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目的了解氨基胍对烫伤大鼠心肌的影响。方法将72只Wistar大鼠随机分为烫伤组、氨基胍组。2组大鼠均造成30%TBSAⅢ度烫伤后常规补液,氨基胍组伤前20 min腹腔内注射氨基胍(40 mg/kg)。于伤前及伤后1、3、6、12、24 h取大鼠动脉血检测血清中心肌肌钙蛋白I(cTnl)浓度、一氧化氮(NO)浓度,另取心肌组织测定NO浓度;观察氨基胍组、烫伤组伤后6 h大鼠的心功能水平。结果伤后3 h烫伤组大鼠血清NO浓度[(59.6±5.4)μmol/L]明显高于伤前[(24.6±0.8)μmol/L,P<0.01],6 h达峰值,24 h明显回落,均明显高于氨基胍组(P<0.01);心肌组织NO浓度的变化趋势同上。与烫伤组比较,氨基胍组伤后各时相点cTnI浓度明显升高。与烫伤组伤后6 h比较,氨基胍组大鼠该时相点的心功能抑制加重。结论氨基胍可抑制NO生成,加重了烫伤大鼠的心肌损害并使其心功能下降,提示NO对烫伤后早期心肌可能具有保护效应。
Objective To investigate the effect of aminoguanidine on myocardium in scalded rats. Methods Seventy two Wistar rats were randomly divided into burn group and aminoguanidine group. Rats in both groups were given routine rehydration after 30% TBSA Ⅲ degree scald while aminoguanidine (40 mg / kg) was injected intraperitoneally in aminoguanidine group 20 minutes before injury. The levels of cTnl, NO and NO in myocardium were measured at 1, 3, 6, 12 and 24 h after injury. The aminoguanidine group and the scald group were sacrificed 6 hours after injury, the heart function of rats. Results Serum nitric oxide levels were significantly higher in the scalded rats 3 h after injury (59.6 ± 5.4 μmol / L vs 24.6 ± 0.8 μmol / L, P <0.01), and peaked at 6 h (P <0.01). The trend of NO concentration in myocardial tissue was the same as above. Compared with scalded group, aminoguanidine group cTnI concentration significantly increased at each time point. Compared with the sham injury group 6 h after injury, the aminoguanidine group rats at the time point of cardiac function suppression increased. CONCLUSION: Aminoguanidine inhibits the production of nitric oxide and aggravates myocardial damage and decreases cardiac function in burned rats, suggesting that nitric oxide may have a protective effect on early postburn myocardium.