目的：探讨难治性鼻出血临床治疗的选择。方法:回顾性分析本科2005年11月～2006年11月收治的难治性鼻出血82例的临床资料。结果:均治愈。其中73例在鼻窦内窥镜下行局部填塞;4例行鼻中隔矫正术;3例鼻腔血管瘤中1例行下鼻甲部分切除术,另2例行双极电凝术。2例因鼻出血严重,经反复前鼻孔或前后鼻孔填塞都无效后,采用颈外动脉血管结扎术。结论:针对难治性鼻出血的不同原因、不同出血部位，应选择不同的治疗方法。
目的 探讨大隐静脉高位结扎及剥脱术后腹股沟切口淋巴瘘发生的原因和防治方法。方法 回顾性分析我院收治的120例(186条患肢)行大隐静脉高位结扎及剥脱术者中术后发生腹股沟切口淋巴瘘患者的临床资料，并对相关文献进行复习。结果 大隐静脉高位结扎及剥脱术后腹股沟切口淋巴瘘发生率为4.3%（8/186）。2例单侧腹股沟切口淋巴瘘患者扩创后予以碘伏纱布填塞创面，于第20天及第23天后淋巴瘘闭合，再行切口二期缝合，7 d后拆线； 3例双侧腹股沟切口淋巴瘘患者切口创面予以医用胶喷洒后碘伏纱布填塞，3 d后淋巴瘘全部闭合，切口二期缝合、加压包扎后7 d拆线。切口均愈合良好。结论 对腹股沟区股根部不恰当的广泛解剖及淋巴结切除的不规范与大隐静脉高位结扎及剥脱术后腹股沟切口淋巴瘘的发生密切相关。术前对大隐静脉准确定位，术中仔细操作、避免广泛剥离、避免切除肿大淋巴结是预防腹股沟切口淋巴瘘的有效措施。淋巴瘘发生后予以医用胶封堵是有效的补救措施。
ObjectiveTo understand the effect of nitric oxide (NO) on the formation of hyperdynamic circulatory syndrome (HCS) and the influence of level of NO on HCS. MethodsAfter establishment of stable HCS in partial portal vein ligated rats,the quantity of NO in blood of portal vein and the activity of nitric oxide synthase (NOS) in liver were determined by pre and post injection of inhabitor of NOS (NGmethylLarginine) and hemodynamics was supervised simultaneously.ResultsThe quantity of NO was paralleled with the activity of NOS and was elevated markedly by 24 hours after operation and reached the top by 48 hours after surgery. These sequential changes were coincided with the dilation of general vascularture. There was a close relation between this changes and the formation of HCS.The quantity of NO and the activity of NOS were decreased significantly to the level of the control group after injection of NGmethylLarginine (LNMMA). LNMMA inhabited the activity of NOS and blocked the production of NO. HCS ameliorated obviously. ConclusionNO plays an important role in initiating the dilation of general vascularture and plays a critical role in the formation of HCS. HCS will be ameliorated obviously or be blocked completely by eliminating the effect of NO and the portal pressure will decreased significantly or recover to normal range.
In order to preserve more normal tissue in situ in case of severe traumatic rupture of spleen, simultaneous ligation of splenic artery and vein was performed successfully on animals and then was applied for clinic use. The preserved splenic tissue all survivied and functioned well. Patients with severe traumatic rupture of spleen grade Ⅳ-Ⅴ were all cured by ligation of both the splenic artery and vein at the same time.
The comparison made between two experimental models with obstructive jaundice, which were newly established reversible model and traditional bile duct ligation and internal drainage model, showed that the new model was superior to the traditional one. This study suggests that the new model would be an ideal model, which could replace the traditional one for studying obstructive jaundice.
Objective To explore the role of renin-angiotensin system( RAS) in acute lung injury( ALI) /acute respiratory dysfunction syndrome( ARDS) by using amouse cecal ligation and puncture ( CLP)model.Methods The ALI/ARDS animal models were assessed bymeasuring blood gas, wet/dry lung weight ratio( W/D) , and lung tissue histology 18 hours after CLP operation. After the ALI/ARDS models was successfully established, immunohistochemistry, western blotting and radioimmunity were used to investigate the changes of several key enzymes of RAS, such as ACE, ACE2 and Ang Ⅱ. In addition, two groups of animals received a separate intraperitoneal injection of angiotensin-converting enzyme ( ACE) inhibitor captopril or recombinant mouse ACE2 ( rmACE2) after CLP, then the changes of RAS in ALI/ARDS modelswere observed. Results The extensive lung injuries can be observed in the lung tissues from CLP-treated animals 18 hours after operation. The CLP-induced ALI/ARDS led to an increase in the wet/dry weight ratio of the lung tissues, and a decrease in the PaO2 /FiO2 [ ( 194. 3 ±23. 9) mm Hg vs ( 346. 7 ±20. 5) mm Hg,P lt;0. 01] . Immunohistochemistry and western blotting tests of the lung tissues from CLP-treated animals showed a decrease in the ACE2 protein level. However, in both the CLP and sham mice there were no significant differences between the two groups. CLP markedly increased Ang Ⅱ level in lungs and plasma of mice, and RAS drugs significantly impacted the Ang Ⅱ levels of mice. Compared with the CLP group,captopril or rmACE2 led to a decrease of the Ang Ⅱ level in mice [ Lung: ( 1. 58 ±0. 16) fmol /mg,( 1. 65 ±0. 21) fmol /mg vs ( 2. 38 ±0. 41) fmol /mg; Plasma: ( 178. 04 ±17. 87) fmol /mL, ( 153. 74 ±10. 24) fmol /mL vs ( 213. 38 ± 25. 44) fmol /mL] . Conclusions RAS activation is one of the characteristics of CLP-induced ALI/ARDS in mice models. ACE and ACE2 in RAS have a different role in the regulation of AngⅡ synthesis, while ACE has a positive effect in generating AngⅡ, and ACE2 shows a negative effect.