FIBROSIS-INDUCED REDUCTION OF ENDOMYOCARDIUM IN THE RAT AFTER ISOPROTERENOL TREATMENT
FIBROSIS-INDUCED REDUCTION OF ENDOMYOCARDIUM IN THE RAT AFTER ISOPROTERENOL TREATMENT
复制标题
DOI：
10.1161/01.res.65.2.258
复制
发表时间：
1989-08-01
影响因子：
20.1
通讯作者：
WEBER, KT
中科院分区：
文献类型：
--
作者：
JALIL, JE;JANICKI, JS;WEBER, KT
异丙肾上腺素治疗导致心内膜心肌纤维化，肌纤维被纤维状胶原包围。这项研究是在大鼠身上进行的，以确定胶原蛋白包裹的肌肉随后是否会坏死或萎缩。为此目的，我们在完成皮下异丙肾上腺素疗程（500μg/kg/天）后立即（10天）和30天后监测心肌胶原的纤维性质、其与肌肉的排列、心内膜心肌的形态，以及舒张期和收缩期心肌僵硬度的反应。我们发现：1）第 10 天和第 30 天左心室肥厚，胶原体积分数增加（p < 0.01），胶原蛋白体积分数由包围心内膜心肌的粗细胶原纤维网组成，2）第 30 天心内膜肌纤维直径不同程度减少，纤维组织包围的肌肉变薄程度最大，3）升高（p < 0.01） 第 10 天和第 30 天的舒张期应力-应变关系的斜率。所形成的收缩期应力-应变关系在 10 天时升高 (p < 0.01)，随着心内膜心肌质量的减少而下降 (p < 0.05)。因此，被纤维状胶原包围的心内膜心肌会随着时间的推移而萎缩，这会导致主动僵硬度的降低。这些发现可能部分解释了乳清进行性心室功能障碍伴随慢性心肌病伴心内膜心肌纤维化。
Isoproterenol treatment leads to endomyocardial fibrosis with muscle fibers encircled by fibrillar collagen. This study was undertaken in the rat to determine if muscle encased in collagen would subsequently become either necrotic or atrophic. For this purpose, we monitored the fibrillar nature of myocardial collagen, its alignment with muscle, and the morphology of the endomyocardium, together with the response in diastolic and systolic myocardial stiffness, immediately on completion (10 days) and 30 days after a course of subcutaneous isoproterenol (500 .mu.g/kg/day). We found 1) left ventricular hypertrophy at 10 and 30 days with an increase in collagen volume fraction (p < 0.01) that consisted of a meshwork of thick and thin collagen fibers that encircled endomyocardial muscle, 2) a variable reduction in endocardial muscle fiber diameter at 30 days with the greatest thinning seen in muscle encircled by fibrous tissue, and 3) an elevation (p < 0.01) in the slope of the diastolic stress-strain relation at 10 and 30 days. The developed systolic stress-strain relation, which was elevated at 10 days (p < 0.01), declined (p < 0.05) with the reduction in endomyocardial muscle mass. Thus, endomyocardial muscle, encircled by fibrillar collgen, will atrophy over time, and this leads to a reduction in active stiffness. Thses findings may, in part, explain whey progressive ventricular dysfunction accompanies chronic myocardial disease with endomyocardial fibrosis.