotoxin at this concentration elicited no significant sustained pyretic or hemodynamic responses. Both endothelium-dependent and independent vasomotor responses were determined in coronary arteries (250–500 μ). Vasorelaxation in response to acetylcholine, but not adenosine diphosphate (ADP), was significantly enhanced in endotoxin-challenged animals (EC50 = 62.6 ±11.1 nM, control vs. 33.97 ± 5.7 nM, endotoxin-challenged; p < .05). Vasoconstriction to PGF2±, but not KCI, was significantly decreased in endotoxin-challenged animals. These results indicate that endothelium-dependent and independent vasomotor responses are altered during chronic endotoxemia and are due, in part, to alterations in signal-transduction mechanisms specific for certain types of receptors.

©1996The Shock Society