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机构地区:[1]第三军医大学西南医院全军烧伤研究所,创伤,烧伤与复合伤国家重点实验室,重庆400038 [2]第三军医大学西南医院麻醉科
出 处:《中华烧伤杂志》2007年第5期327-330,共4页Chinese Journal of Burns
基 金:国家自然科学基金重点项目(30430680);国家杰出青年科学基金(30125040)
摘 要: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 observe the influence of aminoguanidine on cardiac troponin (cTnI) and nitric oxide (NO) levels in serum and myocardium in severely scalded rats. Methods Seventy-two Wistar rats were subjected to 30% TBSA full-thickness scald and randomly divided into scald group(S) and aminoguanidine group( A, with intraperitoneal injection of 40 mg/kg aminoguanidine before scald). The venous blood and myocardial tissue of the rats were harvested for the determination of the level of cTnI and nitrite in both serum and myocardium before scald and at 1,3,6,12 and 24 post-burn hours(PBH). Six sham scalded rats served as control group. The changes in the cTnI level and myocardial function were determined among control group , A and S groups at 6PBH. Results The serum level of NO in S group [ (59.6 ± 5.4) μmol/L] was obviously higher than that before scald[ (24.6 ± 0.8) μmol/L, P 〈 0.01 ] , and it peaked at 6 PBH, then decreased obviously at 24 PBH, which was still markedly higher than that in A group( P 〈 0.01 ). The changes in NO level in myocardium were similar to the above tendency. Compared with S group ,the level of cTnI was significantly increased in A group at each time-point. Compared with A group at 6 PBH, the inhibition of the cardiac function was relatively reduced in S group at 6 PBH. Conclusion Inhibition of NO synthesis by aminoguanidine aggravates cardiac damage and impairment of cardiac function of scalded rats, indicating that NO exerts protective effect on myocardium at early stage after a scald injury.
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