Role of nitric oxide during early phase myocardial ischemic preconditioning in rats

Background To date, there have been no reports on altered nitric oxide （NO） content in ischemia/reperfusion with regard to in vivo preconditioning procedures. These studies are important for understanding the mechanisms of NO during early myocardial ischemic preconditioning. The aim of the present study was to investigate the mechanisms of NO during early myocardial ischemic preconditioning by measuring levels of NO and cyclic guanosine monophosphate （cGMP）, as well as activity of nitric oxide synthase （NOS） in ischemia/reperfusion with respect to preconditioning in rats. Methods Sixty-six female Sprague-Dawley rats were randomly divided into four groups： ischemic preconditioning group （IP）, ischemia/reperfusion group （I/R）, control group （CON）, and preconditioning procedure group （PC）. In the PC group, rats were further divided into PC1-, PC1＋, PC2-, PC2＋, PC3-, and PC3＋ subgroups. Rats underwent left coronary artery occlusion and reperfusion, and subsequently, NOS activity and levels were assessed with spectrophotometric analysis. cGMP contents were measured with radioimmunoassay. Results The level of NO and cGMP, as well as the activity of NOS, were significantly higher in the IP group compared to the I/R and CON groups （P 〈0.05）. During preconditioning prior to prolonged ischemia, NO and cGMP levels varied markedly with ischemia and reperfusion. The levels of NO repeatedly increased when the heart was exposed to three episodes of 5-minute ischemia, and were almost completely reversed during each reperfusion period. NO and cGMP levels were significantly different between the 5-minute period of ischemia and the same period of reperfusion during preconditioning. Conclusions NO plays an important role during early phase myocardial ischemic preconditioning in rats. NO and cGMP could be triggers and mediators of early phase myocardial ischemic preconditioning. Altered NOS activity following ischemic stress could be the primary inducer of higher NO levels detected. NO and cGMP fluctuations might be the trigger for protection during early phase myocardial ischemic preconditioning.

深低温假死技术在创伤失血性休克中应用及对外周血冷诱导RNA结合蛋白表达影响

目的探讨深低温假死技术在创伤失血性休克(THS)中应用及对外周血冷诱导RNA结合蛋白(CIRP)表达的影响。方法选取北部战区总医院实验动物中心10只健康成年小型巴马香猪建立THS模型,并应用我院自行研制的便携式体外生命支持系统,联合深低温假死技术,采集不同时间点外周血样本。外周血采集的时间点包括:THS模型建立后30 min(T0)、体外循环降温结束时(T1)、停循环60 min开始恢复循环时(T2)、恢复核心温度达正常体温时(T3)。采用酶联免疫吸附方法检测CIRP、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)在THS模型建立及深低温假死救治不同时间点血浆中的表达水平。结果所有实验动物均救治成功,存活率100.0%(10/10)。与T0时比较,实验动物T1时的外周血CIRP水平显著升高,差异有统计学意义(P<0.05);与T1时比较,实验动物T2时的外周血TNF-α水平明显升高,差异有统计学意义(P<0.05);与T2时比较,实验动物T3时的TNF-α、IL-6水平显著下降,差异有统计学意义(P<0.05)。结论发生THS后,外周血CIRP首先出现表达升高,IL-6、TNF-α等炎症因子随后表达上升,在经由深低温假死救治策略救治后,表达逐渐恢复到救治前水平。

半旋转动脉干调转术临床应用效果观察

目的观察半旋转动脉干调转术的临床应用效果。方法选取北部战区总医院自2006年11月至2013年12月收治的12例接受半旋转动脉干调转术患者为研究对象,其中,11例为完全性大动脉转位、室间隔缺损合并肺动脉狭窄,1例为右心室双出口、室间隔缺损合并肺动脉狭窄。手术均采用半旋转动脉干调转术,即动脉干调转和重建+冠状动脉移植+左、右心室流出道重建,重建后右心室流出道均行心包补片加宽、肺动脉瓣成形。对患者进行随访,观察手术治疗效果。结果术后早期死亡1例,其余均恢复良好。8例患者随访成功,平均随访时间(5.0±2.2)年。随访结果显示,8例患者心脏功能良好,平均射血分数(0.54±0.02),未见主动脉瓣返流和左、右心室流出道梗阻,出现肺动脉分流轻度4例、轻-中度2例,主动脉和肺动脉呈比例增长。结论半旋转动脉干调转术治疗完全性大动脉转位/右心室双出口、室间隔缺损合并肺动脉狭窄术后血流动力学指标满意,长期随访结果良好,完全恢复解剖,肺动脉和主动脉瓣环均具有生长潜力,肺动脉瓣功能佳。