[Experimental study on the mechanism of injury and proliferation of intima in the process of cerebral aneurysm development].
Under the hypothesis that cerebral aneurysms develop partly because of defective or decreased healing process at the site of intimal injury, namely at the site of cerebral arterial bifurcation, following experiments were performed. Experiment (1): Rats were treated with ligation of one common carotid artery and ligation of posterior branches of renal artery on both sides to induce cerebral aneurysms. Three months after the treatment, the contralateral carotid artery was ligated. Two months after the ligation, they were sacrificed and examined under light and electron microscopes. In 7 of 11 bifurcations which developed small cerebral aneurysms, prominent intimal thickening with proliferated smooth muscle cells and collagen was observed in the lumen of aneurysms. In 3 of 7 bifurcations which showed no aneurysmal development, apparent intimal thickening was also found at the site where aneurysms were expected to grow. In the group treated for inducing cerebral aneurysms but not ligated the contralateral carotid artery, none of 12 bifurcations with or without aneurysms showed such intimal thickening. Experiment (2): Rats were treated for inducing cerebral aneurysms. Three months after the treatment, reserpine was injected (0.75 mg/Kg B.W./day intraperitoneally) for 2 weeks. At the next day of the last injection, they were sacrificed and examined under the light microscope. In 6 of 12 bifurcations which developed small cerebral aneurysms, prominent intimal thickening was observed in the lumen of aneurysms. In 2 of 3 bifurcations which showed no aneurysmal development, apparent intimal thickening was also found at the site where aneurysms were expected to grow. In the group treated for cerebral aneurysms but not injected reserpine, none of 10 bifurcations with or without aneurysms showed such intimal thickening. Experiment (3): Rats were treated for inducing cerebral aneurysms. Two weeks after the treatment, FSF (fibrin stabilizing factor, known as blood coagulation factor XIII) was injected (10 U/100 g B.W./day, intravenously) for 5 days. Twelve days after the start of injection, they were sacrificed and examined under light and electron microscopes. In 11 of 20 bifurcations which developed small cerebral aneurysms, prominent intimal thickening was observed in the lumen of aneurysms. In the most advanced cases, the lumen of aneurysms were completely filled with proliferated smooth muscle cells and collagen. In 5 of 10 bifurcations which showed no aneurysmal development, apparent intimal thickening was found at the site where aneurysms were expected to grow. In the group treated for inducing cerebral aneurysms but not given FSF, none of 15 bifurcations with or without aneurysms showed such intimal thickening.
Kang
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Y
Department of Neurosurgery, Faculty of Medicine, Kyoto University.
D000818:Animals; D001794:Blood Pressure; D002455:Cell Division; D002536:Cerebral Arteries / Q000473:pathology*; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000473:pathology; D002532:Intracranial Aneurysm / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000473:pathology; D051381:Rats; D011919:Rats, Inbred Strains