[Effects of electrical stimulation of lateral hypothalamic area on gastric ischemia-reperfusion injury in rats].

The effects of electrical and chemical stimulation and electrolytic lesion of lateral hypothalamic area (LHA) on gastric ischemia reperfusion injury (GI RI) were investigated in rats whose celiac arteries were clamped for 30 min and reperfused for 60 min by removal of the clamp. The results are as follows. (1) Electrical stimulation of LHA could aggravate GI RI in an intensity dependent manner by using 0 2, 0 4 or 0 6 mA current respectively. Microinjection of L glutamic acid into LHA resulted in a similar effect to that of electrical stimulation of LHA on GI RI. After electrolytic lesion of bilateral LHA, the area of gastric mucosal injury induced by gastric ischemia reperfusion (GI R) was smaller than that by electrical stimulation of LHA plus GI R. (2) Dorsal vagal complex (DVC) lesion or vagotomy could eliminate the effect of electrical stimulation of LHA on GI RI. (3) Electrical stimulation of LHA increased the content of malondialdehyde (MDA) but decreased the activity of superoxide dismutase (SOD) of ischemia reperfusion (I R) gastric mucosa. (4) Electrical stimulation of LHA plus gastric I R increased gastric juice volume and total acid output, but there were no significant changes in acidity, pepsin activity and gastric barrier mucus. These results indicate that the LHA is an area in the CNS exerting aggravative effects on GI RI. The DVC and vagus may be involved in the regulative effects of LHA on GI RI. These effects are associated with increases in gastric mucosal MDA content, gastric juice volume, and total acid output, and a decrease in SOD activity.Acidity, pepsin activity and gastric barrier mucus do not seem to play an important role.