Filaretova Ludmila, Myazina Marina, Bagaeva Tatiana
Pavlov Institute of Physiology, Russian Academy of Sciences, St. Petersburg, Russia.
Ideggyogy Sz. 2016 Sep 30;69(9-10):313-317. doi: 10.18071/isz.69.0313.
To investigate contribution of glucocorticoids to the maintenance of gastric mucosal integrity during stress we predominantly used ulcerogenic stress models. Using these models we demonstrated that glucocorticoids released in response to the ulcerogenic stimuli attenuated their harmful action on the gastric mucosa. In the present study we hypothesized that mild stressors does not damage the gastric mucosa due to gastroprotective action of glucocorticoids released in response to these stressors.
To verify the hypothesis the effects of normally non-ulcerogenic mild stimuli (15-30 min cold-restraint) on the gastric mucosal integrity have been studied under the circumstances of inhibition of the hypothalamic-pituitaryadrenocortical axis in rats. The hypothalamic-pituitary-adrenocortical axis was inhibited by: 1) fast inhibitory action of metyrapone, inhibitor glucocorticoid synthesis; 2) fast inhibitory action of NBI 27914, the selective antagonist of cortricotropin- releasing factor receptor type 1; 3) delayed inhibitory action of a single pharmacological dose of cortisol injected one week before the onset of stress stimulus.
Each of these pretreatments significantly decreased 15-30 min cold-restraint-produced corticosterone levels: 37.2±1 vs 22.5±1.2 (p<0.05) after metyrapone; 52.1±0.9 vs 41.4±1 (p<0.05) after NBI, and 64.2±4.2 vs 16.7±1.5 (p<0.05) after cortisol pretreatment. The inhibition of stress-induced corticosterone rise resulted in an ap - pearance of gastric lesions after the onset of these mild stressors in rats.
The results suggest that in rats with inhibited stress-induced corticosterone rise normally non-ulcerogenic stimuli are transformed into ulcerogenic ones and confirm the hypothesis. The findings further support for the point of view that glucocorticoids released during acute stress are gastroprotective factors.
为研究糖皮质激素在应激期间对维持胃黏膜完整性的作用，我们主要使用了致溃疡应激模型。通过这些模型，我们证明了因致溃疡刺激而释放的糖皮质激素减弱了它们对胃黏膜的有害作用。在本研究中，我们假设轻度应激源不会损伤胃黏膜，这是由于对这些应激源产生反应而释放的糖皮质激素具有胃保护作用。
为验证该假设，我们在抑制大鼠下丘脑 - 垂体 - 肾上腺皮质轴的情况下，研究了通常无致溃疡作用的轻度刺激（15 - 30分钟冷束缚）对胃黏膜完整性的影响。通过以下方式抑制下丘脑 - 垂体 - 肾上腺皮质轴：1）美替拉酮（一种糖皮质激素合成抑制剂）的快速抑制作用；2）促肾上腺皮质激素释放因子1型受体的选择性拮抗剂NBI 27914的快速抑制作用；3）在应激刺激开始前一周注射单剂量药理剂量皮质醇的延迟抑制作用。
每种预处理均显著降低了15 - 30分钟冷束缚产生的皮质酮水平：美替拉酮处理后为37.2±1对比22.5±1.2（p<0.05）；NBI处理后为52.1±0.9对比41.4±1（p<0.
