Lurie K G, Bristow M R, Minobe W A, Masek M, Billingham M E
Pathology Department, Stanford University Medical Center, California 94305.
Am J Cardiovasc Pathol. 1988;2(2):181-91.
Weekly injections of the catecholamine depleting agent 6-hydroxydopamine (6-OHDA) were used to denervate rabbit hearts chemically. Analyses of morphology and beta-adrenergic receptor density were made at 1, 2, and 4 weeks. Changes resulting from subacute and chronic inflammatory processes were evident by light microscopy after 1 week. At that time, electron microscopy revealed marked increases in collagen, large myocytic vacuolizations in myocytes, widened gap junctions, and myofibrillar degeneration and dropout. Receptor density was marginally increased at 2 weeks but was decreased (p less than .05) at 4 weeks (maximal [3H]dihydroalprenolol (DHA) binding in fmol/mg: 69.6 +/- 5.4 in controls vs 49.2 +/- 5.1 in 6-OHDA-treated animals). Basal, isoproterenol-stimulated and F- -stimulated adenylate cyclase activities were decreased in the 6-OHDA-treated group at 4 weeks. We conclude that administration of 6-OHDA may cause severe myocardial damage, and that this process may involve loss of some functional components of the cell membrane.
每周注射儿茶酚胺耗竭剂6-羟基多巴胺（6-OHDA）对兔心脏进行化学去神经支配。在第1、2和4周对形态学和β-肾上腺素能受体密度进行分析。1周后，光镜下可见亚急性和慢性炎症过程导致的变化。此时，电镜显示胶原显著增加、心肌细胞出现大的空泡化、缝隙连接增宽以及肌原纤维变性和缺失。2周时受体密度略有增加，但4周时降低（P<0.05）（最大[3H]二氢阿普洛尔（DHA）结合量，以fmol/mg计：对照组为69.6±5.4，6-OHDA处理组为49.2±5.1）。4周时，6-OHDA处理组的基础、异丙肾上腺素刺激和F-刺激的腺苷酸环化酶活性均降低。我们得出结论，给予6-OHDA可能导致严重的心肌损伤，且这一过程可能涉及细胞膜某些功能成分的丧失。
