ABSTRACT
AIM:To investigate the effects of TRH in DVC on motility of the gallbladder in rabbits.METHODS:fter fasted for 15h-18h, rabbits were anesthetized with urethane (1.0g/kg).Gallbladder pressure (GP) was measured by a frog bladder perfused with normal saline.RESULTS:After microinjection of TRH (8.8nmol,1&mgr;l) into DVC,GP was raised and the frequency of phasic contraction of gallbladder (FPCGB) increased. All the doses of TRH (0.13, 0.25, 0.50, 0.80, 1.30nmol, 1&mgr;l) injected into DVC could excite the motility of gallblader. As the dose of TRH was enlarged, the amplitude and duration of the reaction increased. Effects of TRH in DVC on motility of the gallbladder could be completely abolished by atropine (0.2mg/g, i.v.) or vagotomy, but could not be inhibited by phentolamine iv (1.5mg/g) or propranolol iv (1.5mg/g)or by transecting the spinal cord.CONCLUSION: Thyrotropin-releasing hormone in DVC can excite motility of gallbladder. This effect was mediated by vagus nerves and peripheral M receptor. Its physiological significance may be related to maintaining the phasic contraction of gallbladder in interdigestive period.
ABSTRACT
AIM:To observe the effect of octreotide (OT) and somatostatin (SS) on gallbladder pressure and myoelectric activity of SO in rabbits.METHODS:Male rabbits fasted for 15h-18h and anesthetized with urethane. The mean gallbladder pressure (GP) and myoelectric activity of SO were simutaneously measured with a frog bladder connected to a transducer and a pair of copper electrodes.RESULTS:After injection of OT (10&mgr;g/kg, iv), the GP decreased in 2min and reached the lowest value in about 60min (P < 0.01, n = 19), and completely or partially returned to the normal level in 120min. The frequency of myoelectric activty of SO was reduced, even disappeared in 2min (P < 0.01, n = 19) and returned to normal in about 20min. Injection of SS (10&mgr;g/kg, iv) also decreased GP and myoelectric activity of SO (P < 0.01, n = 7); Before and after injection of OT or SS, injection of CCK-8 (100ng or 200ng) caused similar increase in myoelectric activity of SO and GP (P >0.05). Before and after injection of OT, there were no significant differences in increases of myoelectric activity of SO and GP caused by electric stimulation of dorsal motor nucleus of vagus (P >0.05).CONCLUSION:OT and SS decreased GP and myoelectric activity of SO, demonstrating that effects of OT were similar to those of SS. Intravenous injection of OT did not affect the increase of myoelectric activity of SO and GP caused by CCK-8 or electric stimulation of dorsal motor nucleus of vagus.
