Swenson L J, Pantely G A, Anselone C G, Bristow J D
Am J Physiol. 1987 Jul;253(1 Pt 2):H58-65. doi: 10.1152/ajpheart.1987.253.1.H58.
To investigate the acute effects of complement activation on blood flow, we infused complement-activated plasma into the femoral artery of the isolated hindlimb of 19 anesthetized swine. Femoral artery blood flow decreased abruptly, was lowest at 1 min of the infusion, and thereafter slowly increased despite continued infusion. There was no significant change in femoral artery pressure or femoral vein pressure, confirming an acute increase in vascular resistance. Control infusion of heat-decomplemented-activated plasma caused no change in pressure or flow. Slope of the femoral artery pressure-flow relationship during maximal vasodilation with adenosine was significantly lower after infusion of complement-activated plasma, confirming a persistent increase in vascular resistance. Neither the acute nor the persistent increase in vascular resistance was prevented by alpha-adrenergic blockade with phentolamine or granulocytopenia produced by cyclophosphamide. We conclude that complement-activated plasma infusion in the femoral circulation causes an abrupt increase in vascular resistance that persists during pharmacologically maximal vasodilation, is not due to alpha-mediated vasoconstriction, and is not altered by severe granulocytopenia.
为研究补体激活对血流的急性影响，我们将补体激活的血浆注入19只麻醉猪的离体后肢股动脉。股动脉血流迅速减少，在注入1分钟时降至最低，此后尽管持续注入，血流仍缓慢增加。股动脉压力或股静脉压力无显著变化，证实血管阻力急性增加。注入经热灭活激活的血浆作为对照，压力和血流均无变化。在用腺苷进行最大程度血管舒张时，注入补体激活的血浆后股动脉压力-血流关系的斜率显著降低，证实血管阻力持续增加。用酚妥拉明进行α-肾上腺素能阻断或用环磷酰胺导致粒细胞减少，均不能阻止血管阻力的急性或持续增加。我们得出结论，在股循环中注入补体激活的血浆会导致血管阻力突然增加，这种增加在药理学上最大程度血管舒张时持续存在，不是由α介导的血管收缩引起，且不受严重粒细胞减少的影响。
