Vracko R, Thorning D
Cardiovasc Res. 1985 Feb;19(2):76-84. doi: 10.1093/cvr/19.2.76.
A new method for producing a circumscribed injury in rat myocardium is described. It utilises laparotomy and freeze-thawing across an intact diaphragm. Morbidity and mortality are negligible because the chest and pericardial cavities, the major coronary vessels, and the major branches of the conduction system remain intact. The size and location of the injury are reproducible and its sharp delineation facilitates accurate collection of samples from areas of interest. The myocytes are killed in the area of injury, whereas the capillary, nerve and connective tissue cells are killed centrally but preserved peripherally in a perimeter zone of injury in which capillaries remain patent. The reparative activities are initiated at the border between injured and uninjured myocardium; as they progress over the ensuing 6 weeks, the volume of damaged myocardium diminishes rapidly leaving only a rim of subepicardial scar tissue, and the thickness of ventricular muscle between the scar and endocardium returns almost completely to its pre-injury width. The mechanisms involved in the repair process are being investigated.
本文描述了一种在大鼠心肌中制造局限性损伤的新方法。该方法采用剖腹术并通过完整的膈肌进行冻融。由于胸腔、心包腔、主要冠状动脉血管和传导系统的主要分支保持完整，发病率和死亡率可忽略不计。损伤的大小和位置具有可重复性，其清晰的边界便于从感兴趣区域准确采集样本。损伤区域的心肌细胞死亡，而毛细血管、神经和结缔组织细胞在中央死亡，但在损伤周边区域的外周得以保留，该区域的毛细血管保持通畅。修复活动在损伤心肌与未损伤心肌的边界处启动；在随后的6周内，随着修复进程的推进，受损心肌的体积迅速减小，仅留下心外膜下瘢痕组织的边缘，瘢痕与心内膜之间的心室肌厚度几乎完全恢复到损伤前的宽度。目前正在研究修复过程中涉及的机制。
