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急性输尿管梗阻对大鼠肾脏肾小球血流动力学的影响。

Effects of acute ureteral obstruction on glomerular hemodynamics in rat kidney.

作者信息

Dal Canton A, Stanziale R, Corradi A, Andreucci V E, Migone L

出版信息

Kidney Int. 1977 Dec;12(6):403-11. doi: 10.1038/ki.1977.131.

Abstract

In order to study the effects of acute ureteral obstruction on glomerular hemodynamics, glomerular hydrostatic capillary pressure (PG), pressure in the first-order peritubular capillaries (EAP), and intratubular pressure (PT) were directly measured in superficial nephrons on Munich-Wistar rats by micropuncture with a servo-nulling device, in control conditions and one to two hours after ureteral ligation. Single nephron filtration fraction (SNFF) was calculated from arterial and peritubular blood protein concentration. SNGFR was measured by conventional micropuncture techniques in control conditions and was calculated from efferent arteriole blood flow (EABF) and SNFF during ureteral obstruction. EABF was obtained by timed complete collection of blood from superficial efferent arterioles. Afferent arteriole blood flow (AABF) and resistance of afferent (Ra) and efferent arterioles (Re) were calculated from conventional equations. Ureteral obstruction markedly increased PT from 12.9 +/- 1.4 to 36.8 +/- 6.1 (SD) mm Hg. The fall in SNGFR (from 23.3 +/- 6.4 to 17.9 +/- 5.2 [SD] nl/min) was blunted by the rise in PG (from 45.5 +/- 3.6 to 59.3 +/- 4.0 [SD] mm Hg) and AABF (from 130.0 +/- 59.1 to 144.2 +/- 69.0 [SD] nl/min), secondary to a fall in Ra. These results demonstrate that SNGFR is maintained early after complete ureteral obstruction because of afferent arteriole dilatation.

摘要

为了研究急性输尿管梗阻对肾小球血流动力学的影响,通过使用伺服归零装置进行微穿刺,在对照条件下以及输尿管结扎后一到两小时,直接测量慕尼黑-威斯塔大鼠浅表肾单位的肾小球毛细血管静水压(PG)、一级肾小管周围毛细血管压力(EAP)和肾小管内压力(PT)。根据动脉血和肾小管周围血的蛋白质浓度计算单肾单位滤过分数(SNFF)。在对照条件下通过传统微穿刺技术测量单个肾单位肾小球滤过率(SNGFR),并在输尿管梗阻期间根据出球小动脉血流量(EABF)和SNFF计算得出。通过定时完全收集浅表出球小动脉的血液获得EABF。根据传统公式计算入球小动脉血流量(AABF)以及入球小动脉(Ra)和出球小动脉(Re)的阻力。输尿管梗阻使PT从12.9±1.4显著升高至36.8±6.1(标准差)mmHg。PG升高(从45.5±3.6升高至59.3±4.0[标准差]mmHg)和AABF升高(从130.0±59.1升高至144.2±69.0[标准差]nl/min),继发于Ra下降,使得SNGFR的下降(从23.3±6.4降至17.9±5.2[标准差]nl/min)受到抑制。这些结果表明,在完全性输尿管梗阻后早期,由于入球小动脉扩张,SNGFR得以维持。

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