Atabey A, Im M J, Akgur F M, Kolk C A, Manson P N
Department of Plastic and Reconstructive Surgery, Dokuz Eylul University, Izmir, Turkey.
Br J Plast Surg. 1996 Jul;49(5):321-4. doi: 10.1016/s0007-1226(96)90164-2.
The effects of cobalt chloride on ischaemia-reperfusion injury were evaluated in skin flaps. Groin neurovascular island flaps, 3 x 6 cm, were elevated in rats and subjected to primary and secondary ischaemia. Primary ischaemia was produced by 1 hour occlusion of the femoral artery and vein and, 22 hours later, secondary ischaemia was produced by 3 hours venous occlusion. The treatment group received intraperitoneal cobalt chloride (5 or 10 mg/kg) at the time of secondary ischaemia. Flap survival was 80% in the control, 10 to 20% in the cobalt chloride treated, and 20% in the cobalt plus mannitol group. Mannitol (100 mg/kg) failed to prevent the harmful effects of cobalt. Skin flaps exposed to cobalt chloride exhibited increased thiobarbituric acid reactant (TBAR) levels of 20 to 30 times normal. Of the antioxidant enzymes, glutathione peroxidase activity increased by 40% (P < 0.01), whereas glutathione reductase activity decreased by 40% (P < 0.01) in the cobalt exposed groups. Glucose 6-phosphate dehydrogenase activity was not affected.
在皮瓣中评估了氯化钴对缺血再灌注损伤的影响。在大鼠身上掀起3×6厘米的腹股沟神经血管岛状皮瓣，并使其经历原发性和继发性缺血。原发性缺血通过阻断股动脉和静脉1小时产生，22小时后，通过静脉阻断3小时产生继发性缺血。治疗组在继发性缺血时腹腔注射氯化钴（5或10毫克/千克）。对照组皮瓣存活率为80%，氯化钴治疗组为10%至20%，钴加甘露醇组为20%。甘露醇（100毫克/千克）未能预防钴的有害作用。暴露于氯化钴的皮瓣硫代巴比妥酸反应物（TBAR）水平增加至正常水平的20至30倍。在抗氧化酶中，暴露于钴的组中谷胱甘肽过氧化物酶活性增加了40%（P<0.01），而谷胱甘肽还原酶活性降低了40%（P<0.01）。6-磷酸葡萄糖脱氢酶活性未受影响。
