腺苷延长肌瓣缺血耐受时间的实验研究

目的研究缺血前局部使用腺苷对猪背阔肌瓣缺血耐受的促进作用和机理。方法用不同剂量（０，０．５，２．０ｍｇ）的腺苷从腋动脉穿刺注入肌瓣，肌瓣缺血４，４８小时后切取肌瓣，染色后测定肌瓣成活率，腺苷注射前、后，缺血后分别采取肌肉标本做三磷酸腺苷（ＡＴＰ）定量分析。结果腺苷注射组肌肉坏死率明显低于对照组（对照组：４０．３％±２．２％），０．５ｍｇ组：２０．６％±１．６％，２ｍｇ组：１８．２％±１．０％）。腺苷注入组缺血后肌肉ＡＴＰ水平明显高于对照组。结论缺血前局部使用小剂量腺苷对缺血肌瓣有保护作用，并伴随肌肉ＡＴＰ分解水平的减低     

腺甘延长肌瓣缺血耐受时间的实验研究

目的 研究缺血前局部使用腺苷对猪背阔肌瓣缺血耐受的促进作用和机理。方法 用不同剂量（０，０．５，２．０ｍｇ）的腺苷从腋动脉穿刺注入肌瓣，肌瓣缺血４，４８小时后切取肌瓣，染色后测定肌瓣成活率，腺苷注射前、后，缺血后分别采取肌肉标本做三磷酸腺苷（ＡＴＰ）定量分析。结果 腺苷注射组肌肉坏死率明显低于对照组（对照组：４０．３％±２．２０％），０．５ｍｇ组：２０．６％±１．６％，２ｍｇ组；１８．２％±１．０     

游离皮瓣缺血耐受实验研究

目的：研究游离皮瓣的缺血耐受极限,为减少皮瓣并发症提供理论依据。方法：成年家猪10只,制作颞部。肩胛、胸三角及下腹部血管蒂皮瓣,阻断血管蒂、观察不同缺血时间皮瓣的成活情况。结果：实验组均出现部分或全部坏死,对照组均成活良好,结论：游离皮瓣有一相应缺血耐受极限,如超出此时间,必将出现皮瓣不可逆转并发症甚至坏死。     

猪臂部游离与岛状皮瓣继发性缺血耐受时间的比较

观测猪臂部游离与岛状皮瓣继发性缺血耐受时间。方法臂部岛状皮瓣与游离皮瓣２小时原发性热缺血１２小时再灌注，０、２、４、６、１０小时继发性热缺血，７天后测定皮瓣存活率。结论猪臂部游离皮瓣的继发性缺血耐受时间短于岛状皮瓣，与皮瓣低血流相关。     

猪臀部游离与岛状皮瓣继发性缺血耐受时间的比较

目的观测猪臀部游离与岛状皮瓣继发性缺血耐受时间。方法臀部岛状皮瓣与游离皮瓣2小时原发性热缺血,12小时再灌注,0、2、4、6、10小时继发性热缺血,7天后测定皮瓣存活率。结果岛状皮瓣可耐受10小时继发性缺血,无皮瓣坏死。游离皮瓣坏死发生率依继发性缺血时间0、2、4、6、10小时为0、10％、50％、80％、100％。另一组实验中,用15μm 微球测量两种皮瓣4小时继发性缺血后皮瓣血流,8个血运障碍的游离皮瓣为对侧岛状皮瓣的8％,其余12个血运正常的游离皮瓣是岛状皮瓣的76％。结论猪臀部游离皮瓣的继发性缺血耐受时暗短于岛状皮瓣,与皮瓣低血流相关。     

缝匠肌髂骨瓣经粗隆钻孔移植术治疗股骨头缺血坏死

报道8例成人股骨头缺血坏死病人,采用带缝匠肌的髂骨瓣,经股骨粗隆部钻孔植入,共治疗10个髋关节。经12～20个月随访,疼痛消失7例。髋关节活动度明显增加。经髓腔造影检查,证明静脉瘀滞得到解除。优良率达87.5％。     

腺苷A1受体激动剂诱导心脏缺血预处理延迟效应的实验研究

目的探讨腺苷A1受体激动剂能否诱导心脏缺血预处理的延迟保护及其与锰-超氧化物歧化酶(Mn-SOD)表达的关系.方法按随机数字表法将60只鼠分为6组,每组10只.A组:用腺苷A1受体激动剂2-氯环戊腺苷(CCPA)预处理; B组:为缺血对照,静脉注射生理盐水;C组:注射反义全巯代磷酸化寡核苷酸(ODN)后再注射生理盐水;D组、E组和F组在预处理前分别静脉注射Mn-SOD反义ODN、意义ODN、错配ODN.观察左心室压力变化最大速率(±dp/dtmax)的恢复率,肌酸激酶同工酶(CK-MB)释放活性,心肌三磷酸腺苷(ATP)、丙二醛(MDA)含量和Mn-SOD活性.结果 A组、E组和F组±dp/dtmax恢复率、心肌ATP含量和Mn-SOD活性均高于B组、C组和D组(P<0.05,0.01),而CK-MB释放活性和MDA含量均低于B组、C组和D组(P<0.05).结论腺苷A1受体激动剂可诱导预处理的延迟效应,减轻心肌缺血-再灌注损伤,其机制与Mn-SOD的高表达有关.     

