No abstract

We conclude that ulceration and luminal thrombosis of the atheromatous plaque are the main sources of downstream cerebral microemboli in patients with high-grade internal carotid artery stenosis. Our data support the view that these pathoanatomic features may also play a key role in symptom development.

Chronic carotid dissection can be effectively treated by surgical reconstruction to prevent further ischemic or thromboembolic complications, if medical treatment for 6 months with anticoagulation failed or if carotid aneurysms and/or high-grade carotid stenosis persisted or have newly developed.

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The spatial heterogeneity of myocardial perfusion and metabolism was studied in 11 anaesthetized dogs under resting conditions. In each heart local myocardial blood flow was assessed using the tracer microsphere technique in 256 samples (mean mass: 83.1 mg) taken from the left anterior ventricular wall. In the same samples, the following biochemical parameters were determined: accumulation of [3H]-deoxyglucose (a measure of glucose uptake), free cytosolic adenosine (S-adenosylhomocysteine accumulation technique, a measure of tissue oxygenation and a possible mediator of blood flow regulation), and the specific activities of oxidative (citrate synthase, cytochrome-c-oxidase) and glycolytic (hexokinase, phosphoglycerate kinase) enzymes. Capillary density and mitochondrial and myofibril volume densities were determined by morphometry. Myocardial perfusion in each sample (average 0.77 ml min-1 g-1) varied between 0.1 and 2.5 times the mean (coefficient of variation 0.30+/-0.02). [3H]-deoxyglucose was deposited locally in proportion to perfusion. Samples showing low flow (<0.2 ml min-1 g-1) did not exhibit increased levels of cytosolic adenosine. The specific activities of the oxidative and glycolytic enzymes, however, were uniformly distributed between low and high flow areas. Furthermore, capillary density and mitochondrial and myofibril densities were similar in high and low flow regions. The results show firstly that local glucose metabolism in the heart occurs in proportion to local blood flow, suggesting that high flow regions have a higher than average metabolic rate. Secondly, regions of low flow are not compromized by critical oxygenation and most likely have a lower than average oxygen demand and finally, the homogeneous distribution of oxidative and glycolytic enzymes, as well as the homogeneous myocardial ultrastructure, suggest that areas with high and low blood flow under resting conditions may increase their metabolic rate to similar levels when required.

Renal artery dissection can be effectively treated with surgical revascularization. Primary nephrectomy should be considered only in patients with a large ischemic kidney infarction, with significant deterioration of kidney function, to effectively cure or improve severe renovascular hypertension.

our results demonstrate for the first time the complexity of the dissecting process on a molecular level. The ultimate dissection seems to be the dramatic endpoint of a long-lasting process of degradation and insufficient remodelling of the aortic wall. Altered patterns of gene expression suggest a pre-existing structural failure of the aortic wall, resulting in dissection.

We studied the size of infarcts in 25 dogs 48 hrs after proximal occlusion of the left anterior descending coronary artery. In one group of animals infarct size was measured by histologic criteria, in another group the infarct was measured macrohistochemically using p-NBT and malate to incubate unfixed slices of myocardium. In both groups infarct size was expressed as percentage of the area of perfusion of the occluded artery. Infarct size was 72% of the area-at-risk in the group studied by histology and 74.5% in the macrohistochemical group. The satisfactory agreement of both methods favors the p-NBT technique because of its ease and speed. It is suggested that the expression of infarct size as percentage of the perfusion area is a good definition and should be used in experiments designed to manipulate infarct size. In this way differences in the size of occluded arteries and their respective perfusion areas have no or only a negligible influence on infarct size.