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[出血性胰腺炎:右旋糖酐40和血浆对胰腺微循环障碍的影响]

[Hemorrhagic pancreatitis: effect of dextran 40 and plasma on microcirculation disorders of the pancreas].

作者信息

Becker H, Senninger N

出版信息

Langenbecks Arch Chir. 1985;365(1):57-67. doi: 10.1007/BF01261213.

Abstract

A dog model was used to measure the hemodynamic changes occurring during acute pancreatitis induced by intraductal injection of fresh trypsin-bile-blood mixture. Continuous measurements of pancreatic blood flow, cardiac output, mean arterial blood pressure and pancreatic oxygen consumption were made under normal conditions and during acute pancreatitis. All animals received 100 ml of saline/h during the time of observation. Three methods of therapy then were instituted in the dogs starting 30 min after induction of pancreatitis. 10 dogs served as controls (saline 100 ml/h); in 6 dogs additionally 15 ml/kg plasma was infused over 45 min and 6 dogs received 1.5 ml/kg Dextran 40/h continuously. Hemorrhagic pancreatitis was characterized by a fall in cardiac output and mean arterial pressure and the development of severe impairment of the pancreatic microcirculation with early reduction of pancreatic blood flow followed by a fall in pancreatic oxygen consumption. Administration of plasma produced a significant increase in cardiac output; however, blood pressure and pancreatic blood flow remained low. Low-molecular weight Dextran has no influence on cardiac output, but significantly improved the blood pressure and leads to a normalization in pancreatic blood flow and oxygen consumption. These results suggest that low-molecular weight Dextran appears to reverse the impairment of microcirculation and hypoxia of the pancreas and limits the progression from edematous to hemorrhagic pancreatitis and irreversible pancreatic damage.

摘要

采用犬模型来测量经导管注射新鲜胰蛋白酶 - 胆汁 - 血液混合物诱导急性胰腺炎期间发生的血流动力学变化。在正常条件下以及急性胰腺炎期间,持续测量胰腺血流、心输出量、平均动脉血压和胰腺氧耗量。在观察期间,所有动物每小时接受100毫升生理盐水。在诱导胰腺炎30分钟后,对犬采用三种治疗方法。10只犬作为对照组(每小时100毫升生理盐水);6只犬在45分钟内额外输注15毫升/千克血浆,6只犬持续接受1.5毫升/千克右旋糖酐40/小时。出血性胰腺炎的特征是心输出量和平均动脉压下降,胰腺微循环严重受损,胰腺血流早期减少,随后胰腺氧耗量下降。输注血浆使心输出量显著增加;然而,血压和胰腺血流仍较低。低分子量右旋糖酐对心输出量无影响,但能显著改善血压,并使胰腺血流和氧耗量恢复正常。这些结果表明,低分子量右旋糖酐似乎能逆转胰腺微循环障碍和缺氧,并限制从水肿性胰腺炎向出血性胰腺炎的进展以及不可逆的胰腺损伤。

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