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[Induction and validation of arterial calcium overload in rats]
1National Laboratory of Medical Neurobiology, Shanghai Medical University, Shanghai 200032.
Objective:
To induce arterial calcium overload (ACO) in rats and analyze its features.
Methods:
Arterial calcium content and intracellular calcium content were determined by atomic absorption spectrometer and electron probe microanalysis, respectively. The morphological changes of endothelial cells and vascular smooth muscle cells were studied with scanning and transmission electron microscopes. DNA contents and its mass distribution were determined by DNA imaging analysis. Arterial collagen and elastin contents were determined biochemically.
Results:
Seven days after the induction of ACO with selected regimen, massive calcium was found accumulating in the arterial wall, including the cytoplasm and mitochondrion of the medial smooth muscle cells, indicating both extracellular and intracellular calcium overload. Degeneration of aortic endothelial cells was found at the early stage of ACO under scanning and transmission electron microscope. At the late time of ACO, significant proliferation and sclerotic reactions of arteries occurred, including the proliferation of smooth muscle cells, matrix remodeling, and damage of elastic structure. The average DNA content per smooth muscle cell was elevated, and more cells entered the S phase of proliferating cycle since day 7. On the other hand, total collagen content of aorta was increased 7 days after induction of ACO, and rose continuously at day 14 (P < 0.05). Functional studies showed that arterial elasticity was significantly impaired.
Conclusion:
Our method could induce ACO/constantly in rats, and the ACO model shares the similarities with the characterization of human arteriosclerosis on many aspects.