Upregulation of alveolar liquid clearance after fluid resuscitation for hemorrhagic shock in rats

被引:43
作者
Modelska, K
Matthay, MA
McElroy, MC
Pittet, JF
机构
[1] SAN FRANCISCO GEN HOSP, DEPT ANESTHESIA, SAN FRANCISCO, CA 94110 USA
[2] SAN FRANCISCO GEN HOSP, DEPT MED, CARDIOVASC RES INST, SAN FRANCISCO, CA 94110 USA
[3] UNIV DUBLIN TRINITY COLL, DEPT PHYSIOL, DUBLIN 2, IRELAND
关键词
alveolar epithelium; sodium transport; beta-adrenergic receptor; pulmonary edema; acute lung injury;
D O I
10.1152/ajplung.1997.273.2.L305
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The primary objective of this study was to test the hypothesis that a catecholamine-dependent mechanism would upregulate alveolar liquid clearance after fluid resuscitation from 15 min of hemorrhagic shock. Anaesthetized rats were hemorrhaged to a mean arterial pressure of 35 mmHg for 15 min and were resuscitated with a 4% albumin solution. Alveolar liquid clearance was measured 5 h later by the concentration of protein in the distal airspaces over 1 h after instillation of a 5% albumin solution into one lung. Hemorrhaged rats developed a severe metabolic acidosis that was associated with a significant rise in plasma epinephrine levels throughout the study. There was a 60% increase in alveolar liquid clearance in hemorrhaged and resuscitated rats compared with control rats. Amiloride (10(-4) or 10(-6) M), propranolol (10(-4) M), or bilateral adrenalectomy inhibited the increase in alveolar liquid clearance. This effect was reproduced by the intravenous administration of epinephrine in adrenalectomized and hemorrhaged rats. Thus these data provide evidence for a catecholamine-dependent regulation of sodium transport that protects the airspaces against flooding several hours after fluid resuscitation from hemorrhagic shock.
引用
收藏
页码:L305 / L314
页数:10
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