心房钠尿肽对力竭小鼠心脏抗氧化作用及其分泌机制的研究

目的 观察游泳力竭小鼠心肌组织中乳酸(lactic acid,LD)含量及血浆心房钠尿肽(atria1 natriuretic peptide,ANP)的分泌,以探讨力竭心脏的ANP分泌作用及抗氧化作用机制.方法 ①对小鼠进行分组及负重游泳,力竭即测试心肌LD和血浆ANP含量;②采用家兔离体心房灌流模型,利用不同浓度的乳酸缓冲液(4、8和12 mmo1/L)及其氮气模拟力竭心脏,探讨力竭心脏分泌ANP的机制；③利用氮气复制缺氧家兔离体心房灌流模型模拟力竭心脏,观察力竭心肌MDA含量的变化及其机制探讨.结果 ①游泳力竭小鼠心肌组织LD(P＜0.01)和血浆ANP含量(P＜0.01)与对照组相比均明显增高；②灌流浓度分别为4mmol/L(P ＜0.05)、8 mmo1/L (P＜0 05)和12rmmol/L(P ＜0.001)的乳酸缓冲液与对照组相比并不增加离体心房灌流模型中ANP的分泌,反而抑制ANP的分泌；但缺氧能明显增加心房ANP的释放(与对照组相比,P＜0.001)；③缺氧的离体心房灌流模型显示,缺氧组心肌组织中MDA含量比对照组显著降低(P＜00S),而预处理KT5823(1mmol/L)再给予缺氧组心肌组织中MDA含量明显增高(与缺氧组相比,P＜0.01).结论 ①力竭心脏的缺氧分泌大量ANP,而不是乳酸.②力竭时分泌的ANP对心脏具有抗氧化作用,其作用是通过ANP→cGMP→PKG信号传导途径.

Study on mechanism of ANP release and cardiac antioxidation on exhausted heart

【Objectives】 To observe the secretion of the ANP and study the cardiac antioxidation and mechanism of ANP release on exhausted heart.【Methods】 Experimental animals were grouped and swimmed,the exhausted mouse was tested the lactic acid(LD) and ANP in blood plasma;To observe the effect of hypoxia and LD on ANP secretion in the exhausted heart by the isolated perfused beating rabbit atria;To observed the MDA content in the exhausted myocardium which pretreatment and non-pretreatment KT5823(1 mmol/L)(PKG inhibiter) by isolated perfused beating rabbit atria.【Results】 The LD in myocardium(P <0.01) and ANP in plasma(P <0.01) significantly increased of swimming-induced exhausted mouse compaired with control group.Hypoxia significantly increased atrial ANP secretion(P <0.001 vs control cycle) but not latic acid in the isolated perfused beating rabbit atria;The MDA content in hypoxic myocardium significantly decreased(P <0.05) and this effects blocked by KT5823,an inhibiter of protein kinase G(P <0.01 vs hypoxia).【Conclusion】 ANP was increase by hypoxia but not latic acid in exhausted heart;The antioxidation of ANP on hypoxic myocardium through ANP→cGMP→PKG pathway.