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Cerebral atheroembolism. An animal model.

Human atheromatous material was injected into the cerebral vasculature of anaesthetized rabbits via the left common carotid artery. The lethality of varying dosages was determined and the distribution and general character of occlusive vascular lesions which developed were analyzed by light and transmission electron microscopy. It was found that a dose exceeding 55 mg of the atheromatous material (125 mg/ml saline) was lethal in New Zealand white male rabbits weighing between 3 and 5 kg. In nonsurviving animals, parts of the Circle of Willis and usually one or more of its major tributaries were occluded. Some surviving animals exhibited signs of neurologic deficit evidenced by motor dysfunction. Occlusive vascular lesions found in surviving animals were predominantly localized in ipsilateral cortical and subcortical vessels within the distribution territory of the middle cerebral artery. The character of occlusive lesions showed strong evidence of thrombosis. These results demonstrated that this experimental system may be useful as a model for the study of blood-atheroembolic vascular reactions, cerebral infarction development and the testing of agents potentially prophylactic against the development or stabilization of occlusive lesions.

Animals↗

Short vein grafts for cerebral revascularization.

Experience with the use of a short saphenous vein bypass graft for cerebral revascularization is reviewed. Twenty patients with symptomatic atherosclerotic occlusive disease underwent a total of 21 bypass procedures. Cerebral revascularization was performed using a short (5 to 10 cm) saphenous vein graft (SVG) extending from the superficial temporal artery (STA) trunk anterior to the ear in 19 bypasses, or from the occipital artery (OA) immediately behind the mastoid process to the posterior temporal or angular branch of the middle cerebral artery (MCA) in two bypasses. The early patency rate for the SVG bypasses was 90%. Two of the four patients with SVG occlusion were found to have substantial resolution of a severe inaccessible internal carotid artery stenosis that was present preoperatively. Filling of multiple major branches of the MCA through the SVG was seen in 90% of patients on late postoperative conventional angiography. The STA trunk or proximal OA was consistently found to be enlarged on the late studies. None of the patients had recurrence of cerebral transient ischemic attacks. The procedure may be useful as a primary means of cerebral revascularization or as an alternative approach when a scalp artery cannot be used because of its small size, severity of arteriosclerotic changes (a common occurrence), or damage during its dissection. Cerebral blood flow studies suggest that the use of a short SVG has a more favorable effect upon the cerebral circulation than the conventional bypass procedure.

Arteriosclerosis↗

Permeation and deposition of fibrinogen and low-density lipoprotein in the aorta and cerebral artery of rabbits--immuno-electron microscopic study.

The localization of fibrinogen and low-density lipoprotein (LDL) in the arterial wall has been studied to determine whether they mediate the effects of hypertension and/or hypercholesteraemia on atherogenesis. In untreated control rabbits, fibrinogen was localized in the caveolae and vesicles of the endothelial cells and in the subendothelial spaces of the aorta. No fibrinogen was found in the subendothelial spaces of the cerebral artery. Hypertension or hypercholesteraemia was accompanied by enhanced insudation of fibrinogen into the subendothelial spaces of the aorta and cerebral artery, and fibrinogen deposition was most prominent in the hypercholesteraemic rabbits with induced renovascular hypertension. The insudation of fibrinogen appeared to occur by way of vesicular transport, and to some extent by junctional transport. In the untreated control rabbits, LDL was localized only in the caveolae and vesicles of endothelial cells in both aorta and cerebral artery. LDL was deposited in the subendothelial space of the aorta of hypercholesteraemic rabbits with or without hypertension, and in the cerebral artery of hypercholesteraemic rabbits with hypertension. These findings suggest that fibrinogen insudates into the intima of the aorta and cerebral artery both during hypertension and hypercholesteraemia, and that LDL insudation into the intima of the aorta in hypercholesteraemia is accentuated by hypertension. LDL insudated into the intima of the cerebral artery in the presence of hypercholesteraemia linked to hypertension. Thus, hypertension plays a significant role in the pathogenesis of cerebral atherosclerosis.

Animals↗