receptor overexpression in the lateral hypothalamic area attenuates gastric ischemia-reperfusion injury in rats

Excessive activation of the greater splanchnic nerve (GSN) has previously been determined to contribute to the progression of gastric ischemia-reperfusion (GI-R) injury. The present study was designed to estimate the protective effects of [GABA.sub.A] receptor ([GABA.sub.A]R) overexpression in the lateral hypothalamic area (LHA) against GI-R injury. The GI-R injury model was induced in rats by clamping the celiac artery for 30 min and then reperfusing for 1 h. Microinjection of recombinant adenoviral vectors overexpressing [GABA.sub.A]R (Ad-[GABA.sub.A]R) or control adenoviral vectors (Ad-Con) into the LHA was conducted in GI-R and normal control rats. Significant protective effects were observed on day 2 after Ad-[GABA.sub.A]R treatment in the GI-R injury rats. Ad-[GABA.sub.A]R treatment reduced plasma norepinephrine levels, plasma angiotensin II levels and peripheral GSN activity, but increased the gastric mucosal blood flow, as compared with Ad-Con treatment. These results indicate that adenoviral vector-induced [GABA.sub.A]R overexpression in the LHA blunts GSN activity and subsequently alleviates the effects of gastric injury in GI-R rats. Key words: lateral hypothalamic area, gastric ischemia reperfusion injury, [GABA.sub.A] receptor