• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Augmented central nitric oxide production inhibits vasopressin release during hemorrhage in acute alcohol-intoxicated rodents.
【24h】

Augmented central nitric oxide production inhibits vasopressin release during hemorrhage in acute alcohol-intoxicated rodents.

机译：在急性酒精中毒的啮齿动物中，出血过程中中央一氧化氮产生的增加抑制了加压素的释放。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Acute alcohol intoxication (AAI) attenuates the AVP response to hemorrhage, contributing to impaired hemodynamic counter-regulation. This can be restored by central cholinergic stimulation, implicating disrupted signaling regulating AVP release. AVP is released in response to hemorrhage and hyperosmolality. Studies have demonstrated nitric oxide (NO) to play an inhibitory role on AVP release. AAI has been shown to increase NO content in the paraventricular nucleus. We hypothesized that the attenuated AVP response to hemorrhage during AAI is the result of increased central NO inhibition. In addition, we predicted that the increased NO tone during AAI would impair the AVP response to hyperosmolality. Conscious male Sprague-Dawley rats (300-325 g) received a 15-h intragastric infusion of alcohol (2.5 g/kg + 300 mg.kg(-1).h(-1)) or dextrose prior to a 60-min fixed-pressure hemorrhage ( approximately 40 mmHg) or 5% hypertonic saline infusion (0.05 ml.kg(-1).min(-1)). AAI attenuated the AVP response to hemorrhage, which was associated with increased paraventricular NO content. In contrast, AAI did not impair the AVP response to hyperosmolality. This was accompanied by decreased paraventricular NO content. To confirm the role of NO in the alcohol-induced inhibition of AVP release during hemorrhage, the nitric oxide synthase inhibitor, nitro-l-arginine methyl ester (l-NAME; 250 mug/5 mul), was administered centrally prior to hemorrhage. l-NAME did not further increase AVP levels during hemorrhage in dextrose-treated animals; however, it restored the AVP response during AAI. These results indicate that AAI impairs the AVP response to hemorrhage, while not affecting the response to hyperosmolality. Furthermore, these data demonstrate that the attenuated AVP response to hemorrhage is the result of augmented central NO inhibition.
机译：急性酒精中毒（AAI）会减弱AVP对出血的反应，从而导致血液动力学反调节功能受损。这可以通过中枢胆碱能刺激来恢复，暗示调节AVP释放的信号传导被破坏。 AVP被释放以应对出血和高渗性。研究表明，一氧化氮（NO）对AVP释放起抑制作用。已显示AAI可增加脑室旁核中的NO含量。我们假设AAI对出血的AVP应答减弱是中央NO抑制增加的结果。此外，我们预测在AAI期间NO音升高会损害AVP对高渗性的反应。有意识的雄性Sprague-Dawley大鼠（300-325 g）在60分钟前接受了15小时的胃内酒精（2.5 g / kg + 300 mg.kg（-1）.h（-1））或葡萄糖的输注固定压力出血（约40 mmHg）或5％高渗盐水输注（0.05 ml.kg（-1）.min（-1））。 AAI减弱了对出血的AVP反应，这与心室旁NO含量增加有关。相反，AAI并未损害AVP对高渗性的反应。这伴随着室旁NO含量的降低。为了确认NO在出血期间酒精诱导的AVP释放抑制中的作用，在出血前集中给予一氧化氮合酶抑制剂硝基-1-精氨酸甲酯（I-NAME; 250马克/ 5 mul）。在葡萄糖治疗的动物出血期间，l-NAME并未进一步提高AVP水平;但是，它在AAI期间恢复了AVP响应。这些结果表明，AAI会损害AVP对出血的反应，而不会影响对高渗的反应。此外，这些数据表明对出血的减弱的AVP反应是中央NO抑制作用增强的结果。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号