Kövér G, Szemerédi K, Tost H
Acta Physiol Acad Sci Hung. 1982;59(2):119-29.
To determine whether renal prostaglandins participate in the regulation of renal blood flow, sodium and water excretion during "stress situation", renal function was investigated in two groups of anaesthetized dogs, subjected to minor and to more severe surgical stress under control conditions, and following the administration of 4 mg/kg indomethacin i.v. In the control studies, the renal haemodynamic parameters (CPAH, Cinulin), urine output and sodium excretion were not different in those animals in which the surgical traumatization was more severe from data obtained in similarly anaesthetized dogs. Extracellular volume expansion induced with i.v. infusion of Ringer solution enhanced sodium and water excretion in both groups, however, the increase of sodium excretion was less in the dogs subjected to more severe stress. During indomethacin infusion glomerular filtration did not change in either groups; CPAH decreased by 20-25% in the anaesthetized animals and 35-40% in dogs in which the surgical stress was more severe. In this group the total renal blood flow was reduced by 40% simultaneously with the haemodynamic changes; sodium and water excretion fell in both groups. After indomethacin infusion the diuretic response of the kidneys to extracellular volume expansion was markedly reduced in the anaesthetized dogs, the diuretic and natriuretic effects being almost completely inhibited in the animals subjected to more severe stress. These data suggest that in the anaesthetized dog endogenous prostaglandins may serve to maintain renal blood flow but not the glomerular filtration rate. Inhibition of prostaglandin synthesis during more severe stress results in increased renal vascular resistance and reduced renal blood flow. Accordingly, the data provide evidence that renal prostaglandins counteract in the kidney the vasoconstrictor mechanisms activated during more severe surgical traumatization. The data do not support the direct physiological role of prostaglandins in regulating tubular function.
为了确定肾脏前列腺素是否参与“应激状态”下肾血流量、钠和水排泄的调节,对两组麻醉犬的肾功能进行了研究。一组犬接受轻度手术应激,另一组接受更严重的手术应激,均处于对照条件下,并在静脉注射4mg/kg消炎痛后进行观察。在对照研究中,手术创伤更严重的动物的肾血流动力学参数(对氨基马尿酸清除率、菊粉清除率)、尿量和钠排泄与在同样麻醉的犬中获得的数据没有差异。静脉输注林格溶液诱导的细胞外液量扩张使两组的钠和水排泄均增加,然而,遭受更严重应激的犬的钠排泄增加较少。在输注消炎痛期间,两组的肾小球滤过均未改变;麻醉动物的对氨基马尿酸清除率下降了20%-25%,手术应激更严重的犬下降了35%-40%。在这组中,随着血流动力学变化,总肾血流量同时减少了40%;两组的钠和水排泄均下降。输注消炎痛后,麻醉犬肾脏对细胞外液量扩张的利尿反应明显降低,在遭受更严重应激的动物中,利尿和排钠作用几乎完全被抑制。这些数据表明,在麻醉犬中内源性前列腺素可能有助于维持肾血流量,但不能维持肾小球滤过率。在更严重应激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,这些数据证明肾脏前列腺素在肾脏中可对抗在更严重手术创伤期间激活的血管收缩机制。这些数据不支持前列腺素在调节肾小管功能方面的直接生理作用。