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大鼠和犬模型中心肌梗死后愈合及心室重构过程中胶原蛋白沉积速率

Rate of collagen deposition during healing and ventricular remodeling after myocardial infarction in rat and dog models.

作者信息

Jugdutt B I, Joljart M J, Khan M I

机构信息

Cardiology Division of the Department of Medicine, University of Alberta, Edmonton, Canada.

出版信息

Circulation. 1996 Jul 1;94(1):94-101. doi: 10.1161/01.cir.94.1.94.

Abstract

BACKGROUND

We hypothesized that the rate and amount of infarct collagen deposition during healing after myocardial infarction might influence ventricular remodeling in rat and dog models. The purpose of this study was to compare rates of infarct collagen deposition and ventricular remodeling in the two models.

METHODS AND RESULTS

Infarcted rat and dog hearts were removed at fixed time intervals between 1 and 50 days for measuring remodeling parameters and infarct and noninfarct collagen content (mg/g hydroxyproline). Collagen was less in sham rat (n=29) than dog (n=30) ventricles (3.32 versus 4.57 mg/g, P<.001) and markedly lower in the rat (n=48) than dog (n=59) infarcts throughout healing and by 50 days (9.98 versus 56.74 mg/g, P<.0001). Infarct collagen leveled off earlier and healing (histology) was completed sooner in the rat. Infarct scars were also thinner in the rat, with more (P<.0001) thinning and bulging (mm/g), and greater increase in ventricular volume. Although the mass to volume ratio decreased (P<.001) in both models, global remodeling was different, with greater transverse axis widening and globularity in the dog. Although infarct size, transmurality, heart rate, filling pressure, and blood pressure were greater in the rat, infarcts 10% to 30% in size in both models showed similar differences in infarct collagen and remodeling.

CONCLUSIONS

Compared with dog infarcts, rat infarcts exhibited faster healing and infarct collagen deposition and markedly lower infarct collagen. In addition to larger, more transmural, and thinner infarcts, and greater hemodynamic load, the lower infarct collagen in that model might be an important factor in the greater regional remodeling.

摘要

背景

我们推测,心肌梗死后愈合过程中梗死区胶原沉积的速率和量可能会影响大鼠和犬模型的心室重构。本研究的目的是比较两种模型中梗死区胶原沉积速率和心室重构情况。

方法与结果

在梗死后1至50天的固定时间间隔取出大鼠和犬的梗死心脏,测量重构参数以及梗死区和非梗死区的胶原含量(毫克/克羟脯氨酸)。假手术大鼠(n = 29)心室中的胶原含量低于犬(n = 30)心室(3.32对4.57毫克/克,P <.001),并且在整个愈合过程直至50天时,大鼠(n = 48)梗死区的胶原含量明显低于犬(n = 59)梗死区(9.98对56.74毫克/克,P <.0001)。大鼠梗死区胶原水平更早趋于平稳,且愈合(组织学)完成得更快。大鼠的梗死瘢痕也更薄,变薄和膨出更多(P <.0001,毫米/克),心室容积增加更大。虽然两种模型中的质量与容积比均下降(P <.001),但整体重构情况不同,犬的横轴增宽和球形化更明显。虽然大鼠的梗死面积、透壁性、心率、充盈压和血压更大,但两种模型中10%至30%大小的梗死区在梗死胶原和重构方面表现出相似的差异。

结论

与犬梗死区相比,大鼠梗死区愈合更快,梗死胶原沉积更快,且梗死胶原含量明显更低。除了梗死面积更大、透壁性更强、瘢痕更薄以及血流动力学负荷更大外,该模型中较低的梗死胶原可能是区域重构更明显的一个重要因素。

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