• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Endocardial endothelium in the avascular frog heart: role for diffusion of NO in control of cardiac O2 consumption.
【24h】

Endocardial endothelium in the avascular frog heart: role for diffusion of NO in control of cardiac O2 consumption.

机译：血管蛙心中的心内膜内皮：NO扩散在控制心脏O2消耗中的作用。

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

We investigated the role of nitric oxide (NO) in the control of myocardial O(2) consumption in the hearts of female Xenopus frogs, which lack a coronary vascular endothelium and in which the endocardial endothelium is the only source of NO to regulate cardiac myocyte function. Hence, frogs are an ideal model in which to explore the role of diffusion of NO from the endocardial endothelium (EE) without vascular endothelial or cardiac cell NO production. In Xenopus hearts we examined the regulation of cardiac O(2) consumption in vitro at 25 degrees C and 37 degrees C. The NO-mediated control of O(2) consumption by bradykinin or carbachol was significantly (P < 0.05) lower at 25 degrees C (79 +/- 13 or 73 +/- 11 nmol/min) than at 37 degrees C (159 +/- 26 or 201 +/- 13 nmol/min). The response to the NO donor S-nitroso-N-acetyl penicillamine was also markedly lower at 25 degrees C (90 +/- 8 nmol/min) compared with 37 degrees C (218 +/- 15 nmol/min). When Triton X-100 was perfused into hearts, the inhibition of myocardial O(2) consumption by bradykinin (18 +/- 2 nmol/min) or carbachol (29 +/- 4 nmol/min) was abolished. Hematoxylin and eosin slides of Triton X-100-perfused heart tissue confirmed the absence of the EE. Although endothelial NO synthase protein levels were decreased to a variable degree in the Triton X-100-perfused heart, NO(2) production (indicating eNOS activity) decreased by >80%. It appears that the EE of the frog heart is the sole source of NO to regulate myocyte O(2) consumption. When these cells are removed, the ability of NO to regulate O(2) consumption is severely limited. Thus our results suggest that the EE produces enough NO, which diffuses from the EE to cardiac myocytes, to regulate myocardial O(2) consumption. Because of the close proximity of the EE to underlying myocytes, NO can diffuse over a distance and act as a messenger between the EE and the rest of the heart to control mitochondrial function and O(2) consumption.
机译：我们调查了一氧化氮（NO）在雌性非洲爪蟾蛙的心脏中控制心肌O（2）消耗的作用，它们没有冠状血管内皮，并且心内膜内皮是NO调节心肌细胞的唯一来源功能。因此，青蛙是一种理想的模型，可用于探索NO从心内膜内皮（EE）扩散而没有血管内皮或心肌细胞NO产生的作用。在非洲爪蟾的心脏中，我们研究了体外25°C和37°C时心脏O（2）消耗的调节。缓激肽或卡巴胆碱对O（2）消耗的NO介导的控制在25°C时显着降低（P <0.05） C（79 +/- 13或73 +/- 11 nmol / min）比37摄氏度（159 +/- 26或201 +/- 13 nmol / min）高。与37摄氏度（218 +/- 15 nmol / min）相比，在25摄氏度（90 +/- 8 nmol / min）下，对NO供体S-亚硝基-N-乙酰青霉素胺的响应也明显降低。当Triton X-100灌注到心脏时，取消了缓激肽（18 +/- 2 nmol / min）或卡巴胆碱（29 +/- 4 nmol / min）对心肌O（2）消耗的抑制作用。 Triton X-100灌注心脏组织的苏木和曙红玻片证实了EE的缺失。尽管在Triton X-100灌注心脏中内皮NO合酶蛋白水平降低到不同程度，但NO（2）产生（表明eNOS活性）降低了> 80％。看来，青蛙心脏的EE是NO调节心肌细胞O（2）消耗的唯一来源。当这些细胞被删除时，NO调节O（2）消耗的能力受到严重限制。因此，我们的结果表明，EE产生了足够的NO，从EE扩散到心肌细胞，以调节心肌的O（2）消耗量。由于EE与基础肌细胞非常接近，因此NO可以在一定距离内扩散，并充当EE与心脏其他部分之间的信使，以控制线粒体功能和O（2）消耗。

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