Effect of ibuprofen upon denervated skeletal muscle resistance and compliance vessels during endotoxemia.
The primary aim of these studies was to specifically evaluate the non-neural role of the cyclooxygenase products on the peripheral vascular decompensation associated with endotoxemia. The constant-flow perfused, vascularly isolated, denervated double-canine gracilis muscle preparation in which one muscle is used as a control for the contralateral side was employed. The experimental muscle (GMi) received ibuprofen while the control (GMc) was infused with the vehicle. The results of these studies suggest that endotoxin increases the arterial conductance (i.e., arterial dilation) by 100% and venous compliance (i.e., venoconstriction) by 40%. These observations, which are consistent with venous pooling, were not significantly altered by the continuous intra-arterial infusion of ibuprofen at a peripheral blood concentration of 160 microM. Ibuprofen caused a small but statistically significant increase in the conductance/compliance ratio at 60, 75, and 90 min post endotoxin, suggesting that cyclooxygenase products may play a minor role in the non-neural regulation of capillary fluid dynamics during endotoxemia. Consequently, these studies do not provide convincing evidence that would support a non-neural cyclooxygenase role in the peripheral vascular decompensation reported to occur during systemic endotoxemia.
Bond
R F
RF
Department of Physiology, School of Medicine, University of South Carolina, Columbia 29208.
Krech
L H
LH
Hershey
J C
JC
D000818:Animals; D001158:Arteries / Q000187:drug effects*; D003714:Denervation; D004195:Disease Models, Animal; D004285:Dogs; D004731:Endotoxins / Q000494:pharmacology*; D007052:Ibuprofen / Q000494:pharmacology*; D008833:Microcirculation; D009132:Muscles / Q000187:drug effects*; D012772:Shock, Septic / Q000503:physiopathology*; D014680:Veins / Q000187:drug effects*; D014690:Venous Pressure / Q000187:drug effects
D004731:Endotoxins; D007052:Ibuprofen