Vasoactive mediators and renal haemodynamics in exertional heat stroke complicated by acute renal failure

被引:23
作者
Lin, YF
Wang, JY
Chou, TC
Lin, SH
机构
[1] Tri Serv Gen Hosp, Div Nephrol, Dept Internal Med, Natl Def Med Ctr, Taipei, Taiwan
[2] Natl Def Med Ctr, Dept Physiol, Taipei, Taiwan
关键词
ANGIOTENSIN-CONVERTING ENZYME; LEFT-VENTRICULAR FUNCTION; NITRIC-OXIDE PRODUCTION; TUMOR-NECROSIS-FACTOR; ENDOTHELIAL-CELLS; HEMODYNAMICS; HEATSTROKE; SEPSIS; RHABDOMYOLYSIS; THROMBOMODULIN;
D O I
10.1093/qjmed/hcg029
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Background: Although vasoactive substances may be important in the pathogenesis of some types of acute renal failure (ARF), their potential role in exertional heat stroke (ExHS) with ARF has not been explored. Aim: To evaluate whether changes in concentration of individual vasoactive mediators correlated with alterations in renal function and haemodynamics in patients with ExHS and ARF. Design: Prospective case-control study. Methods: Systemic and renal haemodynamics, circulating vasoactive hormones and urinary vasodilator metabolites were determined in 12 military recruits who developed ExHS with ARF but without other organ failure during a three-year period. The control group consisted of 12 recruits who performed similar exercise under the same conditions without developing ExHS. Results: There were significant elevations in circulating pressor hormones (catecholamines, renin, aldosterone and endothelin-1 (ET-1)) and significant decreases in the vasodilatory hormone prostaglandin E-2 (PGE(2)) in the acute phase of ExHS with ARF when compared to ExC. There was also a significant rise in nitric oxide metabolites (NOx) in the acute phase of ExHS. All of these abnormalities in circulating hormones returned to normal range during the recovery phase of ExHS. The ERPF correlated positively with GFR and urinary PGE(2) and negatively with plasma catecholamines, renin, ET-1 and NOx. Discussion: The changes in the plasma levels of these hormones, together with enhanced NO production, may both contribute to the pathophysiology of ARF in ExHS.
引用
收藏
页码:193 / 201
页数:9
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