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

Prostaglandin E2, thromboxane B2, and 6-oxo-prostaglandin F1 alpha were assayed in blood and cerebrospinal fluid samples from patients after subarachnoid hemorrhage (SAH) and from a control population. The levels found in samples obtained from patients after SAH were compared with those found in controls and were also correlated with a number of clinical and radiological variables, many of which are either significantly associated with or represent evidence of cerebral ischemia. The levels of prostaglandin E2, thromboxane B2, and 6-oxo-prostaglandin F1 alpha in blood samples from patients after SAH and from controls were below the level of sensitivity of the assays. Levels of prostaglandin E2, thromboxane B2, and 6-oxo-prostaglandin F1 alpha in cerebrospinal fluid from patients after SAH were significantly elevated when compared with those found in control samples. There was no significant correlation, however, between the level of each prostaglandin measured and the following variables: clinical grade on admission as assessed by the Glasgow Coma Score and the World Federation of Neurological Surgeons grading system; the amount of subarachnoid blood seen on computed tomographic scan; the occurrence of ischemic deterioration; the occurrence of low density change on computed tomographic scan; the presence of vasospasm on angiography; clinical outcome as assessed by the Glasgow Coma Score 3 months after the ictus; and the incidence of ischemia as a cause of death or disability as assessed 3 months after the ictus. A primary role for prostaglandins in the etiology of delayed cerebral ischemia after SAH is not therefore confirmed.
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PMID:Role of prostaglandins in delayed cerebral ischemia after subarachnoid hemorrhage. 843 77

Cerebral blood flow (CBF) and central conduction time (CCT) were recorded from 58 subarachnoid hemorrhage patients and from 49 age-matched controls. CBF was calculated following Xenon inhalation and CCT was determined from somatosensory evoked potentials (SSEP's) following median nerve stimulation. Each patient had a CT scan on the day of admission which was graded from I-IV. CBF, CCT and neurological grade (Hunt and Hess classification) were concomitantly recorded 1, 4, 7 and 14 days after subarachnoid hemorrhage. Mean CBF was highest in patients with neurological grades I and II (48.6 +/- 12.3 and 48.1 +/- 10.3 ml/100gm/min respectively) and lowest in patients with neurological grade IV (37.3 +/- 9.6 ml/100gm/min). Patients in neurological grade I or II had mean CBF and CCT measurements that were significantly different from those obtained from patients in neurological grade IV (P less than 0.05). Neurological grade and CT scan grade correlated with CBF (P less than 0.0001) better than CCT (P = 0.015). Unexpectedly low CBF's from patients in neurological grades II and III (less than 37 and less than 31 ml/100gm/min respectively) failed to significantly prolong CCT suggesting CCT is unable to detect marginal ischemia. A significant correlation between CBF and CCT occurred only when CBF was less than 30 ml/100gm/min (R = 0.75, P = 0.05). It appears that prolonged CCT is associated with a drop in CBF only when CBF drops below a certain threshold.
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PMID:Correlation between cerebral blood flow, somatosensory evoked potentials, CT scan grade and neurological grade in patients with subarachnoid hemorrhage. 178 9

A review of a series of 56 patients with a giant intracranial aneurysm showed that 28 presented with signs related to the mass effect and 19 with subarachnoid hemorrhage (SAH). Additional clinical signs observed were seizures, ischemia, and endocrinological disturbances. Fourty-five aneurysms involved the carotid artery territory and eleven the vertebrobasilar system. On computed tomography (CT) images partially thrombosed aneurysms (23 cases) showed 1) a marginal or central "target" appearance on contrast enhanced scans corresponding to the non-thrombosed lumen as demonstrated by angiography, 2) capsular enhancement in 16 cases and 3) calcifications in 9. SAH occurred in 13 and 6 cases of non-thrombosed and partially thrombosed aneurysms, respectively. Magnetic resonance imaging (MRI) in 6 cases showed several layers of thrombosis in 4 cases and a small signal void close to the parent artery. In one case of a non-thrombosed aneurysm, thrombosis was mimicked by flow artifacts of MRI.
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PMID:Clinico-radiological spectrum of giant intracranial aneurysms. 179 40

