Glavin G B, Westerberg V S, Geiger J D
Can J Physiol Pharmacol. 1987 Jun;65(6):1182-5. doi: 10.1139/y87-186.
Basal (nonstimulated) gastric acid output was determined in conscious rats fitted with indwelling gastric cannulae. The adenosine deaminase resistant analog of adenosine, R-phenylisopropyladenosine, elevated intraluminal pH beyond 7.0 and decreased gastric acid secretion when given at doses of 0.10 or 1.0 mg/kg, while S-phenylisopropyladenosine at similar doses did not affect either gastric acid output or pH. The potent adenosine receptor antagonist, 8-phenyltheophylline, given at doses of 0.1, 1.0, and 2.5 mg/kg augmented gastric acid output and, at doses of 0.01, 0.1, 1.0, and 2.5 mg/kg, blocked the acid-reducing effect of R-phenylisopropyladenosine (0.1 mg/kg). These data suggest that adenosine systems may be important regulators of gastric function.
在植入了留置胃插管的清醒大鼠中测定基础(非刺激状态下)胃酸分泌量。腺苷的抗腺苷脱氨酶类似物R-苯异丙基腺苷,以0.10或1.0毫克/千克的剂量给药时,可使管腔内pH值升高至7.0以上,并减少胃酸分泌,而类似剂量的S-苯异丙基腺苷对胃酸分泌量或pH值均无影响。强效腺苷受体拮抗剂8-苯甲基茶碱,以0.1、1.0和2.5毫克/千克的剂量给药时可增加胃酸分泌量,以0.01、0.1、1.0和2.5毫克/千克的剂量给药时可阻断R-苯异丙基腺苷(0.1毫克/千克)的胃酸分泌减少作用。这些数据表明腺苷系统可能是胃功能的重要调节因子。