ROLES OF HEMODYNAMIC AND TUBULAR FACTORS IN GENTAMICIN-MEDIATED NEPHROPATHY

被引：18

作者：

HISHIDA, A ^{[1
]}

NAKAJIMA, T ^{[1
]}

YAMADA, M ^{[1
]}

KATO, A ^{[1
]}

HONDA, N ^{[1
]}

机构：

[1] HAMAMATSU UNIV SCH MED, DEPT MED 1, HAMAMATSU, SHIZUOKA, JAPAN

来源：

RENAL FAILURE | 1994年 / 16卷 / 01期

关键词：

AMINOGLYCOSIDE; HYDROXYL RADICAL; RENAL BLOOD FLOW; RENIN-ANGIOTENSIN SYSTEMS; TUBULAR NECROSIS;

D O I：

10.3109/08860229409044852

中图分类号：

R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];

学科分类号：

1002 ; 100201 ;

摘要：

Gentamicin (GM) often causes polyuric acute renal failure (ARF) in humans and animals. GM-mediated ARF in rats was accompanied with activated renin-angiotensin system, increased renal endothelin content, and enhanced lipid peroxidation. Suppression of the renin-angiotensin activity by desoxycorticosterone acetate and saline drinking, and treatment with superoxide dismutase attenuated the GM-induced decline in whole-kidney GFR with well-maintained RBF but did not reduce the severity of tubular necrosis. On the other hand, treatment with dimethylthiourea, a hydroxyl radical scavenger, attenuated the GM-mediated decline in GFR and lessened tubular necrosis but did not ameliorate the reduction in RBF. These data suggest contributions of both vascular and tubular factors to the GM-induced decline in GFR in rats. However, relative importance of these factors probably differs with different doses of the agent.

引用

页码：109 / 116

页数：8

共 24 条

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