间断性低压性缺氧对大鼠下丘脑NOS和生长抑素神经元的影响

EFFECT OF INTERMITTENT HYPOBARIC HYPOXIA ON NOS AND SOMATOSTATIN NEURONS IN RAT HYPOTHALAMUS

本研究采用 NADPH-d组化与生长抑素免疫组化技术探讨了间断性低氧 (每天 6h) 1d、7d、15 d、2 1d和 3 0 d对大鼠下丘脑内一氧化氮合酶 (NOS)和生长抑素的影响。结果表明 :间断性低压性低氧可使下丘脑室旁核、视上核 NOS和室周核生长抑素阳性神经元数量明显增多 ,且低氧第 1d即达高峰 ,7和 15 d维持较高水平 ,2 1d开始下降 ,3 0 d则明显减少。NOS阻滞剂 L-NAME(3 0 mg/kg,ip)明显抑制低氧诱导下丘脑生长抑素阳性神经元数的增多。以上结果说明 ,下丘脑内源性的 NO与生长抑素参与了间断性低压性缺氧反应 ,并与慢性缺氧的适应反应有关 ;此外 。

The effect of hypobaric hypoxia intermittently 6 h daily for 1 d, 7 d, 15 d, 21 d and 30 d on NOS and somatostatin in rat hypothalamus was investigated with the methods of NADPH d histochemistry and somatostatin immunohistochemistry. The results showed that the number of NOS positive neurons in supraoptic nucleus (SON) and paraventricular nucleus (PVN) and somatostain immunoreactive(SST IR)neurons in periventricular nucleus (PeV) increased significantly under 1 d hypoxia, kept high level under 7 d and 15 d hypoxia, lowering began under 21 d hypoxia, decreased significantly under 30 d hypoxia. L NAME(30 mg/kg,i.p.), a blocker of NOS, inhibited the increase of SST IR in hypothalamus caused by hypobaric hypoxia. We conclude that hypothalamic endogenous NO and somatostatin participate in intermittent hypoxic reaction, and are related to adaptive reaction of chronic hypoxia; in addition, NO as hypothalamic endogenous neurotransmitter promotes somatostatin release.