Stroke; a journal of cerebral circulation
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Hyperventilation to extremely low arterial carbon dioxide tension (PaCO2) has been used in the management of persistent pulmonary hypertension in newborn infants. With progressive hypocarbia, cerebral vasoconstriction occurs, raising the concern that extreme hypocarbia may result in cerebral oxygen deprivation. Therefore, I evaluated regulation of the cerebral circulation during acute hypocarbia in 10 newborn lambs. ⋯ Cerebral venous lactate concentration increased significantly (3.49 +/- 0.23 vs. 2.01 +/- 0.22 mM, p less than 0.001) during severe hypocarbia (PaCO2 of less than 22 mm Hg), and the arterial-venous lactate concentration difference became negative. These results demonstrate uniform responses of whole-brain and regional blood flows and stable cerebral oxygen consumption during moderate and severe hypocarbia. Although there is evidence for cerebral lactate production during severe hypocarbia, this is not likely to indicate cerebral hypoxia as oxygen consumption does not change.
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Using logistic regression, we analyzed the predictive value of a number of entry variables with respect to the outcome variables delayed cerebral ischemia, rebleeding, and poor outcome (death or severe disability) in patients with aneurysmal subarachnoid hemorrhage. The entry variables were clinical condition on admission (grades on the Glasgow Coma Scale, Hunt and Hess system), the amount of subarachnoid and intraventricular blood and the presence of hydrocephalus on the admission computed tomogram, and antifibrinolytic treatment with tranexamic acid. We used data from a prospectively studied population of 176 patients admitted within 72 hours after subarachnoid hemorrhage. ⋯ The site of delayed cerebral ischemia was not related to the location of the subarachnoid hemorrhage. Antifibrinolytic treatment was the only entry variable (negatively) predicting the risk of rebleeding. Death or severe disability after 3 months was best predicted by the amount of subarachnoid blood and the initial clinical condition reflected by the grade on the Glasgow Coma Scale.
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Our study describes the anatomy of the middle cerebral artery (MCA) in 65 Sprague-Dawley rats and the spatial distribution of ischemic cortical lesions caused by occluding major MCA branches. The rats characteristically had at least two major MCA branches, frontal and parietal. Many rats had additional branches supplying the pyriform and temporal cortexes. ⋯ In contrast, occlusions of the pyriform branch of the MCA invariably caused infarcts in the frontopyriform region. In about one third of the rats, frontal or parietal branch occlusions produced lesions involving much of the proximal MCA territory; the frontopyriform region was most consistently affected. Combined, these data suggest that the pyriform MCA branch is an end-artery and that the cortical region it supplies is prone to ischemic damage resulting from any reduction of blood flow through the main MCA trunk.(ABSTRACT TRUNCATED AT 250 WORDS)
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Twenty-four patients with subarachnoid hemorrhage due to rupture of a supratentorial aneurysm underwent surgery within 72 hours after subarachnoid hemorrhage. Immediately after clipping of the aneurysm the patients were treated with intravenous nimodipine for at least 7 days and then received the drug orally for another week. Nine patients had a documented or probable intake of aspirin or other nonsteroid anti-inflammatory drug during the days preceding admission. ⋯ Thromboxane B2 concentrations were similar to those of four control patients not receiving nimodipine. In three patients who developed delayed ischemic dysfunction despite "therapeutic" nimodipine plasma concentrations, the thromboxane B2 levels were low or normal. Our present results do not support the idea that nimodipine exerts an effect on platelet function in patients with aneurysmal subarachnoid hemorrhage.
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Although blood lipids and lipoproteins are strongly related to coronary atherosclerosis, their association with cerebrovascular atherosclerosis is less clear. A review of more than 20 publications in which a relation was sought between plasma lipid and lipoprotein concentrations and cerebrovascular atherosclerosis leads to the general conclusion that such a relation exists and that it is stronger in older than in younger individuals. ⋯ Interstudy variations in lipoprotein fraction analyzed, methodology for the analysis of lipids and lipoproteins, arterial segment examined, population sampled, control selection in case-control studies, statistical analytic approach taken, and methodology for the assessment of arterial disease preclude pooled analyses. There is a clear need for further evaluation of this relation using standardized and up-to-date methodologies both for analyses of lipids and lipoproteins and for assessment of cerebrovascular disease in symptom-free volunteers as well as in symptomatic patients.