Previous studies of cerebral oxygen metabolism and extraction in patients with subarachnoid hemorrhage (SAH) have yielded conflicting results. We used positron emission tomography (PET) to measure the regional cerebral metabolic rate for oxygen (rCMRO2), oxygen extraction fraction (rOEF), and cerebral blood flow (rCBF) 16 times in 11 patients with aneurysmal SAH. All studies were performed preoperatively; no patient had hydrocephalus or intracerebral hematoma on brain CT. Eight patients with no arteriographic vasospasm who were studied on days 1-4 post-SAH had a significant 25% reduction in global CMRO2 compared to age-matched controls, and no significant change in global OEF, suggesting a primary reduction in CMRO2 caused by SAH. Four patients studied seven times during arteriographic vasospasm had significantly increased rOEF with unchanged CMRO2 in arterial territories affected by arteriographic vasospasm compared to territories without vasospasm, indicative of cerebral ischemia without infarction. No brain regions studied with PET were infarcted on follow-up CT. We conclude that the initial aneurysm rupture produces a primary reduction in CMRO2, and that subsequent vasospasm causes ischemia.
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PMID:Cerebral oxygen metabolism after aneurysmal subarachnoid hemorrhage. 187 16

A spontaneous dissecting aneurysm of the basilar artery is a rare disorder, usually presenting with ischemia rather than a subarachnoid hemorrhage (SAH). Two cases are described of a dissecting aneurysm of the basilar artery presenting with an SAH. Vertebral angiography revealed a double lumen to the basilar artery. Magnetic resonance (MR) imaging detected the intramural hematoma. One patient was treated conservatively, and the other underwent operative intervention with wrapping of the aneurysm. The usefulness of MR imaging in the diagnosis and the treatment options are discussed.
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PMID:Spontaneous dissecting aneurysms of the basilar artery presenting with a subarachnoid hemorrhage. Report of two cases. 188 81

The efficacy and possible side effects of thromboxane A2 (TXA2) synthetase inhibitor in the treatment of cerebral vasospasm after subarachnoid hemorrhage (SAH) were assessed for 24 patients who presented with grades I to IV of the Hunt and Hess classification. All patients underwent aneurysmal clipping within 48 hours after SAH. Postoperatively, TXA2 synthetase inhibitor, Cataclot [sodium (E)-3-[p-(1H-imidazol-1-ylmethyl)phenyl]-2-propenoate] was administered to 13 patients by continuous drip infusion at a dose of 1 microgram/kg/min for 8 to 14 days (group A). The remaining 11 patients did not receive this drug (group B). Of the 13 patients in group A, seven patients (54%) showed no symptomatic vasospasm after SAH. Four patients (31%) developed a transient deterioration of consciousness and/or motor disturbance. Three of these patients fully recovered, while one of them showed a mild neurological deficit on discharge. One patient (8%) developed permanent dysphasia and hemiparesis as a result of ischemic brain damage due to vasospasm. One patient (8%) died of the side effect. On the other hand, of the 11 patients in group B, only three (27%) showed no symptomatic vasospasm. One (9%) patient presented a transient neurological deficit but fully recovered upon discharge. Four patients (36%) showed permanent neurological deficits, although they all could lead an independent life after discharge. The three remaining patients developed a severe disturbance of consciousness caused by ischemia due to vasospasm, and two of them died within 1 month after the onset of SAH. In the group treated with Cataclot, two patients developed an epidural hematoma late during the administration of the drug. Of these two, one patient died of increased intracranial pressure that was accelerated by the complication. These results indicate that TXA2 synthetase inhibitor is effective in not only decreasing the occurrence of symptomatic vasospasm but also reducing the neurological deterioration due to vasospasm after SAH. However, this drug has a hazardous side effect in that it may promote a tendency to bleed, which caused death in one of our patients.
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PMID:Efficacy and toxicity of thromboxane synthetase inhibitor for cerebral vasospasm after subarachnoid hemorrhage. 189 55

