Myers S I, Hernandez R, Horton J
Department of Surgery, University of Texas Southwestern Medical Center, Dallas 75235.
Prostaglandins Leukot Essent Fatty Acids. 1993 Jul;49(1):509-13. doi: 10.1016/0952-3278(93)90039-y.
This study examined the differential effects of endotoxin on renal and splanchnic vascular (SV + SI) eicosanoid synthesis. Dogs were anesthetized and subjected to a challenge of 1 mg/kg (i.v.) bolus of B-lipopolysaccharide endotoxin followed by a 3 h infusion of endotoxin at 0.5 mg/kg/h. The kidney and SV + SI were cannulated and perfused in vitro with Krebs buffer. The venous effluent from the kidney and SV + SI were assayed for 6-keto-PGF1a (PGI2), PGE2, Leukotriene B4 (LTB4), LTC4, and thromboxane B2 (TXB2) by enzyme immunoassay. Endotoxin treatment markedly increased splanchnic PGI2 release (splanchnic vasodilator) two fold and decreased release of all other measured eicosanoids. Endotoxin treatment markedly increased renal PGE2 (renal vasodilator) but did not significantly increase PGI2. These data showed that endotoxin treatment stimulated both the splanchnic vascular bed and kidney to increase synthesis and release of their major endogenous vasodilator eicosanoids.
本研究考察了内毒素对肾和内脏血管(脾静脉 + 肠系膜上静脉)类花生酸合成的不同影响。将犬麻醉后,静脉注射1 mg/kg的β-脂多糖内毒素推注剂量,随后以0.5 mg/kg/h的速度输注内毒素3小时。将肾脏和脾静脉 + 肠系膜上静脉插管,并用Krebs缓冲液进行体外灌注。通过酶免疫测定法检测肾脏和脾静脉 + 肠系膜上静脉的静脉流出液中的6-酮-前列环素F1α(PGI2)、前列腺素E2(PGE2)、白三烯B4(LTB4)、白三烯C4(LTC4)和血栓素B2(TXB2)。内毒素处理使内脏PGI2释放(内脏血管舒张剂)显著增加两倍,并使所有其他检测的类花生酸释放减少。内毒素处理显著增加了肾PGE2(肾血管舒张剂),但未显著增加PGI2。这些数据表明,内毒素处理刺激了内脏血管床和肾脏,使其增加主要内源性血管舒张类花生酸的合成和释放。