Tozzi-Ciancarelli M G, Di Massimo C, Mascioli A, Tozzi E, Gallo P, Fedele F, Dagianti A
Department of Biomedical Sciences and Technology and Biometry, University of L'Aquila, Italy.
Cardioscience. 1993 Dec;4(4):231-4.
There is evidence that oxidative insult plays a role in the development of acute myocardial infarction. Significance has also been attributed to changes in viscosity of the blood and in the deformability and aggregation of erythrocytes affecting their rheological behavior. In a group of patients with myocardial infarction we found a decreased erythrocyte filtration and an increased blood viscosity with no significant change in plasma viscosity. These changes were accompanied by alterations in the microviscosity of the erythrocyte membrane assessed by measuring the polarization of specific fluorescent molecules. From our data it is evident that there is an increase in the rigidity of the membrane at the lipid/protein boundary, with an associated increase in the fluidity of the deep lipid core of the membrane, while no changes were observed in the dynamic behavior of the membrane proteins. These physico-chemical perturbations in the membrane could be the basis for the decreased filtration of erythrocytes. We found, however, no evidence of lipid peroxidation in the erythrocyte membrane.
有证据表明氧化损伤在急性心肌梗死的发展中起作用。血液粘度、红细胞变形性和聚集性的变化对其流变行为的影响也具有重要意义。在一组心肌梗死患者中,我们发现红细胞滤过率降低,血液粘度增加,而血浆粘度无明显变化。这些变化伴随着通过测量特定荧光分子的极化来评估的红细胞膜微粘度的改变。从我们的数据可以明显看出,脂质/蛋白质边界处的膜刚性增加,同时膜深层脂质核心的流动性增加,而膜蛋白的动态行为未观察到变化。膜中的这些物理化学扰动可能是红细胞滤过率降低的基础。然而,我们在红细胞膜中未发现脂质过氧化的证据。