Abstract: Objective To investigate the relationship between graft flow and incidence of perioperative myocardial infarction (MI) in coronary artery bypass grafting (CABG). Methods Between January 2010 and June 2010, 58 consecutive patients with coronary artery disease who underwent offpump CABG in the First Hospital of Peking University were enrolled in this study. An anastomosis between left internal mammary arteries (LIMA) and left ant erior descending coronary artery (LAD) were performed. And saphenous vein (SV) graft s were used as bypass grafts. Graft flow was measured intraoperatively using a transi t time flowmeter, and the total graft flow of each patient was calculated as a parameter of myocardial revascularization. The 58 patients were divided into a MI group and a nonMI group retrospectively. There were 11 patients in the MI group, including 7 males and 4 females, with an average age of 67.4±10.3 years.There were 47 patients in the nonMI group, 38 males and 9 females, with a mean age of 633±99 years. The graft flow of the two groups was tested and compared, and the preoperative variables were compared. Results There was no statistically significant difference in operation time (205.4±59.6min versus 1834±32.4 min, t=1.691, P=0.096) between the two groups. Therewere also no statistical differences in the average number of grafts (3.00±1.00 branches versus 2.96±0.78 branches, t=0.154, P=0878) or LIMALAD flow (1540±11.37 ml/min versus 16.50±10.83 ml/min, t=0.301, P=0.764) between the two groups. However, a significant difference was found in the total graft flow between the two groups (41.03±19.50 ml/min versus 64.09±32.44 ml/min, t=2.254, P=0.028), with lower total graft flow in the MI group. Further analysis showed [CM(159mm]that a total graft flow lt;48.5ml/min was a risk factor for MI (odds ratio 4.706, 95% confidence interval 1.099 to 20.147). Conclusion Total graft flow could be used to predict the occurrence of perioperative myocardial ischemia, as there is a high probability of MI for patients with a total graft flow of less than 48.5 ml/min.
【摘要】 目的 探讨凋亡抑制蛋白Livin与凋亡蛋白Caspase-3在结直肠腺瘤-癌序列中的表达变化及其相关性。 方法 2006年7月—2009年12月，采用免疫组织化学染色链霉菌抗生物素蛋白-过氧化物酶链接法streptavidin-peroxidese，SP）法检测18例正常黏膜、84例结直肠腺瘤、72例结直肠癌中Livin及Caspase-3的表达情况。 结果 结直肠腺瘤组织中Livin蛋白的阳性表达率明显高于正常黏膜组织（Plt;0.05），而低于腺癌组（Plt;0.05）；腺瘤组内绒毛状腺瘤与管状腺瘤相比较，Livin蛋白表达率差异有统计学意义（Plt;0.05）。结直肠腺瘤组织中Caspase-3的阳性表达率明显高于正常黏膜组织（Plt;0.05）；而腺瘤组织与癌组织之间Caspase-3阳性表达率差异（Plt;0.05）；腺瘤组内绒毛状腺瘤与管状腺瘤相比较，Caspase-3蛋白阳性表达率差异无统计学意义（Pgt;0.05）。Livin表达与Caspase-3表达呈负相关（Plt;0.05）。 结论 凋亡抑制蛋白Livin参与了大肠肿瘤的发生，且在大肠腺瘤-腺癌阶段起到了重要作用；凋亡抑制蛋白Livin与Caspase-3表达呈负相关，抑制Caspase-3蛋白的活性可能是Livin促进结肠癌发生的途径之一。【Abstract】 Objective To investigate the expression of Livin and Caspase-3 among colorectal adenoma-carcinoma sequence, and to identify the relationship between Livin and Caspase-3 expression in colorectal adenoma-carcinoma sequence. Methods Formalin-fixed paraffin embedded colorectal tissues from 174 patients, including 84 adenomas, 72 carcinomas, and 18 normal mucosa, were examined for expression of Livin and Caspase-3 by streptavidin-peroxidase (SP) immunohistochemistry between July 2006 and December 2009. Results The positive rates of Livin protein expression in colorectal adenoma was significantly higher than that in normal mucosa (Plt;0.05), but lower than that in adenocarcinoma (Plt;0.05); the expression of Livin in tubular adenoma was significantly higher than that in villous adenoma (Plt;0.05). The positive rates of Caspase-3 protein expression in colorectal adenoma were significantly higher than that in normal mucosa and carcinoma (Plt;0.05), and the difference in positive rate of Caspase-3 expression was not significant between the villous adenoma and tubular adenoma (Pgt;0.05). Livin expression had negative correlation with the Caspase-3 expression (Pgt;0.05). Conclusion The difference in expression of Livin between adenoma and adenocarcinoma indicates the potential value of it in carcinogenesis of colorectal cancer, which suggestes that suppressing Caspase-3 protein activity is one of the channels by which livin promotes colorectal carcinogenesis.