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在实验性糖尿病中预防肾小球毛细血管高压可避免肾小球的功能和结构损伤。

Prevention of glomerular capillary hypertension in experimental diabetes mellitus obviates functional and structural glomerular injury.

作者信息

Dunn B R, Zatz R, Rennke H G, Meyer T W, Anderson S, Brenner B M

出版信息

J Hypertens Suppl. 1986 Dec;4(5):S251-4.

PMID:3033178
Abstract

Streptozotocin-diabetic rats kept moderately hyperglycaemic by daily injections of ultralente insulin for 4-6 weeks (group DM) demonstrated a higher glomerular transcapillary hydraulic pressure gradient (delta P), glomerular plasma flow rate and single-nephron glomerular filtration rate (GFR) than was observed in age- and weight-matched non-diabetic controls (group C). This rise in delta P was prevented by therapy with the angiotensin I converting enzyme inhibitor enalapril (15 mg/l drinking water, group DM + E) even though glomerular hyperperfusion and hyperfiltration persisted. Fourteen months after induction of diabetes, animals in group DM displayed high levels of albuminuria and an increased incidence of focal glomerular sclerosis; treatment with enalapril maintained these parameters at levels which did not differ from those observed in group C. We conclude that prevention of glomerular capillary hypertension with enalapril therapy obviates functional and structural glomerular injury in experimental diabetes mellitus.

摘要

通过每日注射超长效胰岛素使链脲佐菌素诱导的糖尿病大鼠持续中度高血糖4 - 6周(DM组),其肾小球跨毛细血管液压梯度(ΔP)、肾小球血浆流速和单肾单位肾小球滤过率(GFR)高于年龄和体重匹配的非糖尿病对照组(C组)。尽管肾小球高灌注和高滤过持续存在,但用血管紧张素I转换酶抑制剂依那普利治疗(15 mg/l饮用水,DM + E组)可防止ΔP升高。糖尿病诱导14个月后,DM组动物出现大量蛋白尿,局灶性肾小球硬化发生率增加;依那普利治疗使这些参数维持在与C组无差异的水平。我们得出结论,依那普利治疗预防肾小球毛细血管高血压可避免实验性糖尿病中肾小球的功能和结构损伤。

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