Stroke; a journal of cerebral circulation
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Comparative Study
Hypertension with or without hemodilution after cardiac arrest in dogs.
We studied blood flow-promoting therapies after cardiac arrest in 18 dogs. Our model consisted of ventricular fibrillation (no blood flow) lasting 12.5 minutes, controlled reperfusion with cardiopulmonary bypass and defibrillation within 5 minutes, controlled intermittent positive-pressure ventilation to 20 hours, and intensive care to 96 hours. Group I (control, n = 6) dogs were reperfused under conditions of normotension (mean arterial blood pressure 100 mm Hg) and normal hematocrit (greater than or equal to 35%). ⋯ Total histopathologic damage scores were similar among the groups. A hypertensive bout with a peak mean arterial blood pressure of greater than or equal to 200 mm Hg beginning 1-5 minutes after the start of reperfusion was correlated with good outcome (p less than 0.01). Our results support the use of an initial bout of severe hypertension, but not the use of delayed hemodilution.
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To study the efficacy of mannitol in reducing cerebral edema and improving the ultimate neuropathologic outcome in perinatal cerebral hypoxia-ischemia, 67 7-day postnatal rats were subjected to unilateral common carotid artery ligation followed by exposure to 8% oxygen at 37 degrees C for 3 hours. Twenty-seven rat pups received a subcutaneous injection of 0.1 ml mannitol in a dosage of 4 mg/kg body wt immediately following cerebral hypoxia-ischemia and every 12 hours thereafter for a total of four doses. Control animals received either no therapy (n = 16) or an equivalent volume of normal saline (n = 24). ⋯ Mannitol significantly reduced (p less than 0.001) brain water content, as a reflection of cerebral edema, in both the ipsilateral (88.5% compared with 90.6% in controls) and the contralateral (85.0% compared with 87.2% in controls) cerebral hemispheres. Mannitol therapy did not ameliorate the incidence, distribution, or severity of tissue injury in the cerebral cortex, subcortical white matter, hippocampus, striatum, or thalamus of the ipsilateral cerebral hemisphere compared with the controls. Thus, while mannitol substantially reduces the extent of cerebral edema following hypoxia-ischemia, no beneficial affect on ultimate brain damage occurs.(ABSTRACT TRUNCATED AT 250 WORDS)
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According to several studies, the amount of subarachnoid blood on the initial computed tomogram of patients with aneurysmal subarachnoid hemorrhage has predictive value with respect to infarction and outcome. Of several methods for assessing the amount of subarachnoid blood, none has been subjected to a study of interobserver agreement. ⋯ The Spearman rank correlation coefficients for the sum of the scores for subarachnoid and intraventricular blood were very high. Summed scores for extravasated blood are suitable as a baseline variable in follow-up studies of patients with subarachnoid hemorrhage.
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Comparative Study
Prosthetic valve endocarditis 1976-1987. Antibiotics, anticoagulation, and stroke.
We retrospectively reviewed the clinical characteristics and outcomes of 61 patients with 62 episodes of prosthetic valve endocarditis, paying particular attention to neurologic complications (stroke). Atypical features of the group included a benign outcome of early postoperative infection (18% mortality) and a high stroke morbidity and mortality rate with Staphylococcus epidermidis infections. Eleven patients (18%) suffered an embolic stroke, most less than or equal to 3 days after diagnosis and before the initiation of antimicrobial therapy; the rate of embolic stroke recurrence was low (9%). ⋯ No protective effect of anticoagulation therapy with warfarin was observed. Six patients (8%) suffered brain hemorrhage due to septic arteritis, brain infarction, or undetermined causes; no specific risk of hemorrhagic stroke was evident with anticoagulation therapy. Antibiotic treatment appears to be more important than anticoagulation to prevent neurologic complications in patients with prosthetic valve endocarditis.
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The use of high-dose lidocaine for cerebral protection during ischemia has produced varied results. Our study uses a new, single carotid artery preparation in the rabbit to produce incomplete global ischemia by graded carotid occlusion; specific electroencephalographic changes are used as the end point for the extent of blood flow reduction sustained during 20 minutes. We monitored arterial pressure, intracranial pressure, and internal carotid blood flow that were recorded with an electromagnetic flowmeter after surgical ligation of the opposite internal and the two vertebral arteries, and we studied the electroencephalogram and somatosensory-evoked potentials elicited by stimulation of the sciatic nerve. ⋯ Deep halothane anesthesia alone elicited the slowest recovery, suggesting that the action of lidocaine was independent of its general anesthetic effect. There were very small differences among the groups in the measured arterial pressure, intracranial pressure, and cerebral blood flow, suggesting that lidocaine changed recovery rate without markedly modifying any characteristic of the postischemic cerebral perfusion. The protective effect of lidocaine may be the result of a specific blockade of Na+ channels or a decrease in excitatory neurotransmitter release, either of which would cause a delay in the onset of the events that lead to neuronal damage during ischemia.