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Cerebral infarcts stem from atherosclerosis or arterionecrosis. Arterionecrosis, linked to hypertension and aging, causes microaneurysms leading to small infarcts and hemorrhages.
Area of Science:
- Neurology
- Vascular Biology
- Pathology
Background:
- Cerebral infarctions result from various arterial diseases.
- Understanding the pathogenesis of atherosclerosis and arterionecrosis is crucial for stroke prevention.
Purpose of the Study:
- To elucidate the causes and mechanisms of large and small cerebral infarcts.
- To discuss the pathogenesis and morphogenesis of arterial lesions, including atherosclerosis and arterionecrosis.
- To highlight the role of arterionecrosis in lacunar infarcts and hypertensive cerebral hemorrhage.
Main Methods:
- Analysis of atherosclerosis and thrombosis in proximal cerebral arteries.
- Investigation of arterionecrosis and microaneurysms in distal cerebral arteries.
- Review of factors contributing to endothelial cell injury and arterial wall changes.
- Experimental study of arterionecrosis in hypertensive rats.
Main Results:
- Large infarcts are linked to atherosclerosis in proximal arteries.
- Small infarcts result from arteriosclerosis, arteriosis, atherosclerosis, and arterionecrosis in distal arteries.
- Arterionecrosis-derived microaneurysms cause small infarcts and hypertensive hemorrhages.
- Hypertension, aging, and poor diet contribute to arterionecrosis.
Conclusions:
- Atherosclerosis and arterionecrosis are key causes of cerebral infarction.
- Arterionecrosis is increasingly implicated in small infarcts and hemorrhages.
- Factors like hypertension and aging play significant roles in arterial pathology leading to stroke.
Abstract:
Large cerebral infarctions were caused by atherosclerosis with or without thrombosis in the proximal circumflex (cortical) cerebral arteries. Hypertension, hypercholesterolemia, hypoxidosis, and vasospasm were considered to induce endothelial cell injuries, which might be the primary events not only in atherosclerosis, but also in arteriosclerosis and arteriosis formation. Morphogenesis of atherosclerosis and causes of associated thrombosis were also discussed. Small cerebral infarcts were produced not only by arteriosclerosis, arteriosis, and atherosclerosis, but also by arterionecrosis-derived microaneurysms occluded by thrombi in the distal penetrating (perforating) cerebral arteries. Pathogenesis and morphogenesis of the arterial lesions were discussed. Recent increase of the arterionecrosis occluded by thrombosis in the pathogenesis of small infarcts (lacunes) was noted. The direct cause of hypertensive cerebral hemorrhage was the rupture of arterionecrosis-derived microaneurysms in the distal penetrating cerebral arteries. The primary change of the arterionecrosis was the medial muscle cell necrosis, the causes of which were considered to be hypertension, aging, poor diet low in cholesterol, vasospasm, and the congenitally poor wall structure of the arteries. The development and healing of experimental arterionecrosis in hypertensive rats were also reported.