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[慢性心力衰竭患者运动期间促进氧输送的机制]

[Mechanisms facilitating oxygen delivery during exercise in patients with chronic heart failure].

作者信息

Agostoni P, Assanelli E, Guazzi M, Grazi M, Perego G B, Lomanto M, Cattadori G, Lauri G, Marenzi G

机构信息

Istituto di Cardiologia, Università degli Studi, Milano.

出版信息

Cardiologia. 1997 Jul;42(7):743-50.

PMID:9270180
Abstract

The aim of the study was to estimate the relative importance of the Bohr effect and redistribution of blood from the non-exercising tissues on the arterial-venous oxygen content differences across the exercising extremities and the central circulation in patients with chronic heart failure; the relationship among femoral vein, systemic and pulmonary artery oxygen partial pressure and hemoglobin saturation was determined. It has been reported that the maximal reduction in femoral vein pO2 precedes peak oxygen consumption and lactic acidosis threshold in patients with chronic heart failure and normal subjects during exercise. The increase in oxygen consumption at work rates above lactic acidosis threshold, therefore, must be accounted for by increase in blood flow in the exercising muscles and right-ward shift on the oxyhemoglobin dissociation curve. Since the total cardiac output increase is blunted in patients with chronic heart failure, diversion of blood flow from non-exercising to exercising tissues may account for some of the increase in muscle blood flow. Ten patients with chronic heart failure performed a progressively increasing leg cycle ergometer exercise test up to maximal effort while measuring ventilation and gas concentration for computation of oxygen uptake and carbon dioxide production, breath-by-breath. Blood samples were obtained, simultaneously, from systemic and pulmonary arteries and femoral vein at rest and every minute during exercise to peak oxygen consumption. At comparable levels of exercise, femoral vein pO2, hemoglobin saturation and oxygen content were lower than in the pulmonary artery. PCO2 and lactate concentration increased steeply in femoral vein and pulmonary artery blood above lactic acidosis threshold (due to lactic acid build-up and buffering), but more steeply in femoral vein blood. These increases allowed femoral vein oxyhemoglobin to dissociate without a further decrease in femoral vein pO2 (Bohr effect). The lowest femoral vein pO2 (16.6 +/- 3.9 mmHg) was measured at 66 +/- 22% of peak VO2 and before the lowest oxyhemoglobin saturation was reached. Artero-venous oxygen content difference was higher in the femoral vein than in the pulmonary artery; this difference became progressively smaller as oxygen consumption increased. "Ideal" oxygen consumption for a given cardiac output (oxygen consumption expected if all body tissues had maximized oxygen extraction) was always higher than the measured oxygen consumption; however the difference between the two was lost at peak exercise. This difference positively correlated with peak oxygen consumption and cardiac output increments at submaximal but not at maximal exercise. In conclusion, femoral vein pO2 reached its lowest value at a level of exercise at or below the lactic acidosis threshold. Further extraction of oxygen above the lactic acidosis threshold was accounted for by a right shift of the oxyhemoglobin dissociation curve. The positive correlation between increments of cardiac output vs "ideal" and measured oxygen consumption suggests a redistribution of blood flow from non-exercising to exercising regions of the body. Furthermore the positive correlation between exercise capacity and the difference between "ideal" and measured oxygen consumption suggests that patients with the poorer function have the greater capability to optimize blood flow redistribution during exercise.

摘要

本研究的目的是评估波尔效应以及非运动组织的血液重新分布,对于慢性心力衰竭患者运动肢体和体循环中动静脉氧含量差别的相对重要性;测定股静脉、体循环和肺动脉血氧分压与血红蛋白饱和度之间的关系。据报道,在运动过程中,慢性心力衰竭患者和正常受试者股静脉pO₂的最大降幅先于耗氧量峰值和乳酸酸中毒阈值出现。因此,在高于乳酸酸中毒阈值的工作强度下,耗氧量的增加必定是由于运动肌肉血流量增加以及氧合血红蛋白解离曲线右移所致。由于慢性心力衰竭患者的心输出量总增加量减弱,血液从非运动组织转移至运动组织可能是肌肉血流量增加的部分原因。10例慢性心力衰竭患者进行了逐渐增加负荷的腿部蹬车运动试验,直至竭尽全力,同时测量通气量和气体浓度,以便逐次呼吸地计算摄氧量和二氧化碳产生量。在静息状态以及运动至耗氧量峰值的过程中,每分钟从体循环和肺动脉以及股静脉同时采集血样。在运动水平相当的情况下,股静脉的pO₂、血红蛋白饱和度和氧含量均低于肺动脉。高于乳酸酸中毒阈值时,股静脉和肺动脉血中的PCO₂和乳酸浓度急剧上升(由于乳酸堆积和缓冲作用),但股静脉血中上升更为急剧。这些升高使得股静脉氧合血红蛋白解离,而股静脉pO₂并未进一步下降(波尔效应)。最低股静脉pO₂(16.6±3.9 mmHg)是在峰值VO₂的66±22%时测得,且早于最低氧合血红蛋白饱和度出现之前。股静脉的动静脉氧含量差高于肺动脉;随着耗氧量增加,这种差异逐渐减小。对于给定的心输出量而言,“理想”耗氧量(如果所有身体组织的氧摄取均达到最大化时预期的耗氧量)始终高于实测耗氧量;然而在运动峰值时,两者之间的差异消失。这种差异与次最大运动而非最大运动时的耗氧量峰值和心输出量增量呈正相关。总之,股静脉pO₂在乳酸酸中毒阈值或低于该阈值的运动水平时达到最低值。高于乳酸酸中毒阈值时,氧的进一步摄取是由于氧合血红蛋白解离曲线右移所致。心输出量增量与“理想”和实测耗氧量之间的正相关表明身体血液从非运动区域重新分布至运动区域。此外,运动能力与“理想”和实测耗氧量之间的差异呈正相关,这表明功能较差的患者在运动过程中优化血流重新分布的能力更强。

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