Publications by authors named "Kassell N"

Pharmacodynamic and quantitative autoradiographic studies were performed to characterize the muscarinic receptors on the endothelium and smooth muscle of the rabbit thoracic aorta. The antagonistic effect of atropine and pirenzepine on the relaxation induced by acetylcholine showed that the relaxation was mediated by muscarinic receptors with pA2 values of 9.4 and 6.

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The influence of subarachnoid hemorrhage (SAH) on vasodilatation induced by vasoactive intestinal polypeptide (VIP) was investigated in rabbit basilar arteries. VIP-induced relaxation was measured in ring sections of the basilar arteries precontracted by 10(-5) M serotonin using an isometric tension recording method. The cyclic adenosine monophosphate (cAMP) content was measured using radioimmunoassay as an indicator of the intracellular mechanism in the arterial smooth muscle cells.

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The ability of antithrombin III, an endogenous plasma glycoprotein, to reverse the arterial narrowing in a rabbit model of cerebral vasospasm was evaluated. The vasodilator activity of antithrombin III on rabbit arteries was first assessed in vitro using a myograph-arterial ring preparation. Antithrombin III (10 IU/ml) induced a 55.

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The present work was performed to establish whether the nonglucocorticoid, 21-aminosteroid, U74006F, could prevent the development of delayed cerebral vasospasm after experimental subarachnoid hemorrhage. The subarachnoid hemorrhage was produced by percutaneous injection of 4.5 mL of nonheparinized autologous blood into the cisterna magna of rabbits.

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Thrombosis of the deep cerebral venous system is usually fatal, and patients are frequently stuporous or comatose at presentation. This report describes serial radiological and neuropsychological observations in an 18-year-old woman who remained alert and survived this disorder. In association with diencephalic edema seen on computed tomographic scan, she demonstrated disorientation, abulia, attentional deficits, memory loss, and dyscalculia and had impaired IQ scores: the performance scores were worse than the verbal scores.

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The effects of subarachnoid hemorrhage (SAH) with various degrees of increase in intracranial pressure (ICP) on the staining of prostaglandin F2-alpha (PG F2alpha) were studied in rat brains. SAH was produced in 18 rats by injection of 0.18-0.

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An isometric tension measurement of ring segments was performed in the rabbit basilar and common carotid arteries in vitro to investigate the regional differences in the calcitonin gene-related peptide (CGRP)-induced vasodilation and the effect of subarachnoid hemorrhage on CGRP-induced vasodilation. CGRP elicited vasodilation of the rabbit basilar artery in a dose-dependent fashion when the artery was precontracted by 10(-5) M 5-hydroxytryptamine, whereas almost no relaxation occurred in the rabbit common carotid artery. The relaxation of the basilar artery was 64.

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The time course of the blood-arterial wall barrier disruption following experimental subarachnoid haemorrhage (SAH) was studied in 24 rabbits. Animals with SAH received two successive blood injections through the cisterna magna. Horseradish peroxidase (HRP) was given intravenously 30 minutes before sacrifice to assess the integrity of the barrier.

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An important role of endothelium-dependent relaxation in the local regulation of vascular tone has been suggested. In the present study, the effect of hypoxia on endothelium-dependent relaxation was investigated in canine and rabbit basilar and in rabbit common carotid arteries in vitro, using an isometric tension recording method. Hypoxia was introduced by changing the gas mixture in the in vitro chamber from 95% O2-5% CO2 to 95% N2-5% CO2.

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Disruption of the blood-arterial wall barrier in the major cerebral arteries occurs following subarachnoid haemorrhage (SAH) and may be related to the pathogenesis of cerebral vasospasm. Using FITC dextrans of various sizes, the present study was undertaken to determine if the barrier disruption shortly after SAH occurs equally to various sized tracers. Forty-two Sprague-Dawley rats were divided into 5 groups.

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To determine whether extraluminal or intraluminal hemoglobin inhibits endothelium-dependent relaxation, we measured the vascular responsiveness of rabbit basilar artery in an in vitro perfusion system and we performed immunohistochemical staining for hemoglobin. In the in vitro study, we applied agents from either the intraluminal or the extraluminal side of excised basilar arteries. KCl-induced contraction was the same with either application.

