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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental cerebral vasospasm was induced in the canine basilar artery by an intracisternal injection of fresh autogenous arterial blood. Delayed vasospasm was defined as a reduction to less than 75% of the caliber of control basilar artery 5 days after the intracisternal blood injection. A selective inhibitor of thromboxane A2 synthetase, sodium(E)-3-[4-(3-pyridylmethyl) phenyl]-2-methyl-2-propenoate, was infused intravenously for 1 or 2 hrs at 50 micrograms/kg/min in normal animals exhibiting vasospasm. Angiographic evidence of cerebral vasospasm was not reversed. Mean regional cerebral blood flow was not significantly increased in normal and vasospastic animals, but a mean difference of regional cerebral blood flow was significantly increased only in vasospastic animals. Mean arterial blood pressure and pulse rate were not seriously changed in normal and spastic animals. Another selective thromboxane A2 synthetase inhibitor, (E)-3-[4-(1-imidazolylmethyl)phenyl]-2-propenoic acid hydrochloride monohydrate, showed a similar effect on the caliber of the basilar artery, regional cerebral blood flow, blood pressure, and pulse rate, in vasospastic animals. Venous blood was taken from the internal jugular vein, and the mean platelet aggregation induced by 10 micrograms/ml of collagen was inhibited by the infusion of either selective inhibitor at 50 micrograms/kg/min for 2 hrs. However, mean platelet aggregation rates in vasospastic animals before and after treatment with either selective inhibitor were not significantly different to those in normal animals.
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PMID:Effect of selective inhibitor of thromboxane A2 synthetase on experimental cerebral vasospasm. 653 55

Published studies have seldom examined the in vivo effect of calcium channel blockers on the contractile response of cerebral vessels to receptor mediated constrictors, and have had little success in demonstrating any effect of a single systemic dose of the channel blockers in contrast to the effects of continuous infusions. The present study examines the effect of topical norepinephrine, prostaglandin F2 alpha and serotonin on pial arterioles of the mouse, in the presence of locally applied channel blockers and also 15 and 30 minutes after a single i.p. injection of the blockers. Verapamil, nisoldipine and nimodipine were all effective inhibitors of constriction by either route of administration, and in doses having little or no dilating action. The data not only indicate that single systemic doses can effectively alter contractile behavior of cerebral arterioles, but also demonstrate the importance of testing these drugs against receptor mediated constrictors whose effects, alone or in combination, may be important during initiation or maintenance of cerebral vasospasm.
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PMID:Effects of calcium channel blockers on pial vascular responses to receptor mediated constrictors. 658 78

Two cases of pituitary apoplexy complicated by cerebral vasospasm are described. They emphasize the importance of angiography in the investigation of a protracted clinical course after pituitary apoplexy. The pathophysiology of postapoplectic vasospasm is discussed.
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PMID:Pituitary apoplexy and vasospasm. 663 29

Operative findings of degenerative changes in pituitary adenomas are not uncommon; however, clinical apoplexy is rare. We report the case of a 43-year-old man who presents a sudden right hemiplegia with aphasia and right ophthalmoplegia, in relation with an ischemic pituitary apoplexy and cerebral vasospasm. A few cases of arterial obstruction or vasospasm associated with pituitary apoplexy have been reported in the literature. Cerebral arterial spasm has also been observed after pituitary surgery. Inclusion of blood or necrotic material in the subarachnoid space seems not to be the only mechanism of vasospasm. The role of hypothalamic dysfunction is considered.
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PMID:[Ischemic pituitary apoplexy and cerebrovascular accident]. 666 2

Purified human and bovine thrombin produced comparable tonic contractions in isolated canine basilar arteries. The magnitude of the contractions was closely related to the number of thrombin Units studied rather than to the amount of protein added to the isolation bath. Thrombin had a much slower onset of action, but was more potent in generating sustained contractions than either serotonin or prostaglandin F2 alpha. Moreover, in contrast to serotonin and prostaglandin F2 alpha, the contractions caused by thrombin were not terminated by equivalent washing. The thrombin-induced contractions were significantly inhibited by prostacyclin, meclofenamic acid, phenoxybenzamine and glycerol. Prostacyclin was the most potent of these inhibitors. The results suggest that thrombin in a "free" form may cause vasoconstriction, in addition to platelet aggregation, in hemostasis and could contribute to the genesis of cerebral vasospasm associated with subarachnoid hemorrhage.
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PMID:Cerebral arterial contractions induced by human and bovine thrombin. 699 61

