药剂乳化防止中性粒细胞活化,提高冷缺血和再灌注后心肌功能恢复。

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盖尔SC,戈尔曼GD,科普兰詹,McDonagh PF

药剂乳化防止中性粒细胞活化,提高冷缺血和再灌注后心肌功能恢复。

杂志》2007年3月,138 (1):135 - 40。Epub 2006年12月14日。

PubMed ID

17173933 (在PubMed

]

文摘

背景:在心肺旁路,体外循环激活中性粒细胞,引起缺血再灌注损伤和术后心肌功能障碍。全氟化碳(全氟化物)化合物溶解氧气和具有抗炎和neutrophil-stabilizing特性。我们假设药剂乳液(PFE), PFC,减弱中性粒细胞激活在模拟体外循环(SECC)并将保存在冷缺血后再灌注心肌功能恢复。方法:SECC,稀释血液流通了120分钟,随后用于reperfuse孤立的老鼠心脏2 h后冷(12摄氏度)缺血。三组进行了研究:noncirculated控制;SECC /不加;和SECC / pfizer补充道。在控制和SECC /不添加剂组,全血与plasmalyte 1:1稀释。SECC /工业的血液稀释、plasmalyte 1:1 pfizer (0.075 mL /毫升稀释全血)。血液计数和嗜中性粒细胞活化实验SECC 120分钟之前和之后执行。 Reperfusion was accomplished using a modified Langendorff preparation. Left ventricular developed pressure, dP/dt, and coronary flow were measured at 10, 15, and 20 min of reperfusion. RESULTS: After 120 min SECC, neutrophil activation was significantly reduced in the SECC/PFE group compared to the SECC/no additive group (38.1 +/- 2.3% versus 51.7 +/- 1.0%, P < 0.05). Compared to cold ischemic hearts reperfused with fresh, non-recirculated blood, left ventricular developed pressure and dP/dt were significantly impaired in the cold ischemic hearts reperfused with SECC/no additive blood (P < 0.05). In contrast, myocardial functional recovery was not impaired in the hearts reperfused with SECC/PFE blood. CONCLUSIONS: SECC-induced neutrophil activation was attenuated with Perflubron treatment. In addition, the progressive impairment in myocardial functional recovery after cold ischemia was significantly improved with treatment. PFE has clinical potential to limit neutrophil-mediated reperfusion injury following cold ischemia.

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