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Immunohistochemical staining for prostaglandin F2-alpha (PG F2 alpha) was conducted to identify PG F2 alpha synthesizing or binding sites in anoxic rat brains. Anoxia was produced in 22 rats to lower the arterial oxygen tension (PaO2) to 21 +/- 4 mmHg by ventilation with a 95% nitrogen and 5% carbon dioxide gas mixture. In 8 animals anoxia was continued for 30 sec, and in 14 rats for 3 min.

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Endothelium-dependent relaxation was induced by acetylcholine (ACh), adenosine triphosphate (ATP), and thrombin in isolated cerebral and extracerebral arteries obtained from rabbits and dogs. Using an isometric tension-recording method, the authors then examined the difference in the extent of relaxation between the cerebral and extracerebral arteries. In rabbits, the dose-response curve of the basilar artery for ACh was significantly different (p less than 0.

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We evaluated the results of intracranial operation in 150 consecutive patients surgically treated within seven calendar days of aneurysmal subarachnoid hemorrhage (SAH). Patients in all clinical grades, except those who were moribund, were treated. Those with either anterior or posterior circulation aneurysms were included.

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Vascular contractions in response to KCl and serotonin (5-hydroxytryptamine, 5-HT) in rabbit basilar artery were studied in vitro using an isometric tension-measurement technique. Hemoglobin (10(-5)M) markedly augmented contractions induced by 5-HT (10(-9) to 10(-6)M) and slightly augmented those induced by KCl (20 to 80 mM) in arteries with intact endothelium. On the other hand, the augmentation induced by hemoglobin was almost abolished in arteries that were chemically denuded of endothelial cells by pretreatment with saponin.

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We evaluated the effects of aging and hypertension on endothelium-dependent relaxation of rat common carotid arteries using 14-week-old (young) and 11-month-old (old) Wistar-Kyoto rats (WKY) and age-matched spontaneously hypertensive rats (SHR). Isometric tension of common carotid artery ring segments was measured. With a resting tension of 2.

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The effect of subarachnoid hemorrhage on metabolic rates in rabbit cerebral arteries was investigated by measuring adenosine triphosphate (ATP) content and L-lactate release. The mean +/- SEM ATP content was 0.38 +/- 0.

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The effect of endothelium removal on the contractile responses to KCl, hemoglobin, serotonin (5-HT), norepinephrine (NE), prostaglandin (PG)F2 alpha, PGD2, and PGE2 was investigated in canine and rabbit basilar arteries by an isometric tension-recording method. In canine basilar arteries, endothelium removal elevated the dose-response curves to 5-HT, PGF2 alpha, and PGD2, and PGE2, but not to KCl, hemoglobin, or NE. In rabbit basilar arteries, on the other hand, removal of the endothelium elevated the dose-response curves to 5-HT, NE, PGF2 alpha, and PGD2, but not to KCl or hemoglobin.

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Thromboxane, a highly vasoactive substance, is found in the cerebrospinal fluid of patients and experimental animals following subarachnoid haemorrhage. A stable synthetic analogue of thromboxane A2 was administered intracisternally in rabbits. This resulted in an increase in endothelial permeability of the major cerebral arteries to Evans Blue dye and horseradish peroxidase.

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Anticoagulation with heparin is frequently recommended for patients with progressing ischemic cerebral infarction, yet little data is available detailing the acute results of treatment with this agent. We report the results of continuous intravenous heparin treatment in 36 consecutive patients admitted with progressing ischemic infarction, all of whom had computed tomography scans to exclude the diagnosis of hemorrhage prior to treatment. Overall, 18 of 36 (50%) had continued neurologic worsening despite treatment.

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The changes in prostaglandin F2-alpha (PG F2 alpha) staining over 3 days of recirculation in both fore- and hindbrains were studied. Five minutes of global ischemia was produced in 24 rats by Pulsinelli's method with hypotension around 50 mm Hg of mean arterial blood pressure. Eight rats (including three pretreated with indomethacin) were recirculated for 5 min, three for 1 h, five for 2 h and five for 3 days.

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We evaluated 95 hospitalized patients (50 women and 45 men) aged 15 to 45 who had nontraumatic subarachnoid hemorrhage (SAH). Aneurysmal SAH was identified in 75 patients. Other causes for SAH were ruptured arteriovenous malformations (2 cases), amphetamine arteritis (1 case), and leptomeningeal melanoma (1 case).

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Carotid endarterectomy in rats. Technical note. Carotid endarterectomy is a widely used surgical procedure for stroke-threatened patients.

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