AIM To identify intermittent hypoxic conditions that provide myocardial protection without causing pulmonary hypertension.

METHODS Adult male C57 mice were randomly assigned to the normal oxygen control group and groups exposed respectively to hypoxia at altitudes of 3000 m, 4000 m and 5000 m for a duration of 4 hours per day. Intercostal puncture was performed to measure the right ventricular systolic pressure as an indicator of pulmonary artery pressure changes. Following myocardial ischemia-reperfusion, the extent of myocardial infarction was assessed using Evans blue-TTC double staining and serum troponin I levels were measured using ELISA.

RESULTS Compared with that in the normal oxygen control group, there was no significant change in right ventricular systolic blood pressure in the mice exposed to hypoxia at 3000 m during the first two weeks. However, an increase was observed starting from the third week (P<0.05). In contrast, mice exposed to hypoxia at 4000 m and 5000 m showed increased right ventricular systolic blood pressure after one week of exposure (P<0.01). Mice treated with either normal oxygen or hypoxia at 3000 m for two weeks underwent in vivo myocardial ischemia-reperfusion or isolated myocardial ischemia-reperfusion models, respectively. Both groups exhibited reduced infarct size and decreased serum troponin I content compared with those in the normal oxygen group (P<0.01). Four weeks after returning to a normal oxygen environment, the protective effect provided by hypoxic treatment was lost.

CONCLUSION The intermittent hypoxic myocardial protection condition, achieved through a 2-week treatment of hypoxia at an altitude of 3000 m for 4 hours daily, does not induce pulmonary hypertension. Furthermore, the protective effect persists for up to 3 weeks after discontinuation of the hypoxic environment.