ABSTRACT
A case of acute occlusion of the left common carotid artery is reported. The patient presented with symptoms and signs largely on the left side, ipsilateral to an occluded left carotid artery. Angiography revealed occlusion of the left common carotid artery and ulceration within the lumen of the right internal carotid artery bulb. Computerized tomography showed findings compatible with an old infarct within the right temporal lobe. The diagnosis of interhemispheric steal syndrome was made and the patient was treated successfully with staged surgical procedures on the carotid arteries, beginning with the totally occluded vessel, which was obstructed by fresh clot. The pathophysiology of interhemispheric steal syndrome is reviewed. A policy of operating first on the side of the occluded or more severely stenosed carotid artery is recommended, even though this vessel may be ipsilateral to the patient's symptoms.
Subject(s)
Carotid Artery Thrombosis/complications , Cerebrovascular Circulation , Collateral Circulation , Ischemic Attack, Transient/etiology , Aged , Arteriosclerosis/complications , Arteriosclerosis/diagnostic imaging , Carotid Artery Diseases/diagnostic imaging , Carotid Artery Thrombosis/diagnostic imaging , Carotid Artery Thrombosis/physiopathology , Cerebral Angiography , Humans , Ischemic Attack, Transient/physiopathology , Male , SyndromeABSTRACT
The intraventricular (IVT) administration of angiotensin II (AII) (100 ng.kg-1.min-1) produced significant elevations of arterial blood pressure in pentobarbital-anesthetized dogs on either normal or sodium-deficient diets. In both groups of dogs the intraventricular administration of AII caused comparable and significant elevations in blood pressure averaging 15 +/- 2 and 17 +/- 4 mmHg, respectively, within 10 min after onset of the infusion. The rises in blood pressure were due to increased peripheral resistance (2.87 +/- 1.20 vs. 1.67 +/- 0.43 units). At the peak of the pressor response bradycardia was a constant feature in sodium-depleted animals, but was not present in the normal ones. In both groups of dogs regional cerebral blood flow (rCBF), determined by the xenon-133 washout method, remained unchanged during the development of the pressor response, and peripheral plasma renin activity failed to increase in response to the central infusion of AII. In conclusion, sodium deprivation appears not to influence the sensitivity of the central AII receptor because comparable pressor responses and hemodynamic changes were obtained following the intraventricular administration of AII in both normal and sodium-depleted dogs.
