Role of lysosomes in coronary artery lesions of hypertensive rats

• Published in: Acta pathologica japonica Vol. 36; no. 10; p. 1529
• Main Authors: Suzuki, K, Kawaharada, U, Kobori, K, Takatama, M, Ooneda, G, Fukuda, T
• Format: Journal Article
• Language: English
• Published: Australia 01-10-1986
• Subjects: Acid Phosphatase - analysis; Animals; Coronary Vessels - enzymology; Coronary Vessels - ultrastructure; Hypertension - enzymology; Hypertension - pathology; Lysosomes - enzymology; Lysosomes - ultrastructure; Male; Microscopy, Electron; Muscle, Smooth, Vascular - ultrastructure; Rats; Rats, Inbred Strains
• ISSN: 0001-6632
• DOI: 10.1111/j.1440-1827.1986.tb02824.x

Electron microscopically the role of acid phosphatase (acid P) positive lysosomes in the pathogenesis of intramyocardial coronary artery lesions of hypertensive rats with bilaterally constricted renal arteries was studied. At 3 postoperative weeks, acid P positive lysosomes were increased in endothelial cells of the coronary arteries, but at 5 weeks and thereafter, they were decreased in number. In the intima, intimal smooth muscle cells with acid P positive lysosomes appeared at 3 postoperative weeks, but their number remained small as late as 9 postoperative weeks. The internal elastic lamina was fragmented into amorphous masses from 3 postoperative weeks, at 5 weeks and thereafter the fragmentation and disruption became severer, and at 9 weeks the lamina disappeared because of marked disruption. At 3 postoperative weeks, acid P positive extracellular lysosomes were observed in the gaps of the fragmented internal elastic lamina. At 5 weeks and thereafter, extracellular lysosomes and attenuated processes of medial smooth muscle cells with lysosomes were seen extending through the gaps of the fragmented internal elastic lamina. Necrosis of these extending cell processes and lysosomes remaining after the necrosis were observed. The findings suggested that the fragmentation and lytic change of the internal elastic lamina observed in hypertensive rat intramyocardial coronary arteries might be induced by extracellular lysosomes discharged not only from endothelial cells and intimal smooth muscle cells but also from the extending processes of medial smooth muscle cells into the gaps of the internal elastic lamina.