SKELETAL-MUSCLE OXYGEN AVAILABILITY DURING RESPIRATORY ACID-BASE DISTURBANCES IN CATS

SKELETAL-MUSCLE OXYGEN AVAILABILITY DURING RESPIRATORY ACID-BASE DISTURBANCES IN CATS
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DOI:
10.1016/0034-5687(87)90046-6
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发表时间:
1987-11-01
期刊:
RESPIRATION PHYSIOLOGY
影响因子:
--
通讯作者:
PIANTADOSI, CA
PIANTADOSI, CA
中科院分区:
其他
文献类型:
--
作者:
HAMPSON, NB;JOBSISVANDERVLIET, FF;PIANTADOSI, CA

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呼吸性酸碱失衡引起生理反应,改变O2输送到各种组织。我们已经使用了近红外(NIR)光学技术来监测细胞色素a,a3氧化态,组织O2存储(相对血红蛋白加肌红蛋白氧合),和区域血容量在完整的休息骨骼肌在呼吸酸碱紊乱麻醉猫。通过增加CO2浓度(n = 13)或过度通气(n = 8),在不同的动物组中产生高碳酸酸中毒和低碳酸酸中毒。呼吸性酸中毒降低了后肢肌肉的氧利用率,而呼吸性酸中毒并不改变组织氧合。吸入CO2逐渐减少肌肉血容量,细胞色素a,a3氧化水平,和肌肉氧储存。这些光学反应大大衰减预处理与溴苄铵和失血性低血压,这表明通过交感血管收缩调解。代谢性酸中毒,静脉注射盐酸(n = 8),并没有再现后肢光学反应介导的二氧化碳。这些实验表明,高碳酸酸中毒显著降低了麻醉猫静息骨骼肌的氧供应,可能是通过对CO2的神经调节反应,该反应不依赖于测试pH值范围内动脉[H+]的变化。
Respiratory acid-base disorders elicit physiological responses that alter O2 delivery to various tissues. We have used a near infrared (NIR) optical technique to monitor cytochrome a,a3 oxidation state, tissue O2 store (relative hemoglobin plus myoglobin oxygenation), and regional blood volume in intact resting skeletal muscle during respiratory acid-base disturbance in anesthetized cats. Hypercapnic acidosis and hypocapnic alkalosis were produced in separate groups of animals by ventilation with increasing concentrations of CO2 (n = 13) or hyperventilation (n = 8). Respiratory acidosis decreased oxygen availability to hindlimb muscle while respiratory alkalosis did not change tissue oxygenation. Inspired CO2 progressively decreased muscle blood volume, cytochrome a,a3 oxidation level, and muscle oxygen store. These optical responses were greatly attenuated both by pre-treatment with bretylium and by hemorrhagic hypotension, suggesting mediation through sympathetic vasoconstriction. Metabolic acidosis, produced by intravenous HCl infusion (n = 8), did not reproduce the hindlimb optical responses mediated by CO2. These experiments demonstrate that hypercapnic acidosis significantly decreases oxygen supply to resting skeletal muscle in the anesthetized cat, probably via neuroregulatory responses to CO2 which do not depend on changes in arterial [H+] in the tested pH range.