Buss D D, Bisgard G E
Am J Vet Res. 1977 Mar;38(3):365-71.
Hemodynamics and myocardial contractility were evaluated in 6 unanesthetized ponies during hypocapnic and isocapnic hypoxia and during hypocapnic hypoxia after beta adrenergic blockade with propranolol. Hypocapnic hypoxia, with a mean arterial oxygen pressure (PaO2) of 41.9 mm of Hg, produced a decrease in stroke index and an increase in heart rate, with no change of cardiac index. A moderate increase in left ventricular contractility occurred during hypocapnic hypoxia. Beta adrenergic blockade abolished changes in nearly all indices of left ventricular contractility during hypocapnic hypoxia, suggesting that the antonomic nervous system plays a definite role in the genesis of circulatory changes during acute hypoxia. Isocapnic hypoxia produced a more well-defined increase in left ventricular contractility. Changes in right ventricular contractility were not observed in any of the hypoxia periods when the concurrent effects of a significant increase in afterload was taken into consideration. The tension-time index, measured as a guide to myocardial oxygen consumption, increased during each hypoxia period in both the right and left ventricle, and was not affected by beta adrenergic blockade.
在6只未麻醉的小马身上,评估了低碳酸血症和等碳酸血症性缺氧期间以及用普萘洛尔进行β肾上腺素能阻滞之后的低碳酸血症性缺氧期间的血流动力学和心肌收缩力。低碳酸血症性缺氧时,平均动脉血氧分压(PaO2)为41.9 mmHg,导致每搏指数降低、心率增加,而心脏指数无变化。低碳酸血症性缺氧期间左心室收缩力出现适度增加。β肾上腺素能阻滞消除了低碳酸血症性缺氧期间左心室收缩力几乎所有指标的变化,这表明自主神经系统在急性缺氧期间循环变化的发生中起明确作用。等碳酸血症性缺氧使左心室收缩力出现更明确的增加。当考虑到后负荷显著增加的同时影响时,在任何缺氧期均未观察到右心室收缩力的变化。作为心肌耗氧量指标的张力-时间指数在右心室和左心室的每个缺氧期均增加,且不受β肾上腺素能阻滞的影响。