大花鼠延腦縫合核含血壓胺神經元對血壓的調腔機制

Abstract

以?酯麻醉，並切斷迷走神經及竇神經的雄性成年Long-Evans老鼠，用來研究延腦縫合核區內含血壓胺神經元在血壓調節方面所扮演的角色。由免疫組織化學染色的結果，證實延腦中線縫合核區，有密集之含血壓胺神經元的分佈。電及麩胺酸化學刺激該區，主要得到血壓上升的反應。經腦池內注射神經毒5,7-DHT之處理，有效清除脊髓內血壓胺（減少81﹪）之後，電刺激蒼白縫合核中段所引起的升血壓反應顯著減弱，電刺激黑暗縫合核尾端所引起的升血壓反應卻顯著增加；化學刺激蒼白縫合核尾端及中段、以及黑暗縫合核中段所引起升血壓反應均顯著減弱。這項研究結果顯示：老鼠延腦中線縫合核內含血壓胺的神經元，參與對血壓的調節。其調節的機制，很可能是透過縫合核—脊髓下行神經通路，興奮交感神經的前節神經元，而升高血壓。

An investigation was undertaken to study the involvement of serotonergic neurons of the medullary raphe nuclei (MRN) in the control of blood pressure. Adult male Long-Evans rats were used. A dense congregation of serotonergic neurons were found in the MRN by the immunohistochemical methods. For stimulation experiments, rats were anesthetized with urethane, bilaterally vagotomized and their sinus nerves transsected. Electrical and glutamate activation of the serotonergic neuron-rich areas in the MRN produced primarily pressor responses. Intracisternal 5,7-dihydroxytryptamine treatment was used to destroy the raphe-spinal serotonergic pathway. After cord serotonin was depleted 81%, the pressor responses produced by stimulation of the MRN were significantly attenuated. These data provide evidence that activation of the raphe-spinal pathway produces pressor effect which may be mediated by sympathetic vasoconstrictors.