目的 評估多普勒超聲引導的痔上動脈結扎治療Ⅱ、Ⅲ度內痔的臨床應用價值。方法 對2009 年4～9月期間在我科行多普勒超聲引導的痔上動脈結扎的49 例Ⅱ、Ⅲ度內痔患者從術后肛門括約肌功能、癥狀有效改善情況、疼痛程度及完全恢復正常生活所需時間方面進行評價。結果 術后無患者出現肛門括約肌功能失調；術后1 周、1 個月及3 個月Ⅱ、Ⅲ度內痔分別有77.8%(42/54)、87.0%(47/54)、92.6%(50/54)和59.4%(19/32)、71.9%(23/32)、78.1%(25/32)的患者單項癥狀得到有效改善； 術后6 h及24 h VAS 法疼痛程度評分平均分分別為1.95分和1.63分； 患者完全恢復正常生活所需時間平均為術后2.98 d。結論 多普勒超聲引導的痔上動脈結扎治療Ⅱ、Ⅲ度內痔安全有效，術后疼痛較輕且可以較快地完全恢復正常生活。
【Abstract】 Objective To investigate the effect of verapamil on apoptosis, calcium and expressions of bcl-2 and c-myc of pancreatic cells in ischemia-reperfusion rat model. Methods Wistar rats were randomly divided into three groups: control group （n=10）; ischemia-reperfusion group （n=10）; verapamil treatment group （n=10）. The anterior mesenteric artery and the celiac artery of rats in both ischemia-reperfusion group and verapamil treatment group were occluded for 15 min followed by 12-hour reperfusion. Verapamil （1 mg／kg） was injected via caudal vein to the rats in verapamil treatment group 15 min before occlusion and 1 hour after the initiation of reperfusion, respectively; and ischemia-reperfusion group was given the same volume of salient twice intravenously. Pancreatic tissues were collected from the dead rats after twelve hours since the reperfusion. The pathologic characters of pancreatic tissue were observed under light microscope; The level of calcium in the tissue was measured by atomic absorption spectrometer; TUNEL was used to detect apoptosis of pancreatic cells; and the expressions of c-myc and bcl-2 in the cells were also analyzed by immunohistochemistry technique and flow cytometry. Results The pathologic change in verapamil treatment group was less conspicuous than that of ischemia-reperfusion group. Both the calcium level and the number of apoptotic cells in verapamil treatment group were less than those of ischemia-reperfusion group 〔（411.1±55.8） μg/g dry weight vs （470.9±31.9） μg/g dry weight, P＜0.05 and （9.5±2.9）% vs （18.4±3.1）% 〕, P＜0.05. After taking verapamil, the number of apoptotic cells decreased, whereas the expressions of bcl-2 and c-myc increased. The fluorescent indexes of bcl-2 and c-myc in verapamil treatment group were significantly higher than those of ischemia-reperfusion group (1.72±0.11 vs 1.41±0.07, P＜0.05; 1.76±0.19 vs 1.55±0.13, P＜0.05. Conclusion Ischemia-reperfusion injury can induce apoptosis of pancreatic cells. Verapamil could protect the injured pancreatic tissue by reducing the level of calcium, stimulating the expressions of bcl-2 and c-myc and inhibiting apoptosis of pancreatic cells.