DEVELOPMENT OF CURVE FITTING SOFTWARE FOR NOISY EPR SPECTRA

实验性自身免疫性心肌炎（EAM）模型， 在雌性刘易斯大鼠中， 用于研究急性血液动力学和冠状动脉血管变化。 在注射T细胞后，15只实验动物（在1、2和4小时各5只）被注射。 3周）和8个对照组使用离体心脏进行研究。 的 使用EPR血氧测定法测量pO 2。 流出氧与冠脉 EAM组血流增加，而冠脉阻力降低（p<0.05）， （1、2、3周）。 心率-血压升高时心脏/体重增加 与对照组相比，在1 ℃下，产物+dP/dt和-dP/dt降低（p<.05 一周，但不是两三周。 心肌耗氧量和平均 EAM与对照组的pO 2无差异。 不过相比 对照组EAM心肌pO 2变化范围更广， 通常的范围，表明发生局部缺氧， 高氧区 冠状动脉阻力降低， 血流和pO 2异质性与低 阻力，高流量高氧区，其偷流导致缺氧 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.