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Atrial natriuretic peptide reverses the negative functional effects of stunning in rabbit myocardium.

机译:心钠素逆转家兔心肌电击的负面功能效应。

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We tested the hypothesis that atrial natriuretic peptide (ANP) would decrease both the effects of myocardial stunning and oxygen consumption in rabbit hearts. In two groups of anesthetized open-chest rabbits, myocardial stunning was produced by two 15 min occlusions of the left anterior descending (LAD) artery separated by 15 min of reperfusion. Either ANP (0.2 mg) or vehicle (lactated Ringers) was then injected into the affected area of the left ventricle. In a third group, ANP was injected into the LAD region of non-stunned rabbits. Hemodynamic (heart rate, aortic and left ventricular pressures) and functional (wall thickening (WT), delay of onset of WT, and rate of WT) parameters were measured. Coronary blood flow (microspheres) and O2 extraction (microspectrophotometry) were used to determine myocardial O2 consumption. Stunning was demonstrated by an increase in the time delay to contraction and depressed WT. In the control group, baseline delay to contraction was 25+/-7 ms, and this increased to 84+/-16 following stunning and vehicle administration. In the ANP group, baseline delay was 20+/-6 at baseline and after stunning and ANP administration it was 30+/-7. Wall thickening decreased by approximately 30% with stunning and vehicle but only 8% in the ANP treated hearts. Stunning did not affect regional O2 consumption (6.0+/-1.1 stunned vs. 7.4+/-1.2 mlO2/min/100g non-stunned). ANP administration did not affect O2 consumption (7.3+/-1.7 stunned vs. 6.4+/-1.0 non-stunned). We therefore concluded that ANP administration reversed the effects of stunning without alteration in local O2 consumption in stunned myocardium.
机译:我们测试了心钠素(ANP)会同时降低兔心脏心肌电击和耗氧量的假说。在两组麻醉的开胸兔子中,左前降支(LAD)动脉两个15分钟的阻塞(再灌注15分钟)产生心肌震颤。然后将ANP(0.2毫克)或媒介物(乳酸林格氏液)注射到左心室的患处。在第三组中,将ANP注射到未惊呆的兔子的LAD区域中。测量血流动力学(心率,主动脉和左心室压力)和功能性(壁增厚(WT),WT发作延迟和WT速率)参数。冠状血流量(微球)和氧气提取(显微分光光度法)用于确定心肌的氧气消耗量。收缩和WT下降的时间延迟增加证明了惊人的效果。在对照组中,收缩的基线延迟为25 +/- 7 ms,并且在进行击晕和用药后增加至84 +/- 16。在ANP组中,基线延迟在基线时为20 +/- 6,而在击晕和ANP给药后为30 +/- 7。在使用惊叹剂和媒介物的情况下,壁增厚减少了约30%,但在ANP治疗的心脏中仅增加了8%。惊叹不影响区域O2消耗(6.0 +/- 1.1毫升比7.4 +/- 1.2毫升/分钟/ 100克非惊呆)。 ANP给药不影响O2消耗(7.3 +/- 1.7惊呆与6.4 +/- 1.0惊呆)。因此,我们得出的结论是,ANP给药可逆转惊厥的效果,而不会改变昏迷心肌的局部O2消耗量。

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