Shirley D G, Walter S J
Department of Physiology, Charing Cross and Westminster Medical School, London, UK.
Exp Physiol. 1995 Jul;80(4):619-30. doi: 10.1113/expphysiol.1995.sp003872.
The acute effects of haemorrhage (15 ml (kg body wt)-1) on renal function at whole-kidney and single-nephron levels were studied in Inactin-anaesthetized rats. In order to assess the role of vasopressin in mediating the haemodynamic effects, responses in untreated Long-Evans rats were compared with those in Brattleboro rats (which lack circulating vasopressin) and in Long-Evans rats treated with a V1 receptor antagonist. In time-control animals, there were no significant changes in mean arterial pressure (MAP), excretion rates, glomerular filtration rate (GFR), superficial-nephron GFR (SNGFR) or fluid reabsorption in the superficial proximal tubules during the course of the experiment. Following haemorrhage, the immediate reduction in MAP was followed in each group by partial recovery for 30 min; thereafter, MAP was stable. In untreated Long-Evans rats, haemorrhage was followed by a 26% reduction in GFR (P < 0.001, measured 60-150 min post-haemorrhage) and a larger reduction (45%, P < 0.001) in SNGFR, so that the SNGFR/GFR ratio fell significantly ((27.9 +/- 1.9) x 10(-6), control period; (20.2 +/- 2.2) x 10(-6) post-haemorrhage, P < 0.01). Slightly greater reductions in GFR and SNGFR were seen in Brattleboro rats and V1 antagonist-treated Long-Evans rats, which corresponded to slightly greater haemorrhage-induced reductions in blood pressure in these groups; the falls in the SNGFR/GFR ratio were similar to that in untreated Long-Evans rats. In all three groups of bled rats, fractional reabsorption by the proximal convoluted tubule increased slightly 30-60 min after haemorrhage, but during the subsequent period (60-150 min) returned to values indistinguishable from those during the control period. The results suggest that the renal haemodynamic changes that follow moderate haemorrhage include a preferential reduction in the GFR of superficial nephrons. Vasopressin appears to play no role in this response. Increases in fractional reabsorption in the proximal tubules are seen only during the immediate post-haemorrhage period.
在使用英纳克（Inactin）麻醉的大鼠中，研究了出血（15毫升/千克体重）对全肾和单肾单位水平肾功能的急性影响。为了评估血管加压素在介导血流动力学效应中的作用，将未处理的长-伊文斯（Long-Evans）大鼠的反应与布拉德福德（Brattleboro）大鼠（缺乏循环血管加压素）以及用V1受体拮抗剂处理的长-伊文斯大鼠的反应进行了比较。在时间对照动物中，实验过程中平均动脉压（MAP）、排泄率、肾小球滤过率（GFR）、浅表肾单位GFR（SNGFR）或浅表近端小管中的液体重吸收均无显著变化。出血后，每组MAP立即下降，随后部分恢复30分钟；此后，MAP保持稳定。在未处理的长-伊文斯大鼠中，出血后GFR降低26%（P<0.001，出血后60 - 150分钟测量），SNGFR降低幅度更大（45%，P<0.001），因此SNGFR/GFR比值显著下降（对照期为(27.9±1.9)×10⁻⁶；出血后为(20.2±2.2)×10⁻⁶，P<0.01）。在布拉德福德大鼠和用V1拮抗剂处理的长-伊文斯大鼠中，GFR和SNGFR的降低幅度略大，这与这些组中出血诱导的血压降低幅度略大相对应；SNGFR/GFR比值的下降与未处理的长-伊文斯大鼠相似。在所有三组出血大鼠中，出血后30 - 60分钟近端曲管的分数重吸收略有增加，但在随后的时期（60 - 150分钟）恢复到与对照期无差异的值。结果表明，中度出血后肾脏血流动力学变化包括浅表肾单位GFR的优先降低。血管加压素似乎在这种反应中不起作用。近端小管分数重吸收的增加仅在出血后的即刻出现。
