Exercise response of the denervated heart in long-term cardiac transplant recipients.
Exercise response of the denervated heart in long-term cardiac transplant recipients.
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长期心脏移植受者去神经支配心脏的运动反应。
DOI：
10.1016/0002-9149(80)90060-0
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发表时间：
1980
期刊：
影响因子：
--
通讯作者：
E. Alderman
中科院分区：
文献类型：
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作者：
S. Pope;E. Stinson;G. Daughters;J. Schroeder;N. Ingels;E. Alderman
对9例长期（1年以上）心脏移植受者的左心室对容量负荷和渐进式仰卧自行车运动（3分钟，15、45和90瓦）的反应进行了评估。在手术时植入左心室的不透射线心肌标记物的计算机辅助透视用于测量左心室动力学。监测肺动脉压和左心室压。血浆去甲肾上腺素用放射酶法测定。运动早期平均舒张末期容积（6例）在45瓦时从静息值125增加到138 ml (p < 0.02)，然后在90瓦时降至121 ml。在相应运动水平下，收缩期末期容积由68 ml降至63 ml，再降至49 ml （p < 0.01）。脑卒中容量从57 ml增加到76 ml (p < 0.01)，然后略有下降到71 ml（相对于静息值增加p < 0.02）。心率由102 ~ 116次/min逐渐升高（p < 0.05），而后迅速升高至140次/min （p < 0.01）。因此，在所有运动水平下，心输出量都显著增加，从静止时的5.7升/分钟，到15瓦时的6.5升/分钟（p < 0.02），到45瓦时的8.7升/分钟（p < 0.01），到90瓦时的10.0升/分钟（p < 0.01）。血浆去甲肾上腺素从静止时的233 pcg/ml缓慢上升到45瓦时的460 pcg/ml，然后迅速上升到90瓦时的1,970 pcg/ml。周向纤维缩短速度（Vcf）和心率的增加与去甲肾上腺素浓度的增加相关（Vcf r = 0.92，心率r = 0.79）。在7例患者中，通过抬高腿部负荷导致舒张末期容积、搏量和心输出量显著增加，但心率没有增加，证明了Frank-Starling机制的功能。因此，移植心脏的心输出量增加是在运动早期通过增加预负荷和Frank-Starling机制引起的，而在运动后期通过增加循环儿茶酚胺的变时性和收缩性影响引起的。
The left ventricular response to volume loading and graded supine bicycle exercise (3 minutes at 15, 45 and 90 watts) was assessed in nine long-term (more than 1 year) cardiac transplant recipients. Computer-aided fluoroscopy of radiopaque myocardial markers implanted in the left ventricle at the time of surgery was used to measure left ventricular dynamics. Pulmonary arterial and left ventricular pressures were monitored. Plasma norepinephrine was measured by radio-enzymatic assay at each level of exercise.Early in exercise mean end-diastolic volume (six patients) increased from a resting value of 125 to 138 ml (p < 0.02) at the 45 watt level, then decreased to 121 ml at the 90 watt level. End-systolic volume decreased from 68 to 63 ml and then to 49 ml (p < 0.01) at corresponding exercise levels. Stroke volume increased from 57 to 76 ml (p < 0.01) then declined slightly to 71 ml (p < 0.02 for increase relative to resting value). Heart rate increased gradually from 102 to 116 beats/min (p < 0.05) and then rapidly to 140 beats/min (p < 0.01). Thus cardiac output increased significantly at all levels of exercise from 5.7 liters/min at rest, to 6.5 at 15 watts (p < 0.02), to 8.7 at 45 watts (p < 0.01) and to 10.0 liters/min at 90 watts (p < 0.01). Plasma norepinephrine increased slowly from 233 pcg/ml at rest to 460 at 45 watts, then rapidly to 1,970 pcg/ml at 90 watts. Increases in velocity of circumferential fiber shortening (Vcf) and heart rate were correlated with increasing norepinephrine concentrations (r = 0.92 for Vcf; r = 0.79 for heart rate). A functioning Frank-Starling mechanism was demonstrated in seven patients with volume loading by leg elevation resulting in significant increases in end-diastolic volume, stroke volume and cardiac output in the absence of any increase in heart rate. Thus, cardiac output increases in the transplanted heart were brought about early in exercise by augmented preload and the Frank-Starling mechanism, and later in exercise by chronotropic and inotropic influences of increased circulating catecholamines.