Prevention of lipid peroxidation does not prevent oxidant-induced myocardial contractile dysfunction.
Prevention of lipid peroxidation does not prevent oxidant-induced myocardial contractile dysfunction.
复制标题
预防脂质过氧化并不能预防氧化剂引起的心肌收缩功能障碍。
DOI：
10.1152/ajpheart.1994.267.6.h2371
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Horwitz,LD
中科院分区：
文献类型：
--
作者：
Kong,Y;Lesnefsky,EJ;Ye,J;Horwitz,LD
We tested whether, with exposure to an extraneous iron-catalyzed free radical-generating system, prevention of lipid peroxidation with U74006F, a 21-aminosteroid, could also prevent myocardial contractile dysfunction. Rabbits received either U74006F (10 mg/kg iv) or vehicle (V). Thirty minutes later the hearts were excised and perfused by a non-recirculating Langendorff technique. Six U74006F- and six V-treated hearts were exposed for 7.5 min to a .OH-generating system (H2O2 and Fe(2+)-ADP chelate). Myocardial lipid peroxides were measured by glutathione peroxidase-catalyzed oxidation of exogenous glutathione. With exposure to .OH, cytosolic lipid peroxide levels were increased threefold in V-treated hearts, but there was no increase in U74006F-treated hearts. After 30 min of recovery, developed pressure and maximum first derivative of left ventricular pressure were greater in U74006F-treated hearts than in V-treated hearts but were still 50 and 44% of levels in saline hearts, respectively. Coronary flow was markedly reduced after exposure to free radicals and was only slightly less depressed when U74006F was administered. When coronary flow following oxidant exposure was increased by nitroglycerin, U74006F again only modestly improved systolic function. Thus, although U74006F blocked lipid peroxidation, it only slightly improved the ventricular dysfunction caused by .OH. Therefore, factors other than lipid peroxidation play a major role in oxidant-induced myocardial stunning.
