RELATION BETWEEN CENTRAL AND PERIPHERAL HEMODYNAMICS DURING EXERCISE IN PATIENTS WITH CHRONIC HEART-FAILURE - MUSCLE BLOOD-FLOW IS REDUCED WITH MAINTENANCE OF ARTERIAL PERFUSION-PRESSURE

RELATION BETWEEN CENTRAL AND PERIPHERAL HEMODYNAMICS DURING EXERCISE IN PATIENTS WITH CHRONIC HEART-FAILURE - MUSCLE BLOOD-FLOW IS REDUCED WITH MAINTENANCE OF ARTERIAL PERFUSION-PRESSURE
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DOI:
10.1161/01.cir.80.4.769
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发表时间:
1989-10-01
期刊:
影响因子:
37.8
通讯作者:
COBB, FR
COBB, FR
中科院分区:
医学1区
文献类型:
--
作者:
SULLIVAN, MJ;KNIGHT, JD;COBB, FR

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我们研究了30例慢性心力衰竭患者的中枢血流动力学、腿部血流和代谢反应,这些患者可归因于严重的左心功能不全(射血分数,24。+-)。8%)和12名正常受试者。在运动高峰时,患者的氧耗量降低(15.1±-)。4.8比32.1.+-9.9ml/kg/min,P<0.001),心输出量(8.7±-)。3.2比18.6。+-4.4.L/分钟,P&lt;0.001),平均体动脉压(116.0±-)。15比135。+-。13 mm Hg,p&lt;0.01)。与正常受试者相比,患者的腿部血流量在静息、匹配次最大工作速率和最大运动时减少(2.1.+-)。1.9比6.4.+-L/分钟,均P&lt;0.01)。平均体动脉压在静息状态或匹配的次极量工作速度下在活体组中没有差异,而患者的腿部血管阻力在静息、次极量和最大运动量下高于正常受试者(均P&lt;0.01)。虽然静息时患者的非腿部血流量减少,但两组患者在运动时都没有明显减少。患者和正常人的运动腿血流量与运动心输出量呈正相关(r=0.66,p&lt;0.01;r=0.67,p&t;0.01)。在患者中,腿部血管阻力与静息或运动时的平均动脉压、肺毛细血管楔压、动脉儿茶酚胺、动脉乳酸或股静脉pH值无关。与正常受试者相比,在次极量运动中,患者表现出腿部氧摄取和乳酸生成增加,同时腿部耗氧量减少。因此,在慢性心力衰竭患者中,与正常人相比,骨骼肌在静息和次极量和最大运动量运动时的血流灌注量减少,局部血管阻力增加。我们的数据表明,我们的患者在运动过程中优先维持非腿部血流和动脉血压,但牺牲了腿部低灌注量。与正常受试者相比,这与腿部氧气利用减少和腿部吸氧增加有关,这进一步证明,减少素描肌肉的灌注量是导致这种疾病受试者在运动过程中早期骨骼肌代谢异常的重要原因。尽管这些结果没有确定慢性心力衰竭患者在运动过程中腿部血管阻力增加的机制,但我们的发现表明,在患有这种疾病的患者中,反射介导的外周血管收缩在连接运动对运动的心输出量和骨骼肌血流反应中发挥了作用。
We studied the central hemodynamic, leg blood flow, and metabolic responses to maximal upright bicycle exercise in 30 patients with chronic heart failure attributable to severe left ventricular dysfunction (ejection fraction, 24 .+-. 8%) and in 12 normal subjects. At peak exercise, patients demonstrated reduced oxygen consumption (15.1 .+-. 4.8 vs. 32.1 .+-. 9.9 ml/kg/min, p < 0.001), cardiac output (8.7 .+-. 3.2 vs. 18.6 .+-. 4.4 l/min, p < 0.001), and mean systemic arterial blood pressure (116 .+-. 15 vs. 135 .+-. 13 mm Hg, p < 0.01) compared with normal subjects. Leg blood flow was decreased in patients versus normal subjects at rest and matched submaximal work rates and maximal exercise (2.1 .+-. 1.9 vs. 6.4 .+-. 1.4 l/min, all p < 0.01). Mean systemic arterial blood pressure was no different in the vivo groups at rest or at matched submaximal work rates, whereas leg vascular resistance was higher in patients compared with normal subjects at rest, submaximal, and maximal exercise (all p < 0.01). Although nonleg blood flow was decreased at rest in patients, it did not decrease significantly during exercise in either group. Peak exercise leg blood flow was related to peak exercise cardiac output in patients (r = 0.66, p < 0.01) and normal subjects (r = 0.67, p < 0.01). In patients, leg vascular resistance was not related to mean arterial blood pressure, pulmonary capillary wedge pressure, arterial catecholamines, arterial lactate, or femoral venous pH at rest or during exercise. Compared with normal subjects during submaximal exercise, patients demonstrated increased leg oxygen extraction and lactate production accompanied by decreased leg oxygen consumption. Thus, in patients with chronic heart failure compared with normal subjects, skeletal muscle perfusion is decreased at rest and during submaximal and maximal exercise, and local vascular resistance is increased. Our data indicate that nonleg blood flow and arterial blood pressure were preferentially maintained during exercise at the expense of leg hypoperfusion in our patients. This was associated with decreased leg oxygen utilization and increased leg oxygen extraction when compared to normal subjects, providing further evidence that reduced perfusion of sketal muscle is important in causing early anaurobic skeletal muscle metabolism during exercise in subjects with this disorder. Although these results do not define the mechanisms responsible for increased leg vascular resistance during exercise in subjects with chronic heart failure, our finding that arterial blood pressure in patients was closely regulated suggests a role for reflex-mediated peripheral vasoconstriction in linking the cardiac output and skeletal muscle blood flow responses to exercise in subjects with this disorder.