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Adaptation to hypoxia prevents endothelial dysfunction of coronary and non‐coronary blood vessels during myocardial ischemia and reperfusion injury

Prior adaptation to intermittent hypoxia (AIH) is cardioprotective during myocardial ischemia‐reperfusion injury (IR). This study investigated the possibility that AIH would lessen endothelial dysfunction (EDF) in rat hearts during IR. AIH was performed in a normobaric chamber (5–8 cycles/d for 20 d, FIO2 9.5–10% for 5–10 min/cycle, with intervening 4‐min normoxia). Endothelium‐dependent (ED) function of coronary blood vessels was evaluated by the flow response to acetylcholine (ACH) in Langendorf isolated hearts after in vitro IR. Also, ED relaxation of noradrenaline‐precontracted isolated aortic rings was evaluated by response to ACH after in situ myocardial IR. With no IR, coronary flow and response to ACH were similar in hearts of non‐AIH (n=9) and AIH (n=10) rats. IR injury decreased ED dilation of coronary arteries to 10.4±1.7% of the pre‐IR response to ACH in non‐AIH (n=10) rats and to 76±20% in AIH (n=9) rats (p<0.05). In the aorta, IR reduced ED relaxation from 45±4% (n=8) of the precontraction magnitude to 9.7±1.2% (n=10) in non‐AIH rats and to 30±3% (n=10) in AIH (p<0.05). Therefore, 1) IR heart injury induced EDF of both coronary and remote, non‐coronary blood vessels; and 2) AIH blunted EDF of both coronary and noncoronary vessels. These data suggest that adaptation to hypoxia is not only cardioprotective but also vasoprotective during myocardial IR injury. Supported by RFBR grant 10–04‐00980.