Somatostatin and innervation of the heart of the snake Elaphe obsoleta.

Somatostatin and innervation of the heart of the snake Elaphe obsoleta.
复制标题

生长抑素和蛇锦蛇心脏的神经支配。

DOI:
10.1152/ajpregu.1990.258.4.r1001
复制
发表时间:
1990
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Lillywhite,HB
Lillywhite,HB
中科院分区:
--
文献类型:
--
作者:
Donald,JA;O'Shea,JE;Lillywhite,HB

文献摘要

被引文献

相似文献

用肽免疫组织化学、乙醛酸诱导的儿茶酚胺荧光和离体生理标本研究了锦蛇心脏的神经支配。用戊巴比妥麻醉蛇。在静脉窦、心房和心室中观察到许多生长抑素(SOM)样免疫反应(LI)轴突。在静脉窦、房间隔和房室区的心内神经干中发现了具有SOM-LI的细胞体。SOM-LI轴突和胞体不受6-羟基多巴胺和辣椒素的影响。它们可能是内在副交感神经元。在静脉窦、心房和心室中发现肾上腺素能、神经肽Y-LI、P物质-LI和降钙素基因相关肽-LI轴突。在自发搏动的窦房或电驱动心房准备中,施加SOM(6 x 10(-9)M和6 x 10(-8)M)降低了心房收缩力和/或搏动率。SOM的作用是快速的。SOM对驱动心室的收缩力无影响。刺激左右迷走神经引起负性变时性和变力性反应,然后是刺激后正性变力性和变时性反应。阿托品可消除抑制作用,溴苄铵可消除兴奋作用。在胆碱能和肾上腺素能阻断后,高频迷走神经刺激对心率和收缩力没有影响。因此,虽然有一个广泛的内在SOM-LI神经元分布在心脏中,虽然应用SOM是一个有效的抑制剂的速率和力,SOM在迷走神经元似乎并不作为一个直接的抑制性递质心肌或起搏细胞。
The innervation of the heart of the snake Elaphe obsoleta was examined with peptide immunohistochemistry, glyoxylic acid-induced catecholamine fluorescence, and in vitro physiological preparations. Snakes were anesthetized with Nembutal. Many somatostatin (SOM)-like immunoreactive (LI) axons were observed in the sinus venosus, atria, and ventricle. Cell bodies with SOM-LI were found in the intracardiac nerve trunks of the sinus venosus, the interatrial septum, and the atrioventricular region. The SOM-LI axons and cell bodies were not affected by 6-hydroxy-dopamine and capsaicin. They are probably intrinsic parasympathetic neurons. Adrenergic, neuropeptide Y-LI, substance P-LI, and calcitonin gene-related peptide-LI axons were found in the sinus venosus, atria, and ventricle. In spontaneously beating sinoatrial or electrically driven atrial preparations, applied SOM (6 x 10(-9) M and 6 x 10(-8) M) decreased the force of atrial contraction and/or the rate of beating. The effects of SOM were tachyphylactic. SOM had no effect on the force of contraction of the driven ventricle. Stimulation of the left and right vagus nerves elicited negative chronotropic and inotropic responses followed by poststimulus positive inotropic and chronotropic responses. Atropine abolished the inhibition, and bretylium abolished the excitation. After cholinergic and adrenergic blockade, high-frequency vagal nerve stimulation had no effect on heart rate and the force of contraction. Thus, although there is an extensive distribution of intrinsic SOM-LI neurons in the heart and although applied SOM is a potent inhibitor of rate and force, SOM in the vagal neurons does not appear to act as a direct inhibitory transmitter to the cardiac muscle or pacemaker cells.