THE INVOLVEMENT OF MUSCARINIC RECEPTORS IN GASTRIC LIQUID EMPTYING IN THE CONSCIOUS RAT FOLLOWING ROUX-EN-Y-ANTRECTOMY


ALICAN I., YEGEN C., AKTAN A., OKTAY S., ULUSOY N., YEGEN B.

RESEARCH IN EXPERIMENTAL MEDICINE, cilt.194, sa.4, ss.269-275, 1994 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 194 Sayı: 4
  • Basım Tarihi: 1994
  • Doi Numarası: 10.1007/bf02576388
  • Dergi Adı: RESEARCH IN EXPERIMENTAL MEDICINE
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.269-275
  • Marmara Üniversitesi Adresli: Evet

Özet

The gastric emptying of liquid test meals is dependent on resistance to flow at the pylorus and on pressure gradients between the duodenum and the body of the stomach. In the present study, we investigated the role and subtypes of muscarinic receptors during gastric emptying of various liquid test meals in conscious rats with gastric fistula after Roux-en-Y antrectomy. In the control rats with gastric fistula but with intact reflex pathways and pylorus, the non-selective muscarinic antagonist atropine (7 mg/kg i.p.) and Mi-selective pirenzepine (7 mg/kg i.p.), acting possibly on M1 receptors, delayed saline emptying by suppressing cholinergic tone and thus relaxing the body of the stomach and contracting the pyloric sphincter. On the other hand, in Roux-rats saline and hyperosmolal saline emptying were not significantly affected, while the inhibitory effect of HCl was completely reversed. Furthermore, peptone-induced delay of gastric emptying in control rats was also reduced in Roux-rats. Pirenzepine abolished the facilitating effects of Roux-en-Y operation on acid and peptone emptying and M2-selective antagonist AF DX-116 (7 mg/kg i.p.) did not have any inhibitory effect in this regard. In conclusion, Roux-en-Y gastrectomy without vagotomy does not slow gastric emptying of liquids, and it reverses the inhibitory effects of peptone and acid through an atropine- and pirenzepine-sensitive pathway.