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Dynamic changes of myocardial collagen metabolism in pressure-overloaded rats / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12): 740-743, 2017.
Article in Chinese | WPRIM | ID: wpr-512814
ABSTRACT

AIM:

To observe the dynamic changes of myocardial collagen metabolism in pressure-overloaded rats.

METHODS:

The pressure-overloaded rat model was established by partial abdominal aortic coarctation.The rats underwent surgery but not constrictive were used as sham-operated control group.The rats were euthanized at 3, 4, 8 and 12 weeks.The body mass, heart mass and left ventricular mass were weighed, and the heart mass index (HMI) and left ventricle mass index (LVMI) were calculated.Masson trichrome staining was used on the myocardial sections, alkaline hydrolysis was used to detect the content of myocardial hydroxyproline (HYP), and the serum levels of procollagen type I carboxy-terminal peptide (PICP), procollagen type III amino-terminal peptide (PIIINT), and collagen C telopeptide type I (CTX-I) were also measured.

RESULTS:

Compared with sham-operated control group, the collagen deposition was evident, and collagen volume fraction (CVF) was increased significantly in model group (P<0.01), which further increased over time.HMI, LVMI and HYP significantly increased in model group (P<0.05), and HYP showed a tendency to increase over time.In addition, the serum concentration of PICP was increased significantly in model group, and the difference was significant at 4, 8 and 12 weeks (P<0.05).The serum concentration of PIIINP was increased significantly, but CTX-I was lowered significantly in model group (P<0.01).

CONCLUSION:

In the state of pressure overload, myocardial collagen metabolism is in disorder, and myocardial fibrosis is the major pathological change, which further increases over time.

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2017 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2017 Type: Article