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 探討凋亡抑制蛋白Livin與凋亡蛋白Caspase-3在結直腸腺瘤-癌序列中的表達變化及其相關性。 方法 2006年7月—2009年12月，采用免疫組織化學染色鏈霉菌抗生物素蛋白-過氧化物酶鏈接法streptavidin-peroxidese，SP）法檢測18例正常黏膜、84例結直腸腺瘤、72例結直腸癌中Livin及Caspase-3的表達情況。 結果 結直腸腺瘤組織中Livin蛋白的陽性表達率明顯高于正常黏膜組織（Plt;0.05），而低于腺癌組（Plt;0.05）；腺瘤組內絨毛狀腺瘤與管狀腺瘤相比較，Livin蛋白表達率差異有統計學意義（Plt;0.05）。結直腸腺瘤組織中Caspase-3的陽性表達率明顯高于正常黏膜組織（Plt;0.05）；而腺瘤組織與癌組織之間Caspase-3陽性表達率差異（Plt;0.05）；腺瘤組內絨毛狀腺瘤與管狀腺瘤相比較，Caspase-3蛋白陽性表達率差異無統計學意義（Pgt;0.05）。Livin表達與Caspase-3表達呈負相關（Plt;0.05）。 結論 凋亡抑制蛋白Livin參與了大腸腫瘤的發生，且在大腸腺瘤-腺癌階段起到了重要作用；凋亡抑制蛋白Livin與Caspase-3表達呈負相關，抑制Caspase-3蛋白的活性可能是Livin促進結腸癌發生的途徑之一。【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.
