不同手术应激水平下吲哚美辛对肾功能的影响。

G Kövér, K Szemerédi, H Tost
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摘要

为了确定肾前列腺素是否参与“应激状态”下肾血流量、钠和水排泄的调节,研究了两组麻醉犬的肾功能,在对照组条件下,分别给予轻度和较重度手术应激,并静脉注射4 mg/kg吲哚美辛。在对照组研究中,肾脏血流动力学参数(CPAH、肉桂碱)、从同样麻醉的狗中获得的数据来看,手术创伤更严重的动物的尿量和钠排泄没有什么不同。在两组中,静脉滴注林格氏液诱导的细胞外体积扩大均能促进钠和水的排泄,但在应激较重的犬中,钠排泄的增加较少。在输注吲哚美辛期间,两组患者肾小球滤过均无变化;麻醉动物的CPAH下降了20-25%,手术应激更严重的狗的CPAH下降了35-40%。在血流动力学改变的同时,该组肾总血流量减少40%;两组的钠和水排泄量均下降。在注射吲哚美辛后,麻醉犬的肾脏对细胞外体积扩张的利尿反应明显降低,在承受更严重应激的动物中,利尿和利钠作用几乎完全被抑制。这些数据表明,在麻醉的狗内源性前列腺素可能有助于维持肾血流量,但不是肾小球滤过率。在更严重的应激下抑制前列腺素合成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,证明肾前列腺素抵消肾脏中在更严重的手术创伤中激活的血管收缩机制。这些数据并不支持前列腺素在调节肾小管功能中的直接生理作用。
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Effect of indomethacin on renal function during different levels of surgical stress.

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.

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