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犬心源性水肿:肾血流及肾小球滤过液的分布

Cardiac edema in dogs: distribution of renal blood flow and glomerular filtrate.

作者信息

Boudreau R J, Mandin H

出版信息

Can J Physiol Pharmacol. 1979 Jan;57(1):71-7. doi: 10.1139/y79-011.

DOI:10.1139/y79-011
PMID:427647
Abstract

The injection of Freund's adjuvant into the pericardial sac of 29 dogs resulted in chronic pericardial tamponade with persistent sodium retention. Micropuncture, clearance, and radioactive microsphere experiments were initiated 6--13 days after pericardial injection and 60 min after pericardiocentesis. Pericardiocentesis increased sodium excretion (from 12.2 to 41.3 microequiv./min) and mean arterial pressure (+ 20 mmHg (1 mmHg = 133.322 Pa)). Central venous pressure decreased 6.5 mmHg, as did hematocrit (from 45.7 to 39.8%) and plasma protein concentration (from 5.88 to 5.15 g%). Pericardiocentesis had no significant effect on renal blood flow (RBF), nor plasma flow. Redistribution of glomerular filtrate was suggested by the observation that superficial nephron glomerular filtration rate increased (from 91 to 108 nL/min) while glomerular filtration rate remained unaltered. Determination of intrarenal distribution of RBF revealed that cortical blood flow also distributed superficially. A significant increase in the fraction of RBF perfusing zone 1 (outer cortex) and a decrease in fractional perfusion of zones 2, 3 and 4 (juxtamedullary cortex) were observed in each experiment following pericardiocentesis. RBF distribution examined in a series of six animals prior to and during the development of pericardial tamponade showed the opposite effect. These results indicate that pericardiocentesis causes redistribution of both glomerular filtrate and RBF to superficial nephrons. The development of pericardial tamponade was associated with increased fractional juxtamedullary blood flow. These changes may have been the result of altered blood pressure, hematocrit, plasma protein concentration, or altered renal resistance.

摘要

向29只犬的心包腔内注射弗氏佐剂,导致慢性心包填塞并伴有持续性钠潴留。在心包注射后6 - 13天以及心包穿刺后60分钟,开始进行微穿刺、清除率和放射性微球实验。心包穿刺增加了钠排泄(从12.2微当量/分钟增至41.3微当量/分钟)以及平均动脉压(升高20 mmHg(1 mmHg = 133.322 Pa))。中心静脉压降低了6.5 mmHg,血细胞比容(从45.7%降至39.8%)和血浆蛋白浓度(从5.88 g%降至5.15 g%)也降低。心包穿刺对肾血流量(RBF)和血浆流量均无显著影响。浅表肾单位肾小球滤过率增加(从91 nL/分钟增至108 nL/分钟),而肾小球滤过率保持不变,提示肾小球滤液发生了重新分布。对RBF肾内分布的测定显示,皮质血流也向浅表分布。每次心包穿刺实验后均观察到,灌注1区(外皮质)的RBF比例显著增加,而2区、3区和4区(近髓皮质)的灌注分数降低。在一系列6只动物的心包填塞形成之前和过程中对RBF分布进行检查,结果显示出相反的效应。这些结果表明,心包穿刺导致肾小球滤液和RBF均重新分布至浅表肾单位。心包填塞的发展与近髓血流量分数增加有关。这些变化可能是血压、血细胞比容、血浆蛋白浓度改变或肾阻力改变所致。

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