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Twelve miniature pigs were divided randomly in-to two groups(n=6).One day before thermal in-jury,Swan-Ganz catheter was introduced through theleft jugular vein into the pulmonary artery,acatheter was placed in the portal vein,and tonome-ters were put into both stomach and jejunum.A full-thickness flame burn covering 30% TBSA was pro-duced on the back of each animal under ketamineanesthesia.Fluid resuscitation according to Parklandformula was begun one hour after injury.Group Areceived no drug,while in group B anisodamine wasadministered intravenously in repeated doses of 0.4mg/kg.It-was found that in group A,though thehemodynamic parameters returned to normal range24 hours after burn,the portal blood flow was stillsignificantly lower than its preburn level,and it per-sisted up to the end of 72 hours.The reduced portalflow was accompanied by a rise of lactate content anda lowering of intramural pH(pHi)of both stomachand jejunum.Plasma diamine oxidase(DAO)activi-ty also rose,indicating that there was intestinal mu-cosal injury.Pathological evidence of intestinal mu-cosal damage was marked.Portal bacteremia ap-peared early and its incidence was high,together withan increment in endotoxin level.All these changeswere obviously ameliorated in group B animals.Itwas concluded that anisodamine,together with fluidresuscitation,would relieve mesenteric vasoconstric-tion,improve intestinal mucosal DO_2,lessen is-chemic injury to the intestinal mucosa,and diminishtranslocation of endotoxin and bacteria.The drugmight serve as a useful adjunct in combating burnshock.
Twelve miniature pigs were divided randomly in-to two groups (n = 6). One day before thermal in-jury, Swan-Ganz catheter was introduced through the left jugular vein into the pulmonary artery, acatheter was placed in the portal vein, and tonome -ters were put into both stomach and jejunum. A full-thickness flame burn covering 30% TBSA was pro-duced on the back of each animal under ketamineanesthesia. Fluid resuscitation according to Parklandformula was one hour after injury. Group Areceived no drug, while in group B anisodamine was administered intravenously in repeated doses of 0.4 mg / kg. It-was found that in group A, though thehemodynamic parameters returned to normal range24 hours after burn, the portal blood flow was still more thanificly lower than its preburn level, and it per-sisted up to the end of 72 hours. reduced portalflow was accompanied by a rise of lactate content anda lowering of intramural pH (pHi) of both stomachand jejunum. Plasma mase ofamine (DAO) activi-ty also rose, indicating t hat there was intestinal mu-cosal injury. Pathological evidence of intestinal mu-cosal damage was marked. Portal bacteremia ap-peared early and its incidence was high, together withan increment in endotoxin level. All these changeswere obviously ameliorated in group B animals.Itwas suggests that anisodamine, together with fluidresuscitation, would relieve mesenteric vasoconstric-tion, improve intestinal mucosal DO_2, lessen is-chemic injury to the intestinal mucosa, and diminish transit positions of endotoxin and bacteria. The drugmight serve as a useful adjunct in combating burnshock.