Light and electron microscopic studies on rat arterial lesions induced by experimental arterial contraction

• Published in: Virchows Archiv A Pathological Anatomy and Histology Vol. 385; no. 1; pp. 29 - 39
• Main Authors: Kobori, K, Suzuki, K, Yoshida, Y, Ooneda, G
• Format: Journal Article
• Language: English
• Published: Germany 01-12-1979
• Subjects: Animals; Constriction, Pathologic - pathology; Cytoskeleton - ultrastructure; Endothelium - ultrastructure; Male; Membranes - ultrastructure; Mesenteric Arteries - pathology; Mesenteric Arteries - ultrastructure; Methoxamine; Microscopy, Electron; Muscle, Smooth - ultrastructure; Necrosis; Rats; Time Factors; Vacuoles - ultrastructure
• ISSN: 0340-1227; 1432-2307
• DOI: 10.1007/bf00433538

Experimental contraction was produced in the rat mesenteric arteries and the arterial segments were studied morphologically. When the rat mesenteric artery was exposed in physiological saline solution at 37 degrees C and 2-3 mg of methoxamine hydrochloride (10 mg/ml) was dripped onto it, intense contraction was observed for about 30 min but elevation in blood pressure was slight. During the contraction, numerous vacuoles were seen in the medial smooth muscle cells of the arterial segments, and these vacuoles were shown electron microscopically to have double unit membranes, indicating that they were formed by herniation of a part of the adjacent smooth muscle cell body. In the arteries 1-6 h after the end of the contraction, cellular, nuclear and vacuolar membranes and myofilaments of the medial muscle cells were partially lost. 12-24 h after the contraction the arteries exhibited necrosis and desquamation of endothelial cells and platelet adhesion. In the media, smooth muscle cells were completely deprived of cell membranes, myofilaments, nuclei, intracytoplasmic organelles other than mitochondria, and vacuolar membranes. The cytoplasm was filled with fine granular and granulo-vesicular material, and fibrin insudation was observed in these severely damaged cells. Arterial contraction may be an important factor in the induction of arterial lesions.