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首页> 外文会议>International conference on photonics and imaging in biology and medicine >Adrenergic mechanism responsible for pathological alteration in gastric mucosal blood flow in rats with ulcer bleeding
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Adrenergic mechanism responsible for pathological alteration in gastric mucosal blood flow in rats with ulcer bleeding

机译：溃疡性出血大鼠胃黏膜血流病理改变的肾上腺素能机制

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The adrenergic system plays an important role in regulation of central and peripheral circulation in normal state and during hemorrhage. Because the impaired gastric mucosal blood flow (GMBF) is the major cause of gastroduodenal lesions, including ulcer bleeding (UB), we studied the adrenergic mechanism responsible for regulation of GMBF in rats with a model of stress-induced UB (SUB) using the laser Doppler flowmetry (LDF). First, we examined the effect of adrenaline on GMBF in rats under normal state and during UB. In all healthy animals the submucosal adrenaline injection caused a decrease in local GMBF. During UB the submucosal injection of adrenaline was accompanied by less pronounced GMBF suppression in 30,3% rats with SUB vs. healthy ones. In 69,7% rats with SUB we observed the increase in local GMBF after submucosal injection of adrenaline. Second, we studied the sensitivity of gastric β_2-adrenoreceptors and the activity of two factors which are involved in β_2-adrenomediated vasorelaxation - K_(ATP)-channels and NO. The effects of submucosal injection of isoproterenol, ICI118551 and glybenclamide on GMBF as well as NO levels in gastric tissue were significantly elevated in rats with SUB vs. healthy rats. Thus, our results indicate that high activation of gastric β_2-adrenoreceptors associated with the increased vascular K_(ATP)-channels activity and elevated NO production is the important adrenergic mechanism implicated in the pathogenesis of UB.
机译：肾上腺素系统在正常状态和出血期间在调节中枢和外周循环中起重要作用。由于受损的胃粘膜血流（GMBF）是导致胃十二指肠病变（包括溃疡出血（UB））的主要原因，因此我们使用应激诱导的UB（SUB）模型研究了负责调节GMBF的大鼠的肾上腺素机制。激光多普勒血流仪（LDF）。首先，我们研究了肾上腺素对正常状态和UB期间大鼠GMBF的影响。在所有健康动物中，粘膜下肾上腺素注射引起局部GMBF降低。在UB期间，与健康大鼠相比，在30,3％的SUB大鼠中，肾上腺素的粘膜下注射伴随着不太明显的GMBF抑制。在69.7％的SUB大鼠中，我们观察到粘膜下注射肾上腺素后局部GMBF升高。其次，我们研究了胃β_2-肾上腺素受体的敏感性以及参与β_2-肾上腺素介导的血管舒张的两个因素的活性-K_（ATP）-通道和NO。 SUB大鼠与健康大鼠相比，粘膜下注射异丙肾上腺素，ICI118551和格列本脲对GMBF以及胃组织中NO水平的影响显着提高。因此，我们的结果表明，与增加的血管K_（ATP）通道活性和NO产生增加相关的胃β_2-肾上腺素受体的高激活是牵涉UB发病机理的重要肾上腺素机制。

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