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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Parratt J R, Wadsworth R M

Br J Pharmacol. 1972 Dec;46(4):594-601. doi: 10.1111/j.1476-5381.1972.tb06886.x.

The arterial pO(2) of anaesthetized cats was reduced to 33 mmHg by supplying a mixture of oxygen and nitrogen as the respiratory gas. This produced vasodilatation in the myocardial bed which was not increased after the injection of dipyridamole (1 mg/kg).2. Reactive hyperaemia was observed following occlusion of the left anterior descending coronary artery for 10-120 seconds. The duration of the period of reactive hyperaemia was increased after the injection of dipyridamole. This effect of dipyridamole was most pronounced when the longest periods of occlusion were used.3. These results support the hypothesis that myocardial reactive hyperaemia is at least partly caused by adenosine released from hypoxic myocardial cells. The vasodilatation occurring during systemic hypoxia, on the other hand, is probably mediated via a different mechanism.

Parratt J R, Wadsworth R M

Br J Pharmacol. 1972 Dec;46(4):594-601. doi: 10.1111/j.1476-5381.1972.tb06886.x.

The arterial pO(2) of anaesthetized cats was reduced to 33 mmHg by supplying a mixture of oxygen and nitrogen as the respiratory gas. This produced vasodilatation in the myocardial bed which was not increased after the injection of dipyridamole (1 mg/kg).2. Reactive hyperaemia was observed following occlusion of the left anterior descending coronary artery for 10-120 seconds. The duration of the period of reactive hyperaemia was increased after the injection of dipyridamole. This effect of dipyridamole was most pronounced when the longest periods of occlusion were used.3. These results support the hypothesis that myocardial reactive hyperaemia is at least partly caused by adenosine released from hypoxic myocardial cells. The vasodilatation occurring during systemic hypoxia, on the other hand, is probably mediated via a different mechanism.