SYSTEMIC HYPOXIA ACTIVATES A CORONARY VASOCONSTRICTOR REFLEX RESPONSE THAT IS BLOCKED BY PRAZOSIN

被引:10
作者
DOWNEY, HF
GRICE, DP
JONES, CE
机构
[1] Department of Physiology, Texas College of Osteopathic Medicine, Fort Worth, TX
关键词
CHEMORECEPTOR REFLEX; CORONARY BLOOD FLOW; MYOCARDIAL OXYGEN CONSUMPTION; ALPHA-1-ADRENOCEPTOR BLOCKADE; DOGS;
D O I
10.1097/00005344-199111000-00002
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
We assessed the presence of an alpha-1-adrenoceptor-mediated coronary vasoconstrictor reflex response during acute systemic hypoxia in eight chloralose-anesthetized dogs. We avoided local vasodilator responses to myocardial and coronary hypoxia and to circulating factors by perfusing the left common coronary artery at constant pressure with normoxic blood while the dogs were ventilated with 5% O2-95% N2. Left ventricular afterload was held constant by withdrawing arterial blood during hypoxia-induced peripheral vasoconstriction. Left ventricular (LV) preload, as indicated by left atrial pressure, was unchanged. Beta-adrenoceptor-mediated coronary dilation and positive chronotropic and inotropic responses to hypoxia were blocked by propranolol. Parasympathetic-mediated coronary dilation and bradycardia were blocked by atropine. Under these conditions, systemic hypoxia caused a 19.7 +/- 2.1% decrease in left common coronary blood flow. Blockade of left coronary alpha-1-adrenoceptors with prazosin prevented coronary vasoconstriction during repeated systemic hypoxia. In four other similarly prepared dogs, repeated systemic hypoxia without alpha-1-adrenoceptor blockade reproducibly reduced left coronary blood flow 16.3 +/- 3.5 and 15.7 +/- 3.1%, respectively. The results of this investigation provide the first evidence of a coronary vasoconstrictor reflex response to systemic hypoxia. This response is mediated by alpha-1-adrenoceptors.
引用
收藏
页码:657 / 664
页数:8
相关论文
共 36 条
[1]   EFFECT OF HYPOXIA ON REGIONAL DISTRIBUTION OF CARDIAC-OUTPUT IN DOG [J].
ADACHI, H ;
STRAUSS, HW ;
OCHI, H ;
WAGNER, HN .
CIRCULATION RESEARCH, 1976, 39 (03) :314-319
[2]  
BERNE RM, 1979, HDB PHYSL 2, V1, P873
[3]  
BEVAN JA, 1978, BLOOD VESSELS, V15, P17
[4]  
CAMBRIDGE D, 1977, BRIT J PHARMACOL, V59, pP514
[5]  
CRYSTAL GJ, 1986, P SOC EXP BIOL MED, V182, P17
[6]  
DOHERTY JU, 1984, J LAB CLIN MED, V104, P665
[7]   NONISCHEMIC MYOCARDIAL HYPOXIA - CORONARY DILATION WITHOUT INCREASED TISSUE ADENOSINE [J].
DOWNEY, HF ;
CRYSTAL, GJ ;
BOCKMAN, EL ;
BASHOUR, FA .
AMERICAN JOURNAL OF PHYSIOLOGY, 1982, 243 (04) :H512-H516
[8]   CARDIOVASCULAR RESPONSES TO HYPOXIC STIMULATION OF CAROTID BODIES [J].
DOWNING, SE ;
REMENSNYDER, JP ;
MITCHELL, JH .
CIRCULATION RESEARCH, 1962, 10 (04) :676-&
[9]   BARORECEPTOR AND CHEMORECEPTOR INFLUENCES ON SYMPATHETIC DISCHARGE TO HEART [J].
DOWNING, SE ;
SIEGEL, JH .
AMERICAN JOURNAL OF PHYSIOLOGY, 1963, 204 (03) :471-&
[10]   CORONARY VASCULAR AND MYOCARDIAL RESPONSES TO CAROTID-BODY STIMULATION IN DOG [J].
EHRHART, IC ;
PARKER, PE ;
WEIDNER, WJ ;
DABNEY, JM ;
SCOTT, JB ;
HADDY, FJ .
AMERICAN JOURNAL OF PHYSIOLOGY, 1975, 229 (03) :754-760