Vemulapalli S, Chiu P J, Barnett A
Hypertension. 1984 Jul-Aug;6(4):489-93. doi: 10.1161/01.hyp.6.4.489.
Platelet-activating factor (PAF) has hypotensive effects similar to those of antihypertensive polar renomedullary lipid (APRL), a potent endogenous hypotensive lipid. In this study the cardiovascular and renal effects of PAF were characterized in anesthetized dogs. Intravenous infusion of PAF at 0.1 micrograms/kg/min for 1 hour caused marked reduction in arterial blood pressure and cardiac output and was accompanied by minimal changes in heart rate. Concomitantly, renal blood flow, glomerular filtration rate, urine flow, and fractional excretion of Na+ and K+ fell significantly. Plasma renin activity was greatly stimulated (11.9 +/- 1.66 vs 3.26 +/- 0.45 ng/angiotensin I/ml/hr for the placebo group). There were no significant alterations in any of these parameters following PAF at a lower dose (0.03 micrograms/kg/min for 1 hour). In a separate study, PAF at 0.1 micrograms/kg/min for 20 minutes produced a decrease in left ventricular myocardial contractile force, concomitant with bradycardia and hypotension, which indicated the presence of a negative inotropic activity. It is concluded that systemic administration of PAF has a deleterious effect on kidney function due to arterial hypotension and diminished cardiac output.
血小板活化因子(PAF)具有与强效内源性降压脂质——降压极性肾髓质脂质(APRL)相似的降压作用。在本研究中,对麻醉犬体内PAF的心血管和肾脏效应进行了表征。以0.1微克/千克/分钟的速度静脉输注PAF 1小时,可导致动脉血压和心输出量显著降低,同时心率变化极小。与此同时,肾血流量、肾小球滤过率、尿流量以及Na⁺和K⁺的分数排泄均显著下降。血浆肾素活性受到极大刺激(安慰剂组为3.26±0.45纳克/血管紧张素I/毫升/小时,PAF组为11.9±1.66纳克/血管紧张素I/毫升/小时)。较低剂量(0.03微克/千克/分钟,持续1小时)的PAF给药后,这些参数均无显著变化。在另一项研究中,以0.1微克/千克/分钟的速度输注PAF 20分钟,可导致左心室心肌收缩力下降,同时伴有心动过缓和低血压,这表明存在负性肌力活性。研究得出结论,全身给予PAF会因动脉低血压和心输出量减少而对肾功能产生有害影响。