Analyses of projection route of nitroxidergic nerve and its transmission mechanism

本研究的目的是确定支配血管和海绵体并扩张其平滑肌的氮氧能神经的投射路线，并分析其传递机制。研究总结如下：1。来自翼腭神经节的神经节后神经元在神经NO介导的大脑和眼部血管舒张中起着至关重要的作用，而可能来自上唾核的神经节前神经元通过岩浅大神经支配着猴子和狗的翼腭神经节。血管舒缩中枢的强直性放电在维持脑和眼血管舒张中起着重要作用。支配猪脑动脉的一氧化氮（nitrergic）神经在兴奋时释放NO，但不是NO的稳定产物，作为神经递质产生肌肉松弛，内源性SOD保护神经功能不被超氧阴离子降解。低温可以防止缺氧引起的狗大脑中动脉的氮氧能血管舒张神经功能损伤，这可能部分解释了低温对大脑缺血性神经元损伤的保护作用。犬海绵体神经源性松弛是由神经末梢l -精氨酸合成的NO介导的，该神经来源于靠近海绵体的神经节，而非直接来源于盆腔神经丛。在支配海绵体的氮能扩张神经中，n型而非l型钙通道负责增加胞质游离钙，这是合成NO的先决条件。

The aims of this study are to determine the projection route of nitroxidergic (nitrergic) nerves which innervate blood vessels and corpus cavernosum and dilate their smooth muscles, and to analyze their transmission mechanism. Summary of the study is as follows.1. Postganglionic neurons from the pterygopalatine ganglion play crucial roles in cerebral and ophthalmic vasodilation mediated by NO from the nerve, arid preganglionic neurons, possibly from the superior salivatory nucleus through the greater superficial petrosal nerve, innervate the pterygopalatine ganglion in monkeys and dogs. Tonic discharges from the vasomotor center participate significantly in the maintenance of cerebal and ophthalmic vasodilation.2. Nitroxidergic (nitrergic) nerves innervating porcine cerebral arteries liberate NO, but not stable products of NO, on excitation as a neurotransmitter to produce muscle relaxation, and the nerve function is protected by endogenous SOD from degradation of NO by superoxide anions.3. Hypoxia-induced impairment of the function of nitroxidergic (nitrergic) vasodilator nerve innervating dog middle cerebral arteries is prevented by cooling, which may partially explain the effecacy of hypothermia in protecting against ischemic neuronal injury in the brain.4.Neurogenic relaxation of canine corpus cavernosum is mediated by NO synthesized from L-arginine in nerve terminals, and this nerve is originated from ganglia located close to the corpus cavernosum but not directly from the pelvic nerve plexus.5. N-type, but not L-type, calcium channels are responsible for increasing cytosolic free calcium, a prerequisite for the synthesis of NO, in the nitroxidergic (nitrergic) dilator nerves innervating the corpus cavernosum.