Yoji Yoshida

Morphogenesis of plasmatic arterionecrosis as the cause of hypertensive intracerebral hemorrhage

The morphogenesis of the vascular lesions, which were considered to be the immediate cause of hypertensive intracerebral hemorrhage, was morphologically studied in autopsy cases. The direct cause of the hemorrhage was the rupture of the intracerebral microaneuysms resulted from the plasmatic arterionecrosis. The arterionecrosis was predominantly present in the intracerebral arteries of approximately 150 µ diameter, especially in the external branches of the arteriae corporis striati mediae in the putamen, and characterized by medial smooth muscle cell loss, blood plasma insudation in the intima, histolysis of the internal elastic lamina and intimal collagenous fibers, fibrin deposition (fibrinoid degeneration) in the intima, and luminal dilatation. The morphogenesis of the arterionecrosis was the development of histolysis as well as fibrinoid degeneration caused by blood plasma insudation in the wall of the intracerebral arteries with preceding necrosis and loss of medial smooth muscle cells and subsequent fibrous intimal thickening with dilated lumina. Intracerebral microaneurysms were also formed by the plasmatic arterionecrosis in a narrow sense, in which histolysis due to blood plasma insudation had occurred, but fibrin (fibrinoid substance) deposition in the intima had not yet arisen.

ELECTRON MICROSCOPIC STUDIES ON THE MORPHOGENESIS OF FIBRINOID DEGENERATION IN THE MESENTERIC ARTERIES OF HYPERTENSIVE RATS.

† Department of Pathology, School of Medicine, Gunma University, Maebashi, Japan. The direct cause of apoplectic cerebral hemorrhage (hypertensive intracerebral massive hemorrhage) is the so-called angionecrosis of intracerebral arteries. It is, both histologically and histochemically, very similar to fibrinoid degeneration in the systemic arteries of hypertensive rats which is induced by surgical constriction of the bilateral renal arteries (Ooneda and associates’; Takatama2) . The fibrinoid degeration is observed not only in hypertensive, allergic and collagen diseases, but also in other miscellaneous pathologic conditions (Matsuyama and co-workers3) . As to the morphogenesis of the degeneration, which is characterized by the presence of fibrinoid substance in vascular

Smooth Muscle Cells in the Development of Plasmatic Arterionecrosis, Arteriosclerosis, and Arterial Contraction

Plasmatic arterionecrosis, the causative lesion of hypertensive cerebral hemorrhage, follows upon medial muscle cell necrosis. The development of medial muscle cell necrosis, the earliest cerebral arterial change seen in hypertensive rats, was inhibited when these animals were fed a cholesterol and lard-supplemented diet. Insudation of fibrin was noted in the arterial intima of hypertensive rats with bilaterally constricted renal arteries. Removal of the constriction induced a fall in the elevated blood pressure and an increase of intimal muscle cells. These were responsible for the dissolution of the deposited fibrin, leading to arteriosclerosis. These myointimal cells may originate from the endothelium. Arterial contraction caused by methoxamine hydrochloride often induced the intrusion of one medial muscle cell into another and increased endothelial permeability. 12-24 h after contraction, the arterial segments showed medial muscle cell necrosis, endothelial desquamation with platelet adhesion, and blood plasma infiltration.

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

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° 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.

An electron microscopic study of plasmatic arterionecrosis in the human cerebral arteries

An electron microscopic study of the intracerebral arteries from 9 hypertensive cases was performed in order to elucidate the morphogenesis of the plasmatic arterionecrosis which was considered to be the direct cause of hypertensive intracerebral hemorrhage. In the preceding stage of the arterial lesions, marked necrosis of medial smooth muscle cells and increase of basement membrane-like substance in the intima and media were observed. The lumina of these arteries were slightly dilated. The dilatation and hemodynamic factors were supposed to cause endothelial injury resulting in blood plasma insudation into the intima through the opened spaces between endothelial cells. The insudated blood plasma dispersed and dissolved the basement membrane-like substance, collagen and elastic fibers in the arterial wall, leading to the development of the plasmatic arterionecrosis.

Monoamine-storing cells in the media of the thoracic aorta of Gallus domesticus

SummaryLight, fluorescence and electron microscope studies of chicken and chick embryo aorta reveal the occurrence of cell masses without the characteristics of smooth muscle cells situated within the media, in the transitional region between the aortic arch and the descending thoracic aorta. The cell masses consist of two cell types: one type (G cells) contains large numbers of cytoplasmic granules (900–2200 Å in diameter); the other cell type consists of Schwann cell-axon complexes. G cells are innervated by monoaminergic nerve fibres considered to be efferent ones. Some G cells are in contact with endothelial cells or medial smooth muscle cells. G cells appear in the aortic wall at 9 days in ovo; they do not regress in old chickens.The administration of reserpine results in reduction of the electron opacity of the granules in G cells.

Plasmatic arterionecrosis and its thrombotic occlusion

Abstract The vascular lesions directly responsible for hypertensive intracerebral hemorrhage were studied in autopsy cases, associated with some animal experiments. The immediate cause of the hemorrhage was the rupture of the intracerebral microaneurysms resulted from plasmatic arterionecrosis. At the beginning of the morphogenesis of the arterionecrosis, medial smooth muscle cells of the intracerebral arteries underwent necrosis and disappeared. Subsequently the lumen became somewhat dilated, followed by slight intimal thickening with fibrous tissue. In such intima occurred blood plasma insudation, which induced not only histolysis of the intimal tissue, but also intimal deposition of fibrinoid substance consisting mainly of fibrin. In the striate and thalamic arteries in the basal ganglia, the arterionecrosis and consequent microaneurysms occurred preferably at the bifurcations or in the somewhat distal segments from them. In the medullary arteries in the cortices, however, most of the microaneurysms were found in the just proximal segments from the rectangular bends at the cortico-medullary junction. But they were rarely seen in the straight medullary arteries without bending. These findings suggested the possible role of hemodynamics in the pathogenesis of the arterial lesions. The arterionecrosis was accompanied or not accompanied with the deposition of fibrinoid substance in the intima. In the latter occurred also histolysis due to blood plasma insudation and consequent microaneurysms. The intimal fibrinoid deposition, that is, fibrin deposition, could be considered, like mural thrombi, to have a biological significance of reinforcing the arterial wall that had been affected with marked histolysis. It seemed that microaneurysms most liable to rupture were those revealing the arterionecrosis with neither thrombosis nor dense deposition of abundant fibrin in the intima. The microaneurysms were sometimes occluded by thrombi and saved from rupture. The occluded lesions, however, were one of the causes of cerebral infarction. Twenty-six % of infarcts in the basal ganglia were caused by the occluded microaneurysms. The microaneurysms in the cortices were more liable to be occluded by thrombi than those in the basal ganglia, presumably because of the lower blood pressure in the former according to the law of Hagen-Poiseuille.