Kaye D M, Esler M, Kingwell B, McPherson G, Esmore D, Jennings G
Alfred and Baker Medical Unit, Alfred Hospital, Prahran, Victoria, Australia.
Circulation. 1993 Sep;88(3):1110-8. doi: 10.1161/01.cir.88.3.1110.
The presence of cardiac reinnervation in humans after cardiac transplantation has been widely debated, based on the application of differing methods for the assessment of neuronal function. Some of these techniques have been rather indirect; consequently, the time course and extent of cardiac reinnervation remains uncertain.
To test for the presence of cardiac reinnervation after transplantation, we examined neurochemical (radiolabeled norepinephrine [NE] kinetics) and functional markers (power spectral analysis, heart rate response to exercise) of cardiac sympathetic nerve integrity in 15 cardiac transplantation recipients and 25 healthy control subjects of similar age. Cardiac transplantation subjects were studied 9 weeks to 8 years after cardiac transplantation (10 "early" patients < 18 months and 5 "late" patients > 2 years after cardiac transplantation). At rest, cardiac NE spillover was markedly attenuated early after transplantation (11.2 +/- 18.3 pmol/min) compared with subjects late after transplantation (105 +/- 11 pmol/min, P < .01) or in healthy control subjects (103 +/- 15 pmol/min, P < .01). Heart rate variability (measured by total spectral power) was significantly reduced in cardiac transplantation recipients compared with control subjects (59.4 +/- 30 vs 1673 +/- 516 milliseconds squared; P < .05), with evidence of a trend toward increasing spectral power late after transplantation. During exercise, the cardiac NE spillover was significantly lower in early cardiac transplantation recipients when compared with control subjects (163 +/- 50 vs 1876 +/- 418 pmol/min, P < .01). Late cardiac transplantation subjects showed a response intermediate (1080 +/- 254 pmol/min) between that of the early cardiac transplantation and control groups. However, measurements of the neuronal reuptake process for NE (assessed by the fractional extraction of plasma labeled NE across the heart and tritiated dihydroxyphenylglycol release) were significantly depressed in both early and late cardiac transplantation subjects.
The present study demonstrates a partial restoration of cardiac sympathetic nerve function in humans up to 8 years after heart transplantation.
基于评估神经元功能的不同方法的应用，心脏移植后人类心脏再神经支配的存在一直存在广泛争议。其中一些技术相当间接；因此，心脏再神经支配的时间进程和程度仍不确定。
为了检测移植后心脏再神经支配的存在，我们检查了15名心脏移植受者和25名年龄相仿的健康对照者心脏交感神经完整性的神经化学（放射性标记去甲肾上腺素[NE]动力学）和功能标志物（功率谱分析、运动时心率反应）。心脏移植受者在心脏移植后9周至8年进行研究（10名“早期”患者在心脏移植后<18个月，5名“晚期”患者在心脏移植后>2年）。静息时，与移植后期患者（105±11 pmol/min，P<.01）或健康对照者（103±15 pmol/min，P<.01）相比，移植早期心脏NE溢出明显减弱（11.2±18.3 pmol/min）。与对照者相比，心脏移植受者的心率变异性（通过总谱功率测量）显著降低（59.4±30对1673±516毫秒平方；P<.05），有证据表明移植后期谱功率有增加趋势。运动期间，与对照者相比，早期心脏移植受者的心脏NE溢出显著降低（163±50对1876±418 pmol/min，P<.01）。晚期心脏移植患者的反应介于早期心脏移植组和对照组之间（1080±254 pmol/min）。然而，早期和晚期心脏移植患者中NE的神经元再摄取过程测量值（通过心脏对血浆标记NE的分数提取和氚化二羟基苯乙二醇释放评估）均显著降低。
本研究表明，心脏移植后长达8年，人类心脏交感神经功能可部分恢复。
