Murphy D A, O'Blenes S, Hanna B D, Armour J A
Department of Surgery, Dalhousie University, Halifax, Nova Scotia, Canada.
J Heart Lung Transplant. 1994 Sep-Oct;13(5):847-56.
The capacity of the intrinsic cardiac nervous system to modify the acutely autotransplanted heart was investigated in eight anesthetized open-chest canine preparations in which the adrenal glands had been removed from the circulation. Cardiac effects elicited by isoproterenol and nicotine were also examined before and after heart-lung transplantation. Cardiac augmentation induced by isoproterenol was similar before and immediately after cardiopulmonary transplantation, indicating that the surgery did not obtund cardiac myocyte function significantly. The initial bradycardia induced by nicotine was greater before transplantation. The subsequent augmentation in left atrial systolic pressure, as well as right and left ventricular intramyocardial systolic pressures, induced by nicotine were similar before and after transplantation. When nicotine was administered to transplanted preparations after atropine administration, cardiac augmentation was induced. Cardiac augmentation was not induced by nicotine after subsequent beta-adrenergic blockade. These data indicate that nicotine-sensitive adrenergic neurons which accompany the transplanted heart are capable of inducing considerable cardiac augmentation. Power spectral analysis of heart rate and left ventricular chamber rate of pressure rise variability indicated an almost complete lack of power in these indexes after, as opposed to before, transplantation. Together with intrinsic cardiac cholinergic neurons, intrinsic cardiac adrenergic neurons may be responsible for physiologically and pharmacologically induced alterations in cardiac variables that occur in acutely transplanted hearts.
在八只麻醉开胸犬的实验准备中，研究了心脏固有神经系统对急性自体移植心脏的调节能力，这些犬的肾上腺已从循环中移除。还在心肺移植前后检查了异丙肾上腺素和尼古丁引起的心脏效应。心肺移植前后，异丙肾上腺素引起的心脏增强作用相似，这表明手术并未显著削弱心肌细胞功能。移植前尼古丁引起的初始心动过缓更明显。移植前后，尼古丁引起的左心房收缩压以及右心室和左心室心肌内收缩压的后续增强作用相似。在给移植后的制剂注射阿托品后再给予尼古丁，会引起心脏增强。在随后的β-肾上腺素能阻滞之后，尼古丁不会引起心脏增强。这些数据表明，伴随移植心脏的对尼古丁敏感的肾上腺素能神经元能够引起显著的心脏增强。心率和左心室压力上升变异性的功率谱分析表明，与移植前相反，移植后这些指标几乎完全缺乏功率。与心脏固有胆碱能神经元一起，心脏固有肾上腺素能神经元可能是急性移植心脏中生理和药理诱导的心脏变量改变的原因。
