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心脏增大时心包扩张的机制。

Mechanism of pericardial expansion with cardiac enlargement.

作者信息

Kardon D E, Borczuk A C, Factor S M

机构信息

Department of Pathology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.

出版信息

Cardiovasc Pathol. 2000 Jan-Feb;9(1):9-15. doi: 10.1016/s1054-8807(99)00029-0.

DOI:10.1016/s1054-8807(99)00029-0
PMID:10739902
Abstract

BACKGROUND

The normal pericardial sac accommodates a 250-350 gram heart and 15-50 ml of pericardial fluid. Cardiac enlargement and/or increases in fluid must be accompanied by an increase in pericardial volume and a concomitant expansion of the pericardial sac. The mechanism of such expansion has been debated, but theoretical considerations include fibroblastic proliferation with new connective tissue deposition versus remodeling of the pre-existent connective tissue.

DESIGN

Nineteen pericardia were obtained from consecutive adult autopsies. Total pericardial fluid was measured; the absolute value of pericardial fluid volume and cardiac weight were added to create a total score. Representative pericardial tissue was stained with hematoxylin-eosin (H&E), Masson's trichrome, and Verhoeff's elastin stain (EVG). An additional archival case with the pericardium from a 900-g heart with 1,000-ml of fluid was also included.

RESULTS

None of the sections showed histologic evidence of fibroblastic proliferation. Parameters indicative of collagen stretching or damage were evaluated. The greatest correlative factor in identifying an enlarged pericardium was the average of four measurements of the greatest distance between elastic fibers surrounding obliquely oriented collagen layers. Five of six cases with a cardiac score > 450 showed an average measurement of less than 15 microns, and 10 of 14 cases with a cardiac score < or = 450 showed an average measurement of > 15 microns = 0.0498). Histologic and ultrastructural evidence of collagen damage was identified in the pericardium from the 900-g heart with the 1,000-ml effusion.

CONCLUSIONS

We propose that collagen stretching and slippage of obliquely oriented collagen layers contribute to the increased surface area needed to accommodate larger volumes. When these limits are exceeded, collagen damage ensues.

摘要

背景

正常的心包腔容纳重250 - 350克的心脏及15 - 50毫升的心包液。心脏增大和/或液体增多必然伴随着心包腔容积增加以及心包囊相应扩张。这种扩张的机制一直存在争议,但理论上的考虑包括成纤维细胞增殖伴新结缔组织沉积与已有结缔组织重塑。

设计

从连续的成年尸检中获取19份心包。测量心包液总量;将心包液体积绝对值与心脏重量相加得出总分。取代表性心包组织进行苏木精 - 伊红(H&E)染色、马松三色染色及韦尔霍夫弹性蛋白染色(EVG)。另外纳入1例存档病例,该病例心包来自重900克且伴有1000毫升液体的心脏。

结果

所有切片均未显示成纤维细胞增殖的组织学证据。评估了提示胶原拉伸或损伤的参数。识别心包增大的最相关因素是斜向排列的胶原层周围弹性纤维间最大距离的四次测量平均值。心脏评分>450的6例中有5例该平均测量值小于15微米,而心脏评分≤450的14例中有10例该平均测量值>15微米(P = 0.0498)。在重900克且伴有1000毫升积液的心脏的心包中发现了胶原损伤的组织学和超微结构证据。

结论

我们提出,斜向排列的胶原层的胶原拉伸和滑动有助于增加容纳更大容积所需的表面积。当超过这些限度时,就会发生胶原损伤。

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