VASOACTIVE HORMONES IN THE RENAL RESPONSE TO SYSTEMIC SEPSIS
VASOACTIVE HORMONES IN THE RENAL RESPONSE TO SYSTEMIC SEPSIS
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DOI：
10.1016/s0272-6386(88)80170-7
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发表时间：
1988-01-01
影响因子：
13.2
通讯作者：
LINTON, AL
中科院分区：
文献类型：
--
作者：
CUMMING, AD;DRIEDGER, AA;LINTON, AL
全身性脓毒症中肾功能不全的病理生理学仍不清楚。在这项研究中，在20只容量负荷绵羊手术诱导腹膜炎后24小时，观察到三种肾功能模式。在第1组（n = 8）中，肾小球滤过率（GFR）下降70%，尿量下降85%，绝对钠排泄量下降95%，部分钠排泄量下降83%。第2组（n = 4）表现出类似的钠潴留，但GFR没有下降。第3组（n = 8）显示GFR或尿量无变化，仅极轻微地减少钠排泄。仅第1组平均动脉压下降17%;所有组的中心静脉压、肺毛细血管楔压和血浆容量均维持在或高于术前值。心脏指数增加或不变，所有组的肾血浆流量均维持不变;因此，没有血液动力学证据表明容量收缩。组织学检查仅显示轻微变化，无一致模式。肾功能变化与严重脓毒症的其他表现相关-GFR和钠潴留与心脏指数增加、全身血管阻力降低、肺动脉高压、白细胞减少、低蛋白血症和低血糖显著相关。所有这些变化在第1组中最为显著。在第1和第2组中，血浆肾素活性（PRA）增加，尿激肽释放酶排泄减少。PRA与GFR、尿量和钠排泄呈负相关;尿激肽释放酶排泄与尿量和钠排泄呈正相关。第1组和第2组中6-keto-PGF 1 α的尿排泄增加，并与第1组动物的平均动脉压呈负相关。在脓毒症期间，所有组的尿血栓素B2排泄量均保持在脓毒症前水平。结果表明，不寻常的相互变化的活动的肾素-血管紧张素和肾激肽释放酶-激肽系统可能发挥了作用，在肾反应败血症。PGI 2合成增加，可能影响全身血流动力学和肾功能;血栓素A2在此背景下的作用尚不清楚。
The pathophysiology of renal dysfunction in generalized sepsis remains unknown. In this study, 24 hours after surgical induction of peritonitis in 20 volume-loaded sheep, three patterns of renal function were seen. In group 1 (n = 8), glomerular filtration rate (GFR) decreased by 70%, urine volume by 85%, absolute sodium excretion by 95%, and fractional sodium excretion by 83%. Group 2 (n = 4) exhibited similar sodium retention but GFR did not fall. Group 3 (n = 8) showed no change in GFR or urine volume and only minimally reduced sodium excretion. Mean arterial pressure fell 17% in group 1 only; central venous pressure, pulmonary capillary wedge pressure, and plasma volume were maintained at or above presepsis values in all groups. Cardiac index was either increased or unchanged, and renal plasma flow was maintained in all groups; there was thus no hemodynamic evidence to suggest volume contraction. Histologic examination showed only minor changes with no consistent pattern. Renal functional changes correlated with other manifestations of severe sepsis—GFR and sodium retention correlated significantly with increased cardiac index, decreased systemic vascular resistance, pulmonary arterial hypertension, leukopenia, hypoproteinemia, and hypoglycemia. All of these changes were most marked in group 1. In groups 1 and 2, plasma renin activity (PRA) increased and urinary kallikrein excretion decreased. PRA correlated inversely with GFR, urine volume, and sodium excretion; urinary kallikrein excretion correlated positively with urine volume and sodium excretion. Urinary excretion of 6-keto-PGF1α was increased in groups 1 and 2 and correlated inversely with mean arterial pressure in group 1 animals. During sepsis, urinary thromboxane B2excretion continued at presepsis values in all groups. The results suggest that unusual reciprocal changes in activity of the renin-angiotensin and renal kallikrein-kinin systems may play a role in the renal response to sepsis. PGI2synthesis is increased and may affect systemic hemodynamics and renal function; the role of thromboxane A2in this context is unknown.