HEMODYNAMIC & CORONARY CIRCULAR EFFECTS EXPERIMENTAL AUTOIMMUNE MYOCARDITIS

大鼠实验性自身免疫性心肌炎模型的建立 雌性Lewis大鼠心肌球蛋白多肽特异性T淋巴细胞 用于研究急性血流动力学和冠状动脉血管的变化。 注射T细胞后，15只实验动物(分别为1、2、5只 3周)和8名对照进行研究。这个 用EPR血氧仪测定血氧饱和度。流出的氧气和冠状动脉 EAM增加血流量，降低冠脉阻力(p&lt；0.05) (1、2、3周)。心脏/体重增加，而心率-压力 乘积，与对照组相比，+dp/dt和-dp/dt降低(p&lt；0.05) 一周，但不是在2周或3周。心肌耗氧量和平均耗氧量 EAM组PO2与对照组无明显差异。然而，与 对照组EAM心肌血氧分压的变化范围更广，经常超过 通常的范围，表明发生了局限性低氧和 高氧区。减少冠状动脉阻力，增加冠状动脉 流量和PO2的不均一性与Low的发展相一致 阻力，高流量高氧区，偷流导致缺氧 在其他领域。

A model of experimental autoimmune myocarditis (EAM), induced with cardiomyosin peptide specific T lymphocytes in female Lewis rats, was used to study acute hemodynamic and coronary vasculature changes. After injection of T cells 15 experimental animals (5 each at 1, 2 and 3 weeks) and 8 controls were studied using the isolated heart. The pO2 was measured using EPR oximetry. Effluent oxygen and coronary flow increased while coronary resistance decreased (p<.05) with EAM (1, 2 and 3 weeks). Heart/body weight increased while rate-pressure product, +dP/dt and -dP/dt decreased (p<.05) compared to controls at 1 week but not at 2 or 3 weeks. Myocardial oxygen consumption and mean pO2 were not different for EAM versus control. However, compared to controls EAM myocardial pO2 varied more widely and was often beyond the usual range, suggesting occurrence of localized hypoxic and hyperoxic areas. Decreased coronary resistance, increased coronary flow and pO2 heterogeneity are consistent with development of low resistance, high flow hyperoxic areas which steal flow causing hypoxia in other areas.