Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental subarachnoid hemorrhage was produced in chloralose-anesthetized cats by slow injection of 0.5 ml/kg autologous arterial blood into the cisterna magna. As a result, there was an initial (within 5 min) 25.1% decrease in caudate nuclear blood flow as measured by hydrogen clearance. Between 5 min and 3 h postinjection, there was a further and progressive 25.9% decline in caudate blood flow. The hemorrhage also caused a slow increase in intracranial pressure, a decrease in cerebral perfusion pressure, and an increase in caudate vascular resistance. In contrast, the administration of a single 30 mg/kg i.v. dose of methylprednisolone sodium succinate 30 min after the acute hemorrhage resulted in stabilization of caudate blood flow and vascular resistance and some restoration of those parameters toward prehemorrhage values. This effect was not correlated with a decrease in intracranial pressure or an increase in cerebral perfusion pressure. A 15 mg/kg i.v. dose of the drug had only a slight effect on caudate blood flow. A 60 mg/kg i.v. dose, while initially supportive, lost its effect during the later stages of the experiment, indicating a sharp biphasic dose-response relationship for the effect of methylprednisolone on caudate blood flow after subarachnoid hemorrhage. However, of the three doses, only 60 mg/kg significantly decreased the slow posthemorrhage rise in intracranial pressure. The beneficial effect of the 30 mg/kg i.v. dose of the drug on caudate blood flow, separate from an effect on the slow rise in intracranial pressure, suggests that the steroid support of caudate perfusion is due to a direct protective effect of the drug on the microvasculature. Based on previous studies showing an identical dose-response pattern for the ability of methylprednisolone to prevent posttraumatic lipid peroxidation of central nervous system tissue and progressive ischemia development, the possibility of the drug's inhibition of hemorrhage-initiated vasoconstrictor prostanoid action and microvascular lipid peroxidation is proposed.
 ...
PMID:Attenuation of progressive brain hypoperfusion following experimental subarachnoid hemorrhage by large intravenous doses of methylprednisolone. 334 42

Clinical studies have demonstrated elevated levels of both arachidonic acid and prostaglandins in the cerebrospinal fluid of humans after ischemic stroke and subarachnoid hemorrhage. Such increases in free fatty acid, arachidonic acid, and prostaglandin concentrations suggest excessive production and accumulation of these substances in the ischemic brain. We used a rabbit model of ischemic infarction to examine the relation between controlled central nervous system ischemia and cerebrospinal fluid prostaglandin levels. We found that following stroke PGF2 alpha and not PGD2 was the predominant prostaglandin present in the cerebrospinal fluid. PGF2 alpha also underwent the largest percent increase over control prostaglandin concentrations. This is similar to human and dog cerebrospinal fluid studies, which demonstrate PGF2 alpha as the predominant prostaglandin following ischemic injury. The lack of PGD2 elevation under ischemic conditions may suggest that the rabbit model is more like stroke in humans than the rat or gerbil models. Our preliminary work demonstrates that it is practical to study postischemic prostaglandin changes in cerebrospinal fluid rather than in brain tissue in a rabbit model of central nervous system ischemia.
 ...
PMID:Prostaglandin concentrations in cerebrospinal fluid of rabbits under normal and ischemic conditions. 335 21

Sixty cases with ruptured intracranial aneurysms over 65 years of age were classified as aged group and were compared with 81 cases (control group) between 50 and 59 years of age. The results obtained are as followed: 1. Aneurysms in aged group occur frequently in female (83%) and in internal carotid artery (42%). 2. Cases with "Excellent" operative result in aged group was found significantly lower in ratio (34%) than in control group (59%), which seems attributable to high incidence of their poor results in the cases with serious conditions (Hunt and Kosnik Grade III & VI) and in those operated early after episode of hemorrhage. 3. Symptomatic vasospasm and primary brain damage due to subarachnoid hemorrhage occurred frequently in aged group (22% and 8%, respectively), and are proved to be two major causes of their unfortunate outcome. 4. In aged group difficulty in full enforcement due to cardiovascular complications was considered to make hypervolemia-hypertension therapy less effective to prevent and improve ischemia symptoms due to vasospasm. Accordingly, one has to choose such other means as meticulous and almost complete removal of subarachnoid hematoma in early operation or by some drainage systems. 5. Although the primary brain damage occurred in similar frequency in both aged and control groups, its recovery was significantly lower in aged group than in the control. Under the sustaining conditions of the primary brain damage, one should take care of latently progressing intracranial pathology such as vasospasm.
 ...
PMID:[Clinical analysis of 60 aged patients with ruptured intracranial aneurysms]. 336 95

