Izzo A A, Mascolo N, Autore G, Di Carlo G, Capasso F
Department of Experimental Pharmacology, University of Naples Federico II, Italy.
J Pharm Pharmacol. 1993 Oct;45(10):916-8. doi: 10.1111/j.2042-7158.1993.tb05621.x.
The effects of in-vivo treatment with bisacodyl, phenolphthalein, picosulphate, sulphosuccinate, mannitol and lactulose laxatives were examined on the ex-vivo formation of platelet-activating factor (PAF) by duodenum and colon of rat, mouse, guinea-pig and rabbit. Bisacodyl (10 mg kg-1), phenolphthalein (20 mg kg-1) and picosulphate (10 mg kg-1), but not sulphosuccinate (40 mg kg-1), mannitol (50 mg kg-1) or lactulose (50 mg kg-1), at doses that all caused laxation, markedly increased PAF in the colon (P < 0.01) but not in the duodenum. Intraluminal release of acid phosphatase was also significantly increased in the colon of rats treated with bisacodyl, phenolphthalein and picosulphate, but not in colons of animals treated with sulphosuccinate, mannitol or lactulose. The data show that enhanced generation of PAF is associated with the colonic damage induced by diphenylmethane laxatives, but do not show whether this is a cause or a consequence of the pathophysiological changes.
研究了用比沙可啶、酚酞、匹可硫酸钠、磺基琥珀酸酯、甘露醇和乳果糖泻药进行体内治疗对大鼠、小鼠、豚鼠和兔十二指肠和结肠体外生成血小板活化因子(PAF)的影响。比沙可啶(10毫克/千克)、酚酞(20毫克/千克)和匹可硫酸钠(10毫克/千克),但不包括磺基琥珀酸酯(40毫克/千克)、甘露醇(50毫克/千克)或乳果糖(50毫克/千克),在所有导致腹泻的剂量下,均显著增加结肠中的PAF(P<0.01),但在十二指肠中未增加。用比沙可啶、酚酞和匹可硫酸钠治疗的大鼠结肠中酸性磷酸酶的腔内释放也显著增加,但用磺基琥珀酸酯、甘露醇或乳果糖治疗的动物结肠中未增加。数据表明,PAF生成增强与二苯甲烷类泻药引起的结肠损伤有关,但未表明这是病理生理变化的原因还是结果。