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首页> 外文期刊>American Journal of Physiology >Cardiac performance as a function of intracellular oxygen tension in buffer-perfused hearts.
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Cardiac performance as a function of intracellular oxygen tension in buffer-perfused hearts.

机译:在缓冲液灌注的心脏中,心脏功能随细胞内氧张力的变化而变化。

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摘要

Critical intracellular myocardial oxygen tension was determined by optical spectroscopic measurement of myoglobin oxygen saturation in crystalloid-perfused guinea pig hearts. Accurate end-point determinations of the maximally oxygenated and deoxygenated myoglobin were made. Hearts were subjected to a steady decrease in perfusate oxygen tension while left ventricular developed pressure, maximal left ventricular dP/dt, myocardial oxygen consumption, lactate release, and adenosine release were measured as indices of myocardial function. Intracellular myoglobin was found to be only 72% saturated under baseline conditions with an arterial oxygen tension of >600 mmHg at 37 degrees C. Baseline intracellular oxygen tension was 6.3 mmHg. Myocardial oxygen consumption was decreased by 10% when the oxygen tension fell to 5.7 mmHg, and cardiac contraction decreased 10% when oxygen tension was 4.1 mmHg. Adenosine release and, finally, lactate release began to increase at sequentially lower oxygen tensions. The present results indicate that the buffer-perfused guinea pig heart at 37 degrees C has an intracellular oxygen tension just above the threshold for impaired function.
机译:通过光学光谱法测定晶体灌注的豚鼠心脏中的肌红蛋白氧饱和度,确定了临界细胞内心肌氧张力。进行了最大氧合和脱氧肌红蛋白的准确终点测定。心脏的灌注液氧张力持续下降,同时测量左心室形成压力,最大左心室dP / dt,心肌耗氧量,乳酸释放和腺苷释放作为心肌功能指标。发现在基线条件下细胞内肌红蛋白仅在72℃下饱和72%,在37℃下的动脉氧张力> 600mmHg。基线细胞内氧张力为6.3mmHg。当氧气张力降至5.7 mmHg时,心肌耗氧量减少10%,而当氧气张力为4.1 mmHg时,心肌收缩减少10%。腺苷的释放以及最后乳酸的释放在氧气压力逐渐降低的情况下开始增加。目前的结果表明,在37摄氏度下,缓冲液灌注的豚鼠心脏的细胞内氧张力刚好高于功能受损的阈值。

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