Knowledge of the local incidence of aneurysm rupture permits the conclusion that almost every patient in the population of 933,800 persons served by the authors' institution who was stricken by this catastrophe and survived long enough to be transported was treated at this center (121 patients during 34 months). Of these, 9.1% were admitted late (greater than 72 hours after subarachnoid hemorrhage (SAH]; of the remaining cases, 94.5% were seen within 24 hours and 50% within 6 hours post-SAH. Of the 121 patients, 10% were neurologically devastated on arrival, a late operation was planned for 19%, and the earliest possible surgery and nimodipine administration was selected for 71%. In this latter group, 50% of the operations were begun within 24 hours and 76% within 48 hours post-SAH. Sixty percent of all mortality and morbidity could be linked to the initial aneurysm bleed. The remaining 40% could be ascribed to potentially avoidable causes of unfavorable outcome. No less than 9.6% of all patients admitted within 24 hours after SAH suffered from "ultra-early" rebleeding during transportation or preparation for operation. The mortality rate from such rebleeding was 7.4%, compared with the 9.1% combined mortality rate from complications and late ischemia.
 ...
PMID:Significance of "ultra-early" rebleeding in subarachnoid hemorrhage. 337 85

In 39 patients with a proven subarachnoid hemorrhage (SAH), the clinical status, the amount of subarachnoid blood on a computerized tomography scan obtained within 5 days after SAH, and the flow velocities (FV's) in both middle cerebral arteries (MCA's) measured by transcranial Doppler sonography were recorded daily and correlated. All patients had pathological FV's over 80 cm/sec between Day 4 and Day 10 after SAH. The side of the ruptured aneurysm showed higher FV's than did the unaffected side in cases of laterally localized aneurysms. Increase in FV preceded clinical manifestation of ischemia. A step early increase of FV's portended severe ischemia and impending infarction. Maximum FV's in the range of 120 to 140 cm/sec were not critical and in no case led to brain infarction. Maximum FV's over 200 cm/sec were associated with a tendency for ischemia, but the patients may remain clinically asymptomatic. In cases of no or only a little blood in the basal cisterns, mean FV's in both MCA's increased only moderately whereas, with thick clots of subarachnoid blood, there was a steeper and higher increase of mean FV's.
 ...
PMID:Cerebral vasospasm evaluated by transcranial ultrasound correlated with clinical grade and CT-visualized subarachnoid hemorrhage. 351 99

Based on accumulating evidence of the role of xanthine oxidase (XO) in generating oxygen free radicals and causing tissue damage during ischemia, we examined the possible role of XO in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH). After inducing SAH in dogs by two autologous blood injections 2 days apart, chronic vasospasm of the basilar artery was reliably produced. There was a 3.5-fold elevation in uric acid (UA), the product of XO, in the cerebrospinal fluid (CSF) of these animals. Parenteral administration of allopurinol (i.v., 25 mg/kg, every 6 hours), a specific blocker of XO, successfully abolished the elevation in CSF uric acid levels due to SAH. However, angiographic vasospasm measured on Day 7, morphological changes observed by electron microscope, and elevated CSF prostaglandin levels were not altered by the treatment. It can be concluded that the observed activation of the enzyme XO, which is a well-known source of oxygen free radicals in ischemia in various organs, is not playing a major role in the pathogenesis of chronic cerebral vasospasm in this animal.
 ...
PMID:Production of uric acid in cerebrospinal fluid after subarachnoid hemorrhage in dogs: investigation of the possible role of xanthine oxidase in chronic vasospasm. 361 2

