The relationship of respiratory failure to the oxygen consumption of, lactate production by, and distribution of blood flow among respiratory muscles during increasing inspiratory resistance.
The relationship of respiratory failure to the oxygen consumption of, lactate production by, and distribution of blood flow among respiratory muscles during increasing inspiratory resistance.
复制标题
呼吸衰竭与吸气阻力增加过程中呼吸肌的耗氧量、乳酸产生和血流分布的关系。
DOI：
10.1172/jci108619
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发表时间：
1977
期刊：
影响因子：
--
通讯作者：
Adolph Weinberger
中科院分区：
文献类型：
--
作者：
C. H. Robertson;G. Foster;Robert L. Johnson;Adolph Weinberger
开发了一种动物模型来确定流向呼吸肌的血流是否限制了氧气输送，从而限制了吸气阻力期间的功输出。随着呼吸做功率逐渐增加到静息水平的 15 倍，流向膈肌的血流量呈指数增长 26 倍。流向其他吸气肌和少数呼气肌的血流量增加的程度要小得多，通常仅在工作负荷较大时才增加。心输出量和血压没有变化。隔膜上的动静脉氧含量差异在低工作率时达到最大，此后在较高工作率期间氧输送的所有增加都是通过血流量的增加来实现的。通过血流量乘以氧提取量计算得出的呼吸肌肉组织的耗氧量随着呼吸功的增加而呈指数增加，并且小于每个工作负荷下全身耗氧量的增加。当动物通过最高阻力激发时发生低氧血症和呼吸性酸中毒；血流量和耗氧量甚至高于之前抵抗期间观察到的水平，并且没有证据表明血乳酸和丙酮酸水平转向无氧代谢。在该模型中，呼吸衰竭似乎不是血流不足的结果。
An animal model was developed to determine if blood flow to the respiratory muscles limits oxygen delivery and thus work output during inspiratory resistance. With incremental increases in the rate of work of breathing to 15 times the resting level, blood flow to the diaphragm rose exponentially 26-fold. Blood flow to other inspiratory and a few expiratory muscles increased to a much smaller extent, often only at the greater work loads. Cardiac output and blood pressure did not change. Arterial-venous oxygen content difference across the diaphragm became maximal at low work rates and thereafter all increases in oxygen delivery during higher work rates were accomplished by increments in blood flow. Oxygen consumption of the respiratory musculature calculated by blood flow times oxygen extraction increased exponentially with increasing work of breathing and was less than the increase in total body oxygen consumption at each work load. Hypoxemia and respiratory acidosis occurred when the animals inspired through the highest resistance; blood flow and oxygen consumption were even higher than that observed during previous resistances and there was no evidence of a shift to anaerobic metabolsim in blood lactate and pyruvate levels. Respiratory failure did not appear to be a consequence of insufficient blood flow in this model.