The efficacy of nimodipine in decreasing mortality and morbidity of subarachnoid haemorrhage (HSA) is evaluated in 51 patients admitted to the Neurological and Neurosurgery Departments of the Santa Maria Hospital. Reductions of 2 x (0.65, 6.39) of the incidence of ischemia in the total group and of 2.1 x (0.58, 7.79) of mortality in the sub-group with initial severity of less than 4 points of the Hunt score were observed relatively to a comparable group of patients previously admitted who did not receive nimodipine. Randomized clinical trials that tested the effect of nimodipine in the context of HSA are reviewed.
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PMID:[Nimodipine in subarachnoid hemorrhage]. 195 Jun 63

Among 238 consecutive patients admitted early with ruptured cerebral aneurysms, surgical repair within 48-72 hours was feasible in 200 cases. Unfavorable outcomes among the latter 200 patients are analyzed and discussed in this paper. Preoperatively, 148 patients were in Hunt and Hess grades I-III, 33 were in grade IV, and 19 in grade V. After clipping of the aneurysm, all patients received a regimen of topical intracisternal and intravenous/peroral medication with the calcium antagonist nimodipine. The overall rate of unfavorable outcomes was 25%, ie, outcome with moderate or severe deficit or lethal outcome. The reasons for unfavorable outcomes among these 49 patients were the devastating effect of the bleed (severe subarachnoid hemorrhage or additional intracerebral hemorrhage) in 31 patients (15% of the 200 patients), a surgical complication in 11 (5.5%), preoperative rebleeding in three (1.5%), delayed ischemia from vasospasm in one (0.5%), and various others in three further patients (1.5%). Unfavorable outcome occurred in 11% of patients with preoperative grades I-III, in 52% of patients with grade IV, and in 16 of 19 patients with grade V. Among the 141 patients with subarachnoid hemorrhage but not intracerebral or intraventricular hematoma, 16 made an unfavorable outcome, ie, 11% versus 56% among patients with intracerebral hematoma/intraventricular hematoma on preoperative computed tomography scan. The present data seem to speak in favor of early surgery. Since half of the patients with intracerebral hematoma and poor outcome had suffered previous warning leaks, it appears to be a continuing challenge to diagnose warning leaks before a massive hemorrhage occurs.
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PMID:Unfavorable outcome following early surgical repair of ruptured cerebral aneurysms--a critical review of 238 patients. 199 Apr 84

Adenosine diphosphate-induced platelet aggregation and associated thromboxane B2 release were studied in 52 patients with subarachnoid hemorrhage (SAH) in order to detect a possible association between altered platelet function and development of cerebral ischemic complications after SAH. Compared to the values on admission, the patients showed significantly increased platelet aggregability (p less than 0.05) and thromboxane release (p less than 0.001) 1 to 2 weeks after SAH. The highest values of thromboxane release were seen in patients who deteriorated due to delayed cerebral ischemia with a permanent neurological deficit. Thromboxane release was significantly higher (p less than 0.05) before the onset of severe delayed ischemia in six patients with preoperative ischemia compared to the patients without delayed ischemia. In five others, both ischemic deterioration and elevated thromboxane release occurred after operation. These patients had preoperative values similar to the values in those without ischemic symptoms. The observations suggest that increased platelet aggregability and thromboxane release are associated with delayed cerebral ischemia both before and after surgery.
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PMID:Platelet thromboxane release and delayed cerebral ischemia in patients with subarachnoid hemorrhage. 199 3

Leukotrienes and prostaglandins are formed from arachidonic acid by activation of local phospholipases in pathological conditions such as cerebral ischemia, subarachnoid hemorrhage, cerebral tumors and seizures. These mediators, especially leukotrienes have a very potent vasoconstrictor effect on cerebral arteries. Experