Effects of Centrally Administered Neuropeptides on The Developement of Acute Gastric Lesions in The Rat.

• Project/Area Number: 60570669
• Research Category: Grant-in-Aid for General Scientific Research (C)
• Allocation Type: Single-year Grants
• Research Field: Cerebral neurosurgery
• Research Institution: Nagoya University
• Principal Investigator: NAKANE Toshichi Department of Neurosurgery, Nagoya University School of Medicine, 医学部, 助手 (80172360)
• Co-Investigator(Kenkyū-buntansha): MORISE Kimitomo First Division, Department of Internal Medicine, Nagoya University School of Med, 医学部, 助手 (50182233)
• Project Period (FY): 1985 – 1986
• Project Status: Completed (Fiscal Year 1986)
• Budget Amount: ¥1,600,000 (Direct Cost: ¥1,600,000); Fiscal Year 1986: ¥300,000 (Direct Cost: ¥300,000); Fiscal Year 1985: ¥1,300,000 (Direct Cost: ¥1,300,000)
• Keywords: Acute gastric mucosal lesion / Neuropeptides / TRH / CRF

Research Abstract

It has been reported that various neuropeptides(brain-gut hormones) influence on the development of acute gastric mucosal lesions in the rat. In this work to be presented, we investigated the effects of centrally administered neuropeptides on dynamics of gastric mucosal blood flow(GMBF) and CRF content of rat hypothalamus, especially focused on TRH.
Mean rat GMBF before treatment was 47.2 <+!-> 2.2 ml/min/100gr(Mean <+!-> SE), measured by hydrogen clearance method. After intracisternal injection of TRH, GMBF was decreased significantly by 31.7 <+!-> 4.1 ml/min/100gr within an hour, then restored to normal range. No obvious change was noted in saline-treated rats. Hypothalamic CRF contents after intracisternal administration of various neuropeptides were measured using radioimmunoassay establised by ourselves. CRF content after saline-injection was 1.24 <+!-> 0.06 ng/mg protein, while those in TRH-VIP-bombesin-and neurotensin-treated groups were 0.83 <+!-> 0.03, 0.98 <+!-> 0.06, 1.19 <+!-> 0.09 and 1.08 <+!-> 0.03 ng/mg protein, respectively. Moreover, hypothalamic CRF level after cold-restraint stress, which was widely used to produce experimental gastric lesions, was 0.91 <+!-> 0.06 ng/mg protein. CRF depletion in TRH-treated and cold-restraint rats, was statistically significant compared with that in saline-treated ones.
These results suggest that centrally administered TRH may have similar effect on change of hypothalamic CRF to cold-restraint stress, and decreased GMBF may play a role partly on the development of acute gastric mucosal lesions induced by TRH.