Lonigro A J, Brash D W, Stephenson A H, Heitmann L J, Sprague R S
Am J Physiol. 1982 Jan;242(1):F38-45. doi: 10.1152/ajprenal.1982.242.1.F38.
In anesthetized laparotomized male mongrel dogs with ventilatory rate set at 10 breath.min-1, tidal volume was adjusted so that control arterial pH and PCO2 were within the normal range for unanesthetized dogs. Control renal venous PGE2 and PGF2 alpha concentrations were comparable to those of unanesthetized dogs, namely, 57 +/- 10 and 114 +/- 18 pg.ml-1, respectively. In contrast, control arterial plasma renin activity (PRA), 6.6 +/- 1.2 ng.ml-1.h-1, was considerably greater than in unanesthetized dogs. Stepwise increases in ventilatory rate increased renal venous PGE2 and PGF2 alpha to 109 +/- 18 and 205 +/- 41 pg.ml-1, respectively. Hyperventilation reduced PCO2 and increased pH and PRA but had no effect on renal blood flow, arterial blood pressure, or arterial PGE2 and PGF2 alpha concentrations. When the ventilatory rate was returned to control levels, pH, PCO2, PRA, and renal venous PGE2 and PGF2 alpha concentrations returned to control. Ventilatory rate or some consequence of altering ventilatory rate is, therefore, a determinant of renal venous efflux of PGE2 and PGF2 alpha. Moreover, it may be a more important determinant of "resting" concentrations of prostaglandins in renal venous blood than anesthesia, laparotomy, or PRA.
在通气频率设定为10次/分钟的麻醉开腹雄性杂种犬中,调整潮气量以使对照动脉血pH值和PCO₂处于未麻醉犬的正常范围内。对照肾静脉PGE₂和PGF₂α浓度与未麻醉犬相当,分别为57±10和114±18 pg/ml。相比之下,对照动脉血浆肾素活性(PRA)为6.6±1.2 ng/ml·h⁻¹,明显高于未麻醉犬。通气频率逐步增加使肾静脉PGE₂和PGF₂α分别增至109±18和205±41 pg/ml。过度通气降低了PCO₂,提高了pH值和PRA,但对肾血流量、动脉血压或动脉PGE₂和PGF₂α浓度没有影响。当通气频率恢复到对照水平时,pH值、PCO₂、PRA以及肾静脉PGE₂和PGF₂α浓度均恢复到对照值。因此,通气频率或改变通气频率的某些后果是肾静脉PGE₂和PGF₂α流出量的一个决定因素。此外,与麻醉、开腹手术或PRA相比,它可能是肾静脉血中前列腺素“静息”浓度更重要的决定因素。