Intracerebroventricular calcitonin prevents stress-induced gastric dysfunction

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.

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 microg of calcitonin ICV (10 microl volume), while controls (n = 10) received 10 microl of ICV saline prior to restraint for 2 h at 20 degrees C followed by 2 h at 4 degrees C. Gastric motility data were collected with AT-CODAS and analyzed with ADVANCED CODAS. Gastric volume, pH, and lesions were recorded following the stress.

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).

Pretreatment with 5 microg central sCT prevents the increased amplitude and duration of gastric contractions produced by restraint stress for 2 h, in association with gastroprotection.