Cryer H M, Unger L S, Garrison R N, Harris P D
Department of Surgery, School of Medicine, University of Louisville, KY 40292.
Circ Shock. 1988 Sep;26(1):71-88.
Any beneficial effects of prostaglandin synthesis inhibitors on systemic hemodynamic derangements during sepsis may be offset by the effect of these inhibitors to reduce renal blood flow. To determine the specific role of prostaglandins in maintaining renal perfusion during hyperdynamic live Escherichia coli bacteremia in rats, we used in vivo video-microscopy and optical doppler velocimetry to quantitate changes in renal microvascular blood flow, and to determine if endogenous prostaglandins participate in these responses. E. coli infusions constricted preglomerular arterioles and decreased renal microvascular blood flow in decerebrate animals without drug anesthesia but dilated pre- and postglomerular arterioles in urethane-anesthetized rats. Local inhibition of renal prostaglandin production with mefenamate after E. coli infusion caused renal arteriolar constriction in both groups and decreased renal blood flow to indicate that renal prostaglandin production is an important mechanism for maintenance of renal microvascular blood flow during high cardiac output sepsis.
前列腺素合成抑制剂对脓毒症期间全身血流动力学紊乱的任何有益作用,可能会被这些抑制剂减少肾血流量的作用所抵消。为了确定前列腺素在大鼠高动力性活大肠杆菌菌血症期间维持肾灌注中的具体作用,我们使用体内视频显微镜和光学多普勒测速法来量化肾微血管血流的变化,并确定内源性前列腺素是否参与这些反应。在无药物麻醉的去大脑动物中,输注大肠杆菌会使肾小球前小动脉收缩并减少肾微血管血流,但在氨基甲酸乙酯麻醉的大鼠中,输注大肠杆菌会使肾小球前和肾小球后小动脉扩张。大肠杆菌输注后用甲灭酸局部抑制肾前列腺素生成,导致两组肾小动脉收缩并减少肾血流量,这表明肾前列腺素生成是高心输出量脓毒症期间维持肾微血管血流的重要机制。