短时间一氧化氮吸入对心肌缺血／再灌注损伤的保护机制研究  

作　　者：高宝斌[1] 连庆泉[1] 康定鑫[1] 

机构地区：[1]温州医学院附属第二医院麻醉科,325027

出　　处：《浙江临床医学》2009年第12期1252-1254,共3页Zhejiang Clinical Medical Journal

摘　　要：目的探讨短时间吸入NO对心肌缺血／再灌注损伤的保护机制。方法60只雄性wistar大鼠随机分为三组（Ⅰ、Ⅱ、Ⅲ组），每组20只，通过腹腔注射氯胺酮（120mg／kg）和咪达唑仑（10mg／kg）施行麻醉，同时给予人工通气。结扎左冠状动脉导致心肌缺血10min后开放，再灌注24h。Ⅰ组为对照组，Ⅱ、Ⅲ组分别在再灌注前5min、60rain吸入10％的NO，再灌注24h后结扎左冠状动脉，注入荧光剂，心脏离体冰冻切片，HE染色，测量心肌梗死范围，取大鼠血液和组织中的NO代谢产物定量检测。结果大鼠吸收NO的速度（6．35±0．24）min内基本成线性分布，后趋于稳定。吸入NO后红细胞中的S-亚硝基硫醇、N-亚硝胺和亚硝酰基亚铁血红素水平均明显增加。再灌注前的5min、60min吸入NO的心肌梗死范围较未吸入NO分别减少28％、31％。结论短时间吸入NO能够明显减少心肌再灌注损伤的范围，提示短时间吸入NO对心肌缺血／再灌注也同样有很好的保护作用。其机制可能是迅速通过血液从肺到心脏的NO代谢产物以生物活性形式发挥作用。Objective To investigate the protection mechanism against cardiac ischemia- reperfusion injury by temporary inhalation of nitric oxide. Method Sixty male wistar mice weighing 200 -260g were randomly divided into 3 groups （ Ⅰ , Ⅱ ,Ⅲ;n =20）;Mice were anesthetized by intraperitoneal administration of ketamine （120 mg/kg） and Midazolam （10mg/kg） and ventilated at a fraction of inspired oxygen （FIO2） of O. 99 - 1. 0. Myocardial ischemia was induced by ligation of the left coronary artery for 10 minutes, reperfused for 24h. Nitric oxide （ 10% ） was administered for 60,5 minutes before reperfusion. The artery was re -ligated after 24h. Fluorescent microspheres （0.25 ml, 10μm diameter, ） were injected into the LV to determine the area at risk （AAR）. The heart was excised, and four consecutive 1 -mm cardiac slices were stained with HE for the measurement of myocardial infarction （MI） size. The nitric oxide and the nitric oxide metabolite concentrations achieved in a target tissue and blood. Result Mice absorbed nitric oxide in a nearly linear fashion between 0 to 6. 35 ± 0. 24 minutes,but after this period, the concentration of NO would arrive at a stable level. Breathing nitric oxide rapidly increased the levels of erythrocytic S - nitrosothiols, N - nitrosamines, and nitrosyl - heroes increased dramatically after nitric oxide inhalation. In a murine cardiac ischemia - reperfusion injury model, breathing nitric oxide for either 5 or 60 rain before reperfusion decreased myocardial infarction size as a fraction of myocardial area at risk by 28% or 31%, respectively. Conclusion The temporary nitric oxide inhalation could obviously reduce the area of myocardial ischemia - reperfusion injury. Probability is its function that the metabolite of NO has taken effect by the blood from lung to cardic rapidliy.

关 键 词：一氧化氮 心肌缺血 再灌注损伤 代谢物 

分 类 号：R541[医药卫生—心血管疾病] R542.2[医药卫生—内科学]