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供体心脏保存中再灌注心肌胶原基质变化的机制

Mechanism of changes of the collagen matrix of reperfused myocardium in donor heart preservation.

作者信息

Ohnuki M, Sunamori M, Amano J, Suzuki A

机构信息

Department of Thoracic-Cardiovascular Surgery, Tokyo Medical and Dental University, School of Medicine, Japan.

出版信息

J Thorac Cardiovasc Surg. 1993 Jul;106(1):172-9.

PMID:8320996
Abstract

Isolated canine hearts were preserved for 6 hours at 5 degrees C followed by normothermic reperfusion for 2 hours. Dogs were divided into two groups: group I (group Ia [n = 7] and group Ib [n = 3] with the left ventricle unloaded during reperfusion) received a preservation solution containing potassium (20 mmol/L), and group II (n = 9) received University of Wisconsin solution. Left ventricular diastolic function was better preserved in group II. Degradation and loss of the collagen network during reperfusion, as assessed by scanning electron microscopy, were more extensive and significantly more frequent in group Ia than in group II (6/7 versus 2/9; p < 0.05). Furthermore, extensive disruption of the collagen network was significantly more prevalent in hearts with a left ventricular end-diastolic pressure of more than 20 mm Hg than in hearts with a left ventricular end-diastolic pressure of less than 20 mm Hg (8/10 versus 0/6; p < 0.05), and no disruption of the collagen network occurred in group Ib, regardless of the type of preservation solution. These results suggest that the greatest disruption is caused by barotrauma resulting from an elevated left ventricular end-diastolic pressure after ventricular dysfunction caused by ischemic reperfusion injury.

摘要

将离体犬心在5℃下保存6小时,随后进行2小时的常温再灌注。犬被分为两组:第一组(第一组a [n = 7]和第一组b [n = 3],再灌注期间左心室卸载)接受含钾(20 mmol/L)的保存液,第二组(n = 9)接受威斯康星大学溶液。第二组左心室舒张功能保存较好。通过扫描电子显微镜评估,再灌注期间第一组a的胶原网络降解和丢失比第二组更广泛且明显更频繁(6/7对2/9;p < 0.05)。此外,左心室舒张末期压力超过20 mmHg的心脏中胶原网络的广泛破坏比左心室舒张末期压力低于20 mmHg的心脏中明显更普遍(8/10对0/6;p < 0.05),并且无论保存液类型如何,第一组b中均未发生胶原网络破坏。这些结果表明,最大的破坏是由缺血再灌注损伤导致心室功能障碍后左心室舒张末期压力升高引起的气压伤所致。

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