Hill M F, Singal P K
St Boniface General Hospital Research Centre, and Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Circulation. 1997 Oct 7;96(7):2414-20. doi: 10.1161/01.cir.96.7.2414.
Heart failure subsequent to myocardial infarction (MI) is accompanied by depressed antioxidants and increased oxidative stress in the myocardium. Antioxidant enzyme activities and oxidative stress were examined in the viable left (LV) and right (RV) ventricles in relation to their hemodynamic function.
The left coronary artery in rats was ligated. At 1 week after MI, LV systolic pressure (LVSP), LV end-diastolic pressure (LVEDP), and RV end-diastolic pressure (RVEDP) remained near control values, whereas RV systolic pressure (RVSP) was significantly elevated. In the 4, 8, and 16 week post-MI animals, LVSP was significantly reduced, with values of 112.0+/-1.57, 99.9+/-0.52, and 89.2+/-1.4 mm Hg, whereas LVEDP was significantly elevated, with values of 8.2+/-0.52, 17.4+/-1.7, and 31.4+/-1.5 mm Hg, respectively. RVEDP was higher at 8 and 16 weeks, and RVSP was significantly reduced at 16 weeks. At 1 week after MI, myocardial catalase activity in the LV was maintained near control levels, whereas in the RV, it was 134% compared with its control value. At 4, 8, and 16 weeks, catalase activity in the LV was 71%, 48%, and 28% of respective controls. Catalase activity in the RV was significantly reduced only at 16 weeks. A similar trend was seen with respect to glutathione peroxidase activity. Reduced/oxidized glutathione ratio was significantly depressed in the LV at 1, 4, 8, and 16 weeks, whereas in the RV, this ratio was significantly reduced only at 8 and 16 weeks. Myocardial lipid peroxidation in the LV at 4, 8, and 16 weeks was elevated by approximately 40%, 51%, and 100%, respectively, whereas in the RV, an increase of approximately 50% was seen only at 16 weeks.
These data show that heart failure subsequent to MI is associated with an antioxidant deficit as well as increased oxidative stress, first in the LV, followed by the RV. Furthermore, these changes correlated with the hemodynamic function in each of the ventricles, suggesting their role in the pathogenesis of ventricular dysfunction.
心肌梗死（MI）后发生的心力衰竭伴有心肌中抗氧化剂水平降低和氧化应激增加。研究了存活的左心室（LV）和右心室（RV）中的抗氧化酶活性及氧化应激与其血流动力学功能的关系。
结扎大鼠左冠状动脉。心肌梗死后1周，左心室收缩压（LVSP）、左心室舒张末期压力（LVEDP）和右心室舒张末期压力（RVEDP）接近对照值，而右心室收缩压（RVSP）显著升高。在心肌梗死后4周、8周和16周的动物中，LVSP显著降低，分别为112.0±1.57、99.9±0.52和89.2±1.4 mmHg，而LVEDP显著升高，分别为8.2±0.52、17.4±1.7和31.4±1.5 mmHg。RVEDP在8周和16周时较高，RVSP在16周时显著降低。心肌梗死后1周，左心室中过氧化氢酶活性维持在接近对照水平，而右心室中该酶活性为对照值的134%。在4周、8周和16周时，左心室中过氧化氢酶活性分别为各自对照值的71%、48%和28%。右心室中过氧化氢酶活性仅在16周时显著降低。谷胱甘肽过氧化物酶活性也呈现类似趋势。在1周、4周、8周和16周时，左心室中还原型/氧化型谷胱甘肽比值显著降低，而右心室中该比值仅在8周和16周时显著降低。在4周、8周和16周时，左心室中心肌脂质过氧化分别升高约40%、51%和100%，而右心室中仅在16周时升高约50%。
这些数据表明，心肌梗死后的心力衰竭与抗氧化剂缺乏以及氧化应激增加有关，首先发生在左心室，随后累及右心室。此外，这些变化与每个心室的血流动力学功能相关，提示它们在心室功能障碍发病机制中的作用。
