Intracerebroventricular calcitonin prevents stress-induced gastric dysfunction

Autor: Derek DuBay, Joseph J. Cullen, Kimberly S. Ephgrave, Kimberly A Broadhurst
Rok vydání: 2003
Předmět:
Zdroj: Journal of Surgical Research. 110:188-192
ISSN: 0022-4804
Popis: Background. Restraint stress produces gastric hypercontractility and acidity leading to stress ulceration. Intracerebroventricular (ICV) salmon calcitonin (sCT) decreases restraint injury and acidity, but its effects on restraint-induced hypercontractility are unknown. Methods. Using stereotactic guidance, ICV catheters were placed into the lateral ventricle of adult male rats and calibrated gastric strain gauge transducers were implanted 5 days prior to restraint stress. sCT rats (n = 8) were pretreated with 5 μg of calcitonin ICV (10 μl volume), while controls (n = 10) received 10 μl of ICV saline prior to restraint for 2 h at 20°C followed by 2 h at 4°C. Gastric motility data were collected with AT-CODAS and analyzed with ADVANCED CODAS. Gastric volume, pH, and lesions were recorded following the stress. Results. ICV calcitonin prevented gastric mucosal injury in all animals (0% vs 100%, P < .01) and elevated pH slightly (2.5 ± .3 vs 1.6 ± .1, P < .05). Stress caused the force of contractions to increase from 0.35 ± .1 to 1.38 ± .4 g in controls (P < .01), while treated animal’s force fell from .42 ± .1 to 0.2 ± .05 g (P < .01 vs control). Stress did not affect contractions/min (3.4 + .6 vs 3.5 + .3), but sCT increased frequency (2.5 + .4 to 5.0 + .2, P < .01). Stress prolonged contraction duration (11.5 + 1 to 16.5 + 1.7 s, P < .01), but stress’s effect was prevented by sCT (11.0 + .5 to 11.2 + .3, P < .01 vs control). Conclusions. Pretreatment with 5 μg central sCT prevents the increased amplitude and duration of gastric contractions produced by restraint stress for 2 h, in association with gastroprotection.
Databáze: OpenAIRE
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