Thromboxane B2 in cardiac lymph. Effect of superoxide dismutase and catalase during myocardial ischemia and reperfusion.
Thromboxane B2 in cardiac lymph. Effect of superoxide dismutase and catalase during myocardial ischemia and reperfusion.
复制标题
心脏淋巴中的血栓素 B2。
DOI：
10.1161/01.res.66.4.1040
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发表时间：
1990
影响因子：
20.1
通讯作者：
Entman,ML
中科院分区：
文献类型：
--
作者：
Michael,LH;Zhang,Z;Hartley,CJ;Bolli,R;Taylor,AA;Entman,ML
中性粒细胞与心肌缺血-再灌注损伤的发生有关，其作用机制与活性氧、脂肪酸衍生的前列腺素和白三烯的产生有关。在这项研究中，我们通过研究超氧化物歧化酶（SOD）和过氧化氢酶（CAT）对心肌缺血和再灌注时观察到的血栓素形成增加的影响，来研究活性氧的产生与环氧化酶衍生的类autotacoids之间的潜在关系。在单独输注SOD、单独输注CAT以及SOD和CAT联合输注的情况下，检测闭塞60分钟后清醒犬心脏淋巴中的免疫反应性血栓素B2。缺血60分钟后再灌注导致血栓素B2立即升高。与单独输注SOD一样，SOD和CAT输注可以阻止血栓素B2的升高。SOD-CAT抑制血栓素B2产生的能力在停药后3小时内消失，此时血栓素B2排泄增加。在考虑抗氧化剂对心肌缺血再灌注损伤保护作用的起源时，活性氧对脂肪酸加氧酶的调节可能是一个非常重要的致病因素。
Neutrophils have been implicated in the genesis of myocardial ischemia-reperfusion injury, and their mechanism of action has been linked to the production of reactive oxygen species, fatty acid-derived prostanoids, and leukotrienes. In this study, we examined the potential relation between production of reactive oxygen species and cyclooxygenase-derived autacoids by studying the effects of superoxide dismutase (SOD) and catalase (CAT) on the rise in thromboxane formation observed with myocardial ischemia and reperfusion. Immunoreactive thromboxane B2 was measured in cardiac lymph from conscious dogs during reperfusion after a 60-minute occlusion in the presence of infusions of SOD alone, CAT alone, and a combination of SOD and CAT. Reperfusion after 60 minutes of ischemia causes an immediate elevation in thromboxane B2. SOD and CAT infusion prevented this rise in thromboxane B2 as did infusion of SOD alone. The ability of SOD-CAT to suppress thromboxane B2 production dissipated within 3 hours after the cessation of infusion, at which time thromboxane B2 excretion increased. The modulation of fatty acid oxygenases by reactive oxygen species may be a very important pathogenic factor in considering the origin of the protective effect of antioxidants in the setting of myocardial ischemia-reperfusion injury.