Oliver J A, Sciacca R R, Pinto J, Cannon P J
J Clin Invest. 1981 Jan;67(1):229-37. doi: 10.1172/JCI110018.
To determine whether renal prostaglandins participate in the regulation of renal blood flow during acute reduction of cardiac output, cardiac venous return was decreased in 17 anesthetized dogs by inflating a balloon placed in the thoracic inferior vena cava. This maneuver decreased cardiac output from 3.69+/-0.09 liters/min (mean+/-SEM) to 2.15+/-0.19 liters/min (P < 0.01) and the mean arterial blood pressure from 132+/-4 to 111+/-5 mm Hg (P < 0.01) and increased total peripheral vascular resistance from 37.6+/-2.5 to 57.9+/-4.8 arbitrary resistance units (RU) (P < 0.01). In marked contrast, only slight and insignificant decreases in the renal blood flow from 224+/-16 to 203+/-19 ml/min and renal vascular resistance from 0.66+/-0.06 to 0.61+/-0.05 arbitrary resistance units (ru) were observed during inflation of the balloon. Concomitant with these hemodynamic changes, plasma renin activity and plasma norepinephrine concentration increased significantly in both the arterial and renal venous bloods. Plasma concentration of prostaglandin E(2) in renal venous blood increased from 34+/-6 to 129+/-24 pg/ml (P < 0.01). The subsequent administration of indomethacin or meclofenamate had no significant effect on mean arterial pressure, cardiac output, and total peripheral vascular resistance, but reduced renal blood flow from 203+/-19 to 156+/-21 ml/min (P < 0.01) and increased renal vascular resistance from 0.61+/-0.05 to 1.05+/-0.21 ru (P < 0.01). Simultaneously, the plasma concentration of prostaglandin E(2) in renal venous blood fell from 129+/-24 to 19+/-3 pg/ml (P < 0.01). Administration of indomethacin to five dogs without prior obstruction of the inferior vena cava had no effect upon renal blood flow or renal vascular resistance. The results indicate that acute reduction of cardiac output enhances renal renin secretion and the activity of the renal adrenergic nerves as well as renal prostaglandin synthesis without significantly changing renal blood flow or renal vascular resistance. Inhibition of prostaglandin synthesis during acute reduction of cardiac output results in an increased renal vascular resistance and reduced renal blood flow. Accordingly, that data provide evidence that renal prostaglandins counteract in the kidney the vasoconstrictor mechanisms activated during acute reduction of cardiac output.
为了确定在急性心输出量减少期间肾前列腺素是否参与肾血流量的调节，通过向置于胸段下腔静脉的球囊充气，使17只麻醉犬的心脏静脉回流量减少。此操作使心输出量从3.69±0.09升/分钟（平均值±标准误）降至2.15±0.19升/分钟（P<0.01），平均动脉血压从132±4降至111±5毫米汞柱（P<0.01），并使总外周血管阻力从37.6±2.5增加至57.9±4.8任意阻力单位（RU）（P<0.01）。与之形成显著对比的是，在球囊充气期间，仅观察到肾血流量从224±16降至203±19毫升/分钟以及肾血管阻力从0.66±0.06降至0.61±0.05任意阻力单位（ru）出现轻微且无显著意义的下降。伴随这些血流动力学变化，动脉血和肾静脉血中的血浆肾素活性及血浆去甲肾上腺素浓度均显著增加。肾静脉血中前列腺素E2的血浆浓度从34±6升至129±24皮克/毫升（P<0.01）。随后给予吲哚美辛或甲氯芬那酸对平均动脉血压、心输出量和总外周血管阻力无显著影响，但使肾血流量从203±19降至156±21毫升/分钟（P<0.01），并使肾血管阻力从0.61±0.05升至1.05±0.21 ru（P<0.01）。同时，肾静脉血中前列腺素E2的血浆浓度从129±24降至19±3皮克/毫升（P<0.01）。对5只未预先阻塞下腔静脉的犬给予吲哚美辛对肾血流量或肾血管阻力无影响。结果表明，急性心输出量减少可增强肾素分泌、肾肾上腺素能神经活性以及肾前列腺素合成，而肾血流量或肾血管阻力无显著变化。在急性心输出量减少期间抑制前列腺素合成会导致肾血管阻力增加和肾血流量减少。因此，这些数据提供了证据表明肾前列腺素在肾脏中可对抗急性心输出量减少期间激活的血管收缩机制。
