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心脏停搏下手术冠脉阻力及其内皮细胞功能变化
发表时间：2008-07-26 发表者：张红超
(访问人次：241)
1张红超，1于鲁峰，1黄菊梅，1李卫红，1扬军民，2Tao W.K
(1空军总医院心外科,100036； 2美国西南医学中心外科中心实验室)
[摘要]观察心脏停搏温血灌注心肌手术中EC功能变化及其与冠状动脉阻力（CAR）变化的关系。临床资料与方法： 随机选取风湿性心脏瓣膜病（RHVD）的二尖瓣替换（MVR）病例。A组：风湿性心脏瓣膜病(RHVD)瓣膜替换术（对照组），B组：RHVD瓣膜替换术＋ECC中使用抑肽酶（实验组），各组均为20例。所有病人于阻断开始、阻断30min、阻断60min、开放前温血灌注末留取静脉血本，待分离CEC，测定血小板颗粒膜蛋白(GMP-140)、 6-酮-前列腺素F1α(6-K-F1α) 、组织型纤活酶激活物(t-PA)。记录每次温血灌注的压力及流量。结果：体外循环中各组CEC均升高，尤其是在阻断60 min；A组CEC的变化显著高于B组。与EC分泌相关的有关因子在阻断60 min有相应的升高，比较明显的是6-K-F1α在阻断后60min B组显著高于A组, 并且其高峰滞后。主动脉阻断中，可以看出B组在阻断60分和末次温血灌注中冠脉阻力明显低于A组，尤其在末次温血灌注中明显阻力显著低于对照A组。讨论：，在心脏停搏下手术时，内皮细胞功能与冠脉血管的张力调节密切相关，抑肽酶可以保护主动脉阻断温血灌注中内皮细胞的调节功能。
The variety of coronary artery resistance(CAR) during heart arrest with warm blood cardioplegia.
ZHANG Hong-chao, YU Lu-feng ,HUANG Ju-ei.(The cardiac surgery department,the general airforce hospital, Beijing 100036,China); TAO Weike. (The surgery core Lab, Southwestern medical center,Dallas,TX,75390)
Abstract:
Objective: The aim is to observe the variations of endothelial cell and coronary artery resistance(CAR) during heart arrest with warm blood cardioplegia with or without aprotinin. Methods: There were 40 patents suffered rheumatic heart disease selected randomly. The 20 patients of them were administered aprotin during ECC as B group,and control group as A. The blood samples from vine were taken at aortic clamping, 30min,60min after aortic clamping, and end warm blood perfusion. The tissue-plasminogen activator (t-PA)、the platelet granulate membrane protein 140 (GMP140) and the 6-keto-PGF1α(6-K-F1α) ，circulating endothelial cell[CEC ]were observed. The pressure and flux were recorded during warm blood cardioplegia. Results: ECC led to CEC to increase，peaking up at 60min after aortic crossclamp. The EC related proteins increased at that time, but the peak of 6-K-F1 in group B was markedly higher than than group A and was delayed to reperfusion. CAR of group B was lower than A, and reaching to signifcent difference at 60 min after aortic crossclamp. Conclusions: ECC led to EC excessive activition, injury and dysfunction. Aprotinin attenuated the process via protecting EC function.
Key words:
Extrocorporeal circulation(ECC) Endothelial cell(EC) Rheumatic heart disease
coronary artery resistance(CAR)
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