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实验性胰腺炎不会导致肺动脉高压。

Experimental pancreatitis does not produce pulmonary hypertension.

作者信息

Steinberg S M, Gower W R, Martin D, Carey L C, Cloutier C T

出版信息

Surg Gynecol Obstet. 1983 Dec;157(6):530-3.

PMID:6648772
Abstract

The onset of experimental hemorrhagic pancreatitis in dogs was rapidly followed by a deterioration of CO, blood pressure, LVSW and RVSW, along with significant elevations of Hct, SVR and PVR. These alterations could all be reversed by the administration of Ringer's lactate. These findings support the concept that the major physiopathologic characteristic of severe acute pancreatitis is a loss of effective plasma and extracellular fluid volumes and that the replacement of fluid losses corrects the hemodynamic alterations. In neither of the experimental groups did pulmonary hypertension develop. We found no evidence in this model of hemorrhagic pancreatitis for a circulating pulmonary vasoactive substance.

摘要

犬实验性出血性胰腺炎发作后,很快出现心输出量、血压、左心室每搏功和右心室每搏功下降,同时血细胞比容、全身血管阻力和肺血管阻力显著升高。给予乳酸林格液后,这些改变均可逆转。这些发现支持了以下观点:重症急性胰腺炎的主要病理生理特征是有效血浆和细胞外液量的丧失,补充液体丢失可纠正血流动力学改变。两个实验组均未出现肺动脉高压。在这个出血性胰腺炎模型中,我们没有发现循环中存在肺血管活性物质的证据。

相似文献

1
Experimental pancreatitis does not produce pulmonary hypertension.实验性胰腺炎不会导致肺动脉高压。
Surg Gynecol Obstet. 1983 Dec;157(6):530-3.
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[Hemodynamic effects of naloxone in early acute pancreatitis in the dog and its efficacy in treating acute pancreatitis].[纳洛酮对犬早期急性胰腺炎的血流动力学影响及其治疗急性胰腺炎的疗效]
Zhonghua Wai Ke Za Zhi. 1989 Mar;27(3):173-6, 190.

引用本文的文献

1
Review of experimental animal models of acute pancreatitis.急性胰腺炎实验动物模型的综述。
HPB (Oxford). 2006;8(4):264-86. doi: 10.1080/13651820500467358.
2
Role of reactive oxygen metabolites in early cardiopulmonary changes of acute hemorrhagic pancreatitis.
Dig Dis Sci. 1989 Oct;34(10):1581-4. doi: 10.1007/BF01537114.