目的研究高压氧预处理对皮瓣组织缝隙连接蛋白43(Cx43)和肿瘤坏死因子-α(TNF—α)表达的影响。方法24只雄性sD大鼠按数字表法随机分为高压氧预处理组(高压氧组)和对照组,每组12只。高压氧组在手术前2d行高压氧治疗,每天2次,每次1h,2次之间间隔12h。对照组处于常压空气中。麻醉后在大鼠腹部形成以右侧腹壁下浅动脉为蒂的扩大腹部皮瓣,皮瓣用显微血管夹阻断血供3h后恢复血供。术后第5天处死大鼠,沿皮瓣血管轴在皮瓣近端、中间和远端取材。HE染色观察组织炎症浸润,免疫组织化学方法观察组织Cx43表达,悬浮芯片法测定组织TNF.仪表达。结果HE染色显示,相同取材部位高压氧组皮瓣组织炎症细胞浸润较对照组轻。对照组和高压氧组Cx43分别为(3.87±0.28)、(5.22±0.26)个/高倍镜视野,2组比较差异有统计学意义(t=10.559,P〈0.01);TNF—α分别为(593.72±107.95)、(253.40±47.84)ng/L,2组比较差异有统计学意义(t=5.816,P〈0.05)。结论高压氧预处理可促进Cx43表达,抑制TNF-α表达,减轻皮瓣缺血再灌注炎症反应。
Objective To study the effect of HBO preconditioning on the expressions of Cx43 and TNF - α in skin flaps. Methods Twenty-four male SD rats were randomly divided into 2 groups : the control group (n= 12) and the HBO preconditioning group (n = 12). Two days before surgery, the rats in the HBO preconditioning group received HBO therapy, two sessions a day, for a duration of one hour and with an interval of 12 hours. Rats in the control group lay intact in the normal air. After anesthesia, an extended epigastric adipocutaneous flap was formed, based on the fight superficial epigastric artery and vein. Three hours after flap ischemia induced by clamping the pedicle vessels with micro-vascular clamps, blood flow recovered. On the fifth day after surgery, the rats were sacrificed and samples were collected at the proximal, intermediate and distal portions of the flaps. Tissue inflammatory infiltration was detected by using HE, the expression of Cx43 was monitored with immunochemistry and expression of tissue TNF-α was also analyzed. Results HE staining showed that inflammatory cell infiltration in the same sampled portions was less serious for the animals in the HBO preconditioning group. The expressions of Cx43 for the control group and the HBO group were respectively 3.87± 0.28 and 5.22± 0.26, with statistical difference ( t = 10. 559, P 〈 0. 01 ). The expressions of TNF-α was (593.72±107.95 ) and (253.40 ± 47.84) ng/L respectively, also with statistical significance (t = 5. 816, P 〈 0.05 ). Conclusions HBO preconditioning could enhance Cx43 expression, on the other hand could depress TNF-a expression, and also could decrease inflammatory response induced by repeffusion, following ischemia of he skin flaps.