Cerebrovascular and cardiac alterations evoked by intravascular volume expansion with whole blood, a popular adjunct in the clinical prevention or therapy of the focal ischemic deficits of cerebral vasospasm and acute stroke, were studied in splenectomized dogs. Clipping of the right distal internal carotid and proximal middle cerebral arteries in eight dogs reduced regional cortical blood flow (rCoBF) by 49% to 58% without altering cardiac output (CO), and produced about 10% hemispheric infarction. Eight dogs underwent similar cerebral arterial occlusion and eight dogs underwent arterial manipulation without clipping. Both latter groups received two autologous whole blood infusions within 2 hours, each equal to 20% of the respective dog's total blood volume. Despite significant CO elevations after the infusions, rCoBF in the middle cerebral arterial territory did not rise. These whole-blood infusions did not significantly alter mean arterial blood pressure, hematocrit, intracranial pressure, or, in dogs with clipped cerebral arteries, the relative size of infarction. These data suggest that nondilutional hypervolemia neither elevates collateral perfusion to ischemic regions of the brain nor reduces infarction. In addition, elevations in CO do not appear to augment blood flow in either ischemic or normal brain.
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PMID:Failure of intravascular volume expansion without hemodilution to elevate cortical blood flow in region of experimental focal ischemia. 705 23

A model for producing chronic cerebral vasospasm in monkeys by injecting autologous blood into the basal cistern is described. Spasm/narrowing was observed by angiography one hour after SAH in 8 out of 10 monkeys and in 5 of these 8, spasm was observed both one and two weeks later. No narrowing of the vessels was observed in the control cases. In monkeys that showed spasm one week after SAH, narrowing of the extracranial vertebral arteries was also observed. Repeated injections of blood at intervals of one and two weeks caused intensification of spasm in the intracranial portion of vertebral arteries and the basilar arteries. It is suggested that cerebral vasospasm following SAH may in part be mediated by a central control mechanism acting through the sympathetic nervous system in that extracranial vessels remote from direct contact with blood showed reactive narrowing.
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PMID:Angiographic study of vasospasm following subarachnoid hemorrhage in monkeys. 710 47

The elastic properties of the basilar artery were studied in control and treated dogs in which 3 ml of blood was injected intracisternally. Vascular specimens were resected transclivally as cylindrical segments and their external diameters were measured in vitro in the pressure range from 0 mm Hg to 250 mm Hg in the active condition of smooth muscle in Krebs-Ringer solution and in the passive condition in saline solution. The development of cerebral vasospasm was confirmed comparing the diameter difference between these two conditions. The experimental data indicated that vasospasm was most prominent on the 7th day after the treatment of blood injection. In the passive condition no significant dimensional change (i.e. radius and wall thickness) was observed between the control and the treated arteries at various pressure levels. These results imply that the luminal narrowing under vasospasm is not attributable to an irreversible organic change in the wall but to the constriction of vascular smooth muscle. The treated arteries are more distensible and have lower elastic moduli than the control arteries, possibly due to a change in the content of their connective tissues. These changes of the passive elastic properties of arterial walls after blood injection might be one of the factors affecting the development of cerebral vasospasm.
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PMID:Experimental cerebral vasospasm arterial wall mechanics and connective tissue composition. 712 91

Fourteen experiments have been completed to develop an improved primate model of chronic cerebral vasospasm. Results show that by placing a 0.4 mm needle through the intracranial internal carotid artery and percutaneously removing it the following day, cerebral vasospasm is regularly present five days later. There has been no mortality. The results of two monkeys followed with serial angiograms suggest that spasm first appears four days following the subarachnoid hemorrhage and lasts at least eleven days. The results of all experiments show that the most affected vessel in each experiment is reduced to 62% of control diameters. Vasospasm involves cerebral arteries both ipsilateral and contralateral to the site of hemorrhage and extends to the most distal vessels which can be measured. Finally, a neurological defect has been regularly demonstrated on the side contralateral to the site of hemorrhage.
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PMID:A primate model of chronic cerebral vasospasm. 712 92

Interventional neuroradiology is a dynamic subspecialty which is rapidly gaining new applications in the treatment of neurological diseases. The most common therapeutic role is still in the treatment of brain AVMs, aneurysms and fistulae in close association with neurosurgical support. Endovascular treatment of aneurysms with thrombogenic coils is a promising technique which can be performed with low morbidity. The goal of complete aneurysm occlusion, including the neck, has not yet been achieved in all cases and the procedure has not been shown to possess clear advantages over surgical clipping. Pre-operative embolization of tumours and spinal lesions are common procedures in some centres. Angioplasty and papaverine infusion for treatment of cerebral vasospasm are being performed in most neurosurgical teaching centres. Although angiographic results are often impressive, corresponding clinical improvement is not always seen, particularly when treatment is delayed. Thrombolysis for treatment of acute stroke and angioplasty for treatment of cerebrovascular atherosclerosis are new techniques which await scientific validation before being accepted as standard therapies.
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PMID:Interventional neuroradiology. 749 22


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