Leak L V, Ferrans V J, Cohen S R, Eidbo E E, Jones M
Department of Anatomy, Howard University College of Medicine, Washington, D.C. 20059.
Am J Anat. 1987 Dec;180(4):373-90. doi: 10.1002/aja.1001800408.
To study the evolution of pericardial inflammation, we have developed a model of pericarditis in sheep by surgically injecting heat-killed staphylococci and Freund's adjuvant into the pericardial cavity under sterile conditions. The pericarditis evolved through the following phases: 1) inflammatory response, 2) mesothelial cell injury and desquamation, and 3) fibrotic phase. At 3-24 hr there was increased microvascular permeability, which resulted in the exudation of fluid, neutrophils, macrophages, and fibrin into the pericardial cavity and the pericardial interstitium. By 72 hr, large numbers of inflammatory cells were aggregated on the mesothelial surfaces and dispersed throughout the pericardial cavity, either as free-floating cells or located between strands of fibrin. At 6 days, fibrinolysis was apparent along the mesothelial surfaces; and newly formed collagen fibrils were deposited throughout the interstitial spaces and among the aggregated cells. These fibrils provided a matrix for the growth of new blood and lymphatic vessels into new connective tissue on both parietal and visceral pericardial surfaces. At 2 weeks, intrapericardial fibrosis had produced focal adhesions between the pericardial surfaces. At 1 month, extensive areas of the pericardial cavity were obliterated. By 9 months, there was a marked reduction in the numbers of cells and blood vessels and increased deposition of collagen and elastic fibers. The intrapericardial injection of heat-killed staphylococci and adjuvant provides a reproducible animal model to study the time course of pericardial inflammation.
为研究心包炎的演变过程，我们通过在无菌条件下将热灭活的葡萄球菌和弗氏佐剂手术注入绵羊心包腔，建立了绵羊心包炎模型。心包炎的演变经历以下阶段：1）炎症反应，2）间皮细胞损伤和脱落，3）纤维化阶段。在3 - 24小时，微血管通透性增加，导致液体、中性粒细胞、巨噬细胞和纤维蛋白渗出到心包腔和心包间质。到72小时时，大量炎症细胞聚集在间皮表面，并以游离细胞形式或位于纤维蛋白束之间散布于心包腔内。在6天时，间皮表面出现明显的纤维蛋白溶解；新形成的胶原纤维沉积在整个间质空间以及聚集的细胞之间。这些纤维为新的血管和淋巴管生长到壁层和脏层心包表面的新结缔组织中提供了基质。在2周时，心包内纤维化导致心包表面出现局灶性粘连。在1个月时，心包腔的大片区域被闭塞。到9个月时，细胞和血管数量显著减少，胶原和弹性纤维沉积增加。心包腔内注射热灭活的葡萄球菌和佐剂提供了一个可重复的动物模型，用于研究心包炎的病程。
