Effect of increasing biliary tract pressure on house rabbit blood dynamics in acute cholangitis of severe type

In this study 12 Japanese long ear rabbits were used as models of acute cholangitis of severe type (ACST), and also an increasing pressure apparatus of self-made caecus to form high pressure of the biliary tract. The animals were observed for changes in blood dynamics in an attempt to explore the ef...

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Bibliographic Details
Published inJournal of Tongji Medical University Vol. 14; no. 4; p. 230
Main Authors Zheng, Q C, Qi, L H, Hu, Y H, Guan, M L, Wang, D X
Format Journal Article
LanguageEnglish
Published China 01.12.1994
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Summary:In this study 12 Japanese long ear rabbits were used as models of acute cholangitis of severe type (ACST), and also an increasing pressure apparatus of self-made caecus to form high pressure of the biliary tract. The animals were observed for changes in blood dynamics in an attempt to explore the effect and relation of high pressure of biliary tract and infective element in pathogenesis of ACST. It was found that when the biliary pressure was increased within 120 min in the 20 kPa group, the blood endotoxin level showed no obvious increment (P > 0.05), but the decreased range of average MAP (mean artery pressure) was over 4 kPa, and the cardiac output also decreased evidently (P < 0.05), and that when the biliary pressure was decreased, MAP and cardiac output were restored to normal gradually. Of these animals 3 didn't restore their normal condition when the blood pressure decreased to zero and died finally. Meanwhile the electric discharge frequency of the right greater splanchnic nerves increased (P < 0.05), but when pressure was reduced, the frequency slowed down. From the above findings, the authors came to the conclusion that the rapid increase of the biliary tract pressure is the important factor leading to a decrease in blood pressure of ACST, and even bringing about irreversible shock, which is involved in the activity of splanchnic nerves.
ISSN:0257-716X
DOI:10.1007/BF02897675