腺苷促进猪横行腹直肌肌皮瓣成活的实验研究

目的研究腺苷对猪横行腹直肌肌皮瓣成活率的影响。方法横行腹直肌肌皮瓣以左侧腹壁下动脉为供血血管,肌蒂宽6cm,皮瓣面积8cm×30cm。20头猪分为生理盐水对照组和1mg、2mg、5mg 腺苷注射实验组,掀起皮瓣前从腹壁上动脉注射不同剂量的腺苷和生理盐水。术后7天注射荧光素,以模片法记录腹直肌同侧皮瓣、对侧皮瓣和整个皮瓣的成活率。结果 2mg 和5mg 腺苷注射组,肌皮瓣成活率明显高于生理盐水对照组(P<0.05)。结论小剂量术中局部使用腺苷可增加猪横行腹直肌肌皮瓣成活率。     

带肌蒂比目鱼肌肌腱瓣延长修复跟腱缺损的疗效分析

目的 通过对应用带肌蒂比目鱼肌肌腱瓣延长修复跟腱缺损的病例随访,以评价疗效.方法 于跟腱近端将位于深层的比目鱼肌腱与位于浅层的腓肠肌腱分开,并向近端分离,根据缺损范围预留肌腱长度,横向切断比目鱼肌腱纤维,形成带有肌蒂的肌腱瓣,向下牵拉延长,与跟腱远端缝接,肌腱瓣近端与腓肠肌腱缝接,缝合跟腱两侧,完成跟腱重建.治疗26例,获得随访18例.结果 18例获随访14～72个月,应用Termann跟腱损伤的临床评价标准进行评定:优13例,良4例,可1例,优良率达94.4%.其中开放性损伤1例术后皮肤发生部分坏死,经行皮瓣转移术后延期愈合;余17例伤口均Ⅰ期愈合.无感染发生及跟腱再次断裂.结论 带肌蒂比目鱼肌肌腱瓣延长重建跟腱术,具有损伤小、操作简便、功能康复好的优点,适用于缺损范围在7.5 cm以内的各种类型的闭合性跟腱缺损的修复重建.     

术中预缺血对猪骨骼肌保护作用的实验研究

目的　研究术中预缺血对骨骼肌缺血坏死的保护作用及相关的肌肉代谢变化。方法　１０ 只猪背阔肌瓣在４ｈ 缺血前先进行３ 个循环１０ ｍｉｎ 的术中预缺血,４８ｈ 后用染色法记录肌肉成活率,于肌肉缺血前、缺血后２ ,４ｈ 和再灌流１５ｈ 分别作肌肉活检。结果　４ｈ 缺血后的肌瓣,术中预缺血组成活率高出对照组４４ ％ ,肌肉活检三磷酸腺苷（ Ａ Ｔ Ｐ） 增加和乳酸降低（ Ｐ＜ ００５） 。结论　术中预缺血可增加骨骼肌对缺血坏死的保护作用,这与肌肉中能量代谢的减低相关。     

术中预缺血对猪骨骼肌保护作用的实验研究

目的研究术中预缺血对骨骼肌缺血坏死的保护作用及相关的肌肉代谢变化。方法 10只猪背阔肌瓣在4h 缺血前先进行3个循环10min 的术中预缺血,48h 后用染色法记录肌肉成活率,于肌肉缺血前、缺血后2,4h 和再灌流1.5h 分别作肌肉活检。结果 4h 缺血后的肌瓣,术中预缺血组成活率高出对照组44％,肌肉活检三磷酸腺苷(ATP)增加和乳酸降低(P<0.05)。结论术中预缺血可增加骨骼肌对缺血坏死的保护作用,这与肌肉中能量代谢的减低相关。     

The liver protective effect of ischemic preconditioning may be mediated by adenosine

Abstract We investigated the involvement of adenosine in ischemic preconditioning (IPC) by the unspecific antagonist, 8‐phenyltheophylline (8‐PT). Anesthetized Wistar rats were treated as follows: 1. nonischemic controls, 2. ischemic controls: 60 min of clamping of the common hepatic artery followed by 60 min reperfusion, 3. IPC: 10 min ischemia followed by 15 min reperfusion, prior to the identical ischemia‐reperfusion (IR) period as in group 2, 4. 8‐PT + IPC: 8‐PT 10 mg/kg i. v. was given 10 min prior to the identical procedure as in group 3. The peripheral liver blood flow was monitored by laser‐Doppler flowmetry. Blood alanine aminotransferase (ALT) was analyzed once every 60 min. IPC significantly reduced impairment of liver blood flow, as well as ALT increase during reperfusion. This effect was abolished by pretreatment with 8‐PT. Adenosine appears to be a crucial effector in IPC. Clinical studies need to be undertaken to explore a possible effect of IPC in liver transplantation.     

腺苷A1受体系统在兔脑预缺血延迟相保护效应中的作用

目的 探讨腺苷A1受体系统在兔脑预缺血延迟相保护效应中的作用。方法 股动脉放血至平均动脉压35－40mmHg时,阻断双侧颈总动脉诱导脑缺血。脑缺血3min存活3d（预缺血处理）后、脑缺血10min（预缺血延迟相保护模型）;用腺苷A1受体激动剂氮6－环戊基腺苷（CPA）代替预缺血处理,用其拮抗剂8－环戊基－1,3－二丙基黄嘌呤（DPCPX）阻断该受体;免疫组化分析热休克蛋白70（SHP70）表达。观察缺血3d后海马CA1区正常神经密度和HSP70的表达。结果 （1）CPA能减轻脑缺血损害,但其保护作用不如预缺明显（约占后者的70％）,DPCPX阻断该受体后,预缺血延迟相保护作用消失;（3）3min脑预缺血神经元无损害,但伴HSP70明显表达;DPCPX阻断腺苷A1受体后,3min脑预缺血发生明显损害,且HSP70表达明显削弱。结论 （1）预缺血延迟相保护作用与腺苷A1受体系统激活有关;（2）DPCPX阻断预缺血延迟相保护作用的机制与削弱HSP70表达有关。     

缺血预处理后热休克蛋白对皮瓣成活的影响及作用机理

目的 探索提高皮瓣成活率有有效方法和途径。方法 采用大鼠背部轴型皮瓣，制成活体原位缺血预处理模型，观察缺血预处理对超长跨区供血皮瓣成活率的影响及热休克蛋白70的表达。结果 缺血预处理后即刻断蒂组（A组）和缺血预处理后24h断蒂组（B组）皮瓣平均存活面积明显高于对照组，A组和B组的皮瓣平均存活面积差异无显著性意义；A组和B组中免疫组化染色可见大量阳性表达，对照组免疫组化染色仅见微量弱阳性表达。结论 缺血预处理能提高超长跨区供血皮瓣的存活率, 其机理可能与缺血预处理后热休克蛋白合成增加所引发的机体自身的保护作用有关。     

Closure of a tracheocutaneous fistula by two hinged turnover skin flaps and a muscle flap: A case report

INTRODUCTIONTracheocutaneous fistula is a complication of tracheostomy. Tracheocutaneous fistulectomy followed by primary closure carries a high possibility of complications.PRESENTATION OF CASEAn 11-year-old boy underwent surgery to repair a tracheocutaneous fistula, using skin and muscle flaps. A vertical incision was made around the fistula and 3 skin flaps were prepared: 2 hinge flaps, and 1 to cover the skin defect (advanced flap). The 2 hinged turnover flaps were invaginated by multiple layered sutures, and a strap muscle flap was placed over the resulting tracheal closure. An advanced skin flap was used to cover the area of the previous defect. The patient was extubated immediately after surgery. He was discharged on the sixth postoperative day without tracheal leakage or subcutaneous emphysema. The patient is currently doing well, with no respiratory symptoms and no recurrence at the postoperative 5 months.DISCUSSIONOur technique is minimally invasive and has a low risk of lumen stenosis, other complications, or recurrence.CONCLUSIONThis technique demonstrates the multiple-layered closure of a tracheocutaneous fistula, using skin flaps and a muscle flap.     

Expression of inducible nitric oxide synthase in muscle flaps treated with ischemic postconditioning

Background/Objective

Preconditioning has been considered promising for the treatment of ischemic flaps. In this study, the therapeutic effect of postconditioning was compared with that of preconditioning during ischemia/reperfusion (I/R) injury, and a role of inducible nitric oxide synthase (iNOS) in postconditioning treatment was also explored.

Methods

Sixty rats were randomly divided into four groups with 15 rats in each group. Ischemic injury was induced in a rat’s gracilis muscle flap model. Preconditioning and postconditioning were performed respectively on the flaps in the pre-con group and the post-con group. No treatment was given to the flaps in the control group, and flaps without I/R injury were used as a sham control. Muscle viability ratio, histology, and gene expression of iNOS were examined at different time intervals (3, 12, and 18 h).

Results

A significantly higher survival ratio was observed in both the pre-con group (78.98 ± 3.39, 62.74 ± 3.7, and 54.42 ± 4.45 %) and the post-con group (77.42 ± 4.14, 59.74 ± 6.67, and 49.52 ± 4.13 %) than the control group (45.22 ± 3.69, 42.44 ± 3.76, and 33.2 ± 3.29 %) at 3, 12, and 18 h postoperatively (P < 0.05). There was no statistical difference between the pre-con group and the post-con group (P > 0.05). Histological examination showed delayed and attenuated tissue damage in both the pre-con group and the post-con group when compared to that of the control group. A higher expression of iNOS was observed in both the pre-con group and the post-con group than the control group and the sham group (P < 0.05).

Conclusions

Significant improvement of flap survival could be achieved by both preconditioning and postconditioning treatments; however, better protection could be provided by preconditioning. The higher expression of iNOS may play an important role in the therapeutic effect of postconditioning during I/R injury.