摘要
正常血压兔侧脑室注射(ICV)促甲状腺素释放激素(TRH)后,平均动脉压(MAP)与脉压(PP)分别由给药前的12.6±1.0kPa与7.2±1.3k pa上升到16.3±1.4k Pa与8.4±2.4k Pa(P均<0.01);但心率(HR)却由给药前的282±56b/min减慢为236±76b/min(P<0.01)。失血性休克兔和中毒性休克兔ICV TRH后,MAP分别由给药前的7.2±1.2k Pa与5.1±2.1k Pa上升到13.5±2.0k Pa与10.3±1.4k Pa(P均<0.01);PP分别由给药前的4.5±1.4k Pa与2.1±0.4k Pa增加到7.2±2.3k Pa与4.4±1.2k Pa(P均<0.01);HR分别由给药前的224±39 b/min与220±20 b/min增加到238±42b/min与233±25 b/min(P均<0.01),动物存活时间延长。若在ICV TRH之前预先向延髓腹外侧区头端(rVLM)微量注射阿托品则可阻断TRH的升压效应。提示ICV TRH对失血性休克和中毒性休克兔均有明显的升压抗休克作用。TRH的升压效应可能需要VLM区胆碱能神经元功能的完整。
After the injection of thyrotropin-releasing hormone ( TRH) into the lateral cerebral ventricle of the rabbit with normal blood pressure, the mean arterial pressure (MAP) and the pulse pressure (PP) are increased from 12.6±1.0kPa and 7.2±1.3kPa before administration to 16.3±1.4kPa and 8.4±2.4kPa ( P<0.01), but the heart rate (HR) slowed down to 236±76b/min from 282±56 b/min ( P<0.01 ) . After TRH is injected into the lateral cerebral ventricle in the hemorrhagic shock and the toxic shock, MAP rises to 13.5±2.0kPa and 10.3±1.4kPa from 7.2±1.2kPa and 5.1±2.lkPa before treatment, respectively ( P<0.01), PP is increased to 7.2±2.3kPa and 4.4±1.2kPa from 4.5±1.4kPa and 2.1±0.4kPa ( P<0.01 ) . HR is increased to 238±42b/min and 233±25 b/min from 224±39b/min and 220±20b/min. respectively (P<0.01). The survival time of the animals is prolonged. If a trace of atropine is injected into the rostral ventrolateral medulla before the injection of TRH into the lateral cerebral ventricle, the pressor response of TRH will be blocked. These results suggest that the injection of TRH into the lateral cerebral ventricle has great pressor and anti-shock effects. The pressor response may be related to the integrity of the function of the cholinergic neuron in the ventrolateral medulla area.
出处
《温州医学院学报》
CAS
1991年第3期129-134,共6页
Journal of Wenzhou Medical College
基金
浙江省教委
浙江省卫生厅资助
关键词
TRH
休克
胆碱能神经元
延髓
thyrotropin-releasing hormone (TRH)
hemorrhagic shock
toxic shock
ventrolateral medulla
cholinergic neuron
atropine
