AIM To investigate the effect and regulation of electrical stimulation on the paraventricular nucleus (PVN)of hypothalamus using rat gastric ischemia-reperfusion injury (I-RI)induced ulcer model.METHODS Adult male Sprague-Dawley rats weighing 150 g-250 g were used. The surgically prepared ratswere kept fasting for 24 h, but allowed free access to water. They were then anesthetized with urathane(1 g/kg), the celiac artery was clamped with a small clip (holding force 145 g) for 30min, reperfusion wasestablished by removal of the clamp, 60min after reperfusion, the rats were killed and their stomachs wereremoved and perfused intragastrically with 100 mL/L formalin for 30min, and the ulcer index was scoredaccording to Guth et al. The PVN was obtained according to atlas of Paxinos and Watson. The electrodesand cannula were inserted into the PVN for the electrical stimulation, electrical injury and PVN injection，RESULTS In control group (30min ischemia and 60ain reperfusion only), ulcer index was 184.70±60.80(n = 8); in electrical stimulations of PVN (0.2mA, 0.4mA and 0.6mA) + I-RI group, ulcer indexes were102.40±20.39, 85.37±39.76 and 45.00±19.04 (n =8) respectively. Compared with the control groupthere was significant difference ( P < 0.01) in a dose-dependent manner. In electrical lesion of bilateral PVN+ I-RI group, ulcer index was greatly increased (230.00±47.30, n = 8). Microinjection of 3% L-glutamate0.5μL into PVN could produce similar effect to that of PVN stimulation (ulcer index 75.14±37.18, n = 8).A further study indicated that the MDA, pepsin activity and gastric acidity were reduced by PVN stimulationbut no obvious changes of gastric juice volume, total acid output and gastric mucus barrier were observed.CONCLUSION The PVN is one of the specific CNS areas capable of protecting the gastric ischemic-reperfusion injury in rats, and related to decreased MPA, pepsin activity, gastric acidity, while gastric juicevolume, total acid output and gastric mucus do not likely play any important role in it.