Venho V M, Mattila M J
Acta Pharmacol Toxicol (Copenh). 1979 Jul;45(1):36-40. doi: 10.1111/j.1600-0773.1979.tb02357.x.
In order to confirm our previous findings of increased sulphafurazole (sulfisoxazole, SF) inactivation by intestinal occlusion, SF was given intravenously 20 mg/kg to rats with a low small intestinal occlusion and to sham-operated controls 40-45 hours after the operation. Occlusion did not cause major changes in the distribution of SF to various tissues, but there were some indications of increased SF acetylation after occlusion. The occlusion rats produced ascitic fluid into the abdominal cavity and the total SF levels in the ascitic fluid were almost identical to those in blood, also after oral administration of SF, 50 mg/kg. After intraperitoneal administration of 2 ml of SF (60 microgram/ml) more SF accumulated into the small intestinal wall in occlusion rats than in controls, and the acetyl SF levels were increased in the small and large intestine. So, our previous suggestion of an increased excretory function of the large intestine in occlusion states may not be the only explanation for increased drug levels in the large intestine found after oral administration of SF. Part of the SF in the intestinal wall can also result from ascitic fluid SF, and ascites must be taken into account when considering drug pharmacokinetics.
为了证实我们之前关于肠道梗阻会增加磺胺异恶唑（SF）失活的发现，在术后40 - 45小时，给小肠低位梗阻的大鼠静脉注射20mg/kg的SF，并给假手术对照组同样剂量的药物。梗阻并未导致SF在各组织中的分布发生重大变化，但有一些迹象表明梗阻后SF的乙酰化增加。梗阻大鼠腹腔内产生腹水，口服50mg/kg的SF后，腹水中SF的总水平与血液中的几乎相同。腹腔注射2ml SF（60μg/ml）后，梗阻大鼠小肠壁中积累的SF比对照组更多，并且小肠和大肠中乙酰化SF的水平均升高。因此，我们之前提出的在梗阻状态下大肠排泄功能增强的观点，可能不是口服SF后大肠中药物水平升高的唯一解释。肠壁中的部分SF也可能来自腹水SF，在考虑药物药代动力学时必须考虑腹水的因素。