Cerebral ischemia from vasospasm is a major cause of death and disability following aneurysmal subarachnoid hemorrhage (SAH). This study examines and compares the relative utility of the initial neurologic examination and early CT in predicting cerebral ischemia after SAH. The influence of antifibrinolytic drugs (AFD) in the development of cerebral ischemia was also studied. AFD increased the risk of cerebral ischemia regardless of the admitting neurologic condition or the findings of CT. Among patients given AFD, impaired orientation or alertness was associated with a higher risk of ischemia. Other neurologic signs were not predictive of ischemia. Clinical features were not predictive of ischemia among patients not given AFD. Focal, thick collections of blood on CT were highly predictive of ischemia, whether or not patients received AFD. Admitting CT is the best prognostic indicator for the development of cerebral ischemia after SAH. It should be used to supplement the clinical examination in selecting patients best suited for therapy to prevent vasospasm.
 ...
PMID:Predicting cerebral ischemia after aneurysmal subarachnoid hemorrhage: influences of clinical condition, CT results, and antifibrinolytic therapy. A report of the Cooperative Aneurysm Study. 365 61

We describe total management results in a prospective series of 264 patients with aneurysmal subarachnoid hemorrhage (SAH) admitted to a neurologic unit. Referrals were actively solicited from general physicians as well as neurologists in the area. The diagnosis was based on computed tomography (CT). Secondary deteriorations were analyzed clinically and with serial CT scanning. Outcome was assessed 3 months after SAH. There were no relevant differences between the analyses of patients with and without an aneurysm confirmed by angiography or autopsy. One third of the patients either died within 1 day (12%) or remained in a poor clinical condition that precluded surgery (22%). One third were in good clinical condition, but contraindications to surgery were judged present or serious complications occurred before surgery could be performed. One third of all patients underwent surgery. Overall mortality in our series was 52%; only 26% made a good recovery. The risk of rebleeding was not related to the patients' initial clinical condition, but all other intracranial complications occurred significantly more often in patients graded poor compared with patients in good clinical condition. The most important causes of death and severe disability were hemorrhage (16%), recurrent hemorrhage (18%), and delayed cerebral ischemia (15%). The most important surgical complication was delayed deterioration caused by ischemia (20% of operated patients). We estimated that recognition of 'warning leaks,' surgery in patients over 65, and improvement of our surgical technique could decrease mortality from 52% to approximately 41%.
 ...
PMID:Aneurysmal subarachnoid hemorrhage. Complications and outcome in a hospital population. 368 78

The risk of carotid endarterectomy in acute cerebral ischemic situations is well documented. By using the superficial temporal or occipital artery, it is possible to provide relatively low flow revascularization conduits, potentially avoiding the risk of postoperative hemorrhage. Eighteen patients at The University of Texas Health Science Center at Dallas, Texas, have been treated recently with extracranial to intracranial bypass in the setting of acute neurological deficit, stroke in evolution, or recent completed infarction. Angiographic causes of these deficits included cervical carotid occlusion in 5 patients, carotid siphon disease in 2 patients, middle cerebral stenosis or occlusion in 3 patients, and delayed cerebral ischemia following subarachnoid hemorrhage in 8 patients. Neurological improvement was demonstrated within 24 hours following revascularization in 15 cases (83%); 3 patients were unchanged following bypass, and no patient's condition was worsened. The only case of postoperative intracerebral hemorrhage occurred 1 week following a long saphenous vein graft from the subclavian to the middle cerebral artery. After an average follow-up of 19 months, 7 patients are neurologically normal, 8 patients have mild to moderate deficits, and 3 patients have died. Low flow revascularization procedures appear to be safe in the setting of acute cerebral ischemia and may in selected patients boost regional cerebral blood flow from levels of symptomatic ischemia into a range compatible with normal neuronal function.
 ...
PMID:Potential roles for early revascularization in patients with acute cerebral ischemia. 370 87

A 60-year-old man with vertebrobasilar ischemia unrelieved by anticoagulation was found to have a midbasilar stenosis with an inadequate basilar collateral circulation. He underwent a right superficial temporal-superior cerebellar artery bypass. Following this operation he had a subarachnoid hemorrhage and right third nerve palsy that was due to formation of a pseudoaneurysm at the site of the anastomosis. This aneurysm was managed by ligation of the right superficial temporal artery. Subsequently it became necessary to perform a left superficial temporal artery-superior cerebellar artery bypass because of severe posterior circulation ischemic symptoms.
 ...
PMID:Pseudoaneurysm complicating superficial temporal artery-superior cerebellar artery bypass. 373 23


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>