The exercising heart at altitude

被引：26

作者：

Calbet, Jose A. L. ^{[1
,2
]}

Robach, Paul ^{[3
,4
]}

Lundby, Carsten ^{[2
,5
]}

机构：

[1] Univ Las Palmas Gran Canaria, Dept Phys Educ, Las Palmas Gran Canaria 35017, Canary Islands, Spain

[2] Rigshosp, Copenhagen Muscle Res Ctr, DK-2200 Copenhagen N, Denmark

[3] Ecole Natl Ski & Alpinisme, Chamonix Mt Blanc, France

[4] Univ Paris 13, ARPE, EA 2363, Lab Reponses Cellulaires & Fonct Hypoxie, Bobigny, France

[5] Aarhus Univ, Dept Sport Sci, Aarhus N, Denmark

来源：

CELLULAR AND MOLECULAR LIFE SCIENCES | 2009年 / 66卷 / 22期

关键词：

Hypoxia; Contractility; Cardiac output; Nitric oxide; Cardioprotection; Infarct; Oxygen; Adenosine; NITRIC-OXIDE SYNTHASE; PULMONARY GAS-EXCHANGE; MUSCLE BLOOD-FLOW; PROTEIN-KINASE-C; MYOCARDIAL OXYGEN-CONSUMPTION; ISCHEMIA-REPERFUSION INJURY; HYPOXIA-INDUCIBLE FACTOR-1; INDUCED ARTERIAL HYPOXEMIA; RAT VENTRICULAR MYOCYTES; BRAIN-STEM PREPARATION;

D O I：

10.1007/s00018-009-0148-6

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Maximal cardiac output is reduced in severe acute hypoxia but also in chronic hypoxia by mechanisms that remain poorly understood. In theory, the reduction of maximal cardiac output could result from: (1) a regulatory response from the central nervous system, (2) reduction of maximal pumping capacity of the heart due to insufficient coronary oxygen delivery prior to the achievement of the normoxic maximal cardiac output, or (3) reduced central command. In this review, we focus on the effects that acute and chronic hypoxia have on the pumping capacity of the heart, particularly on myocardial contractility and the molecular responses elicited by acute and chronic hypoxia in the cardiac myocytes. Special emphasis is put on the cardioprotective effects of chronic hypoxia. (Part of a multi-author review.).

引用

页码：3601 / 3613

页数：13

共 195 条

[71] Muscarinic cholinergic regulation of cardiac myocyte ICa-L is absent in mice with targeted disruption of endothelial nitric oxide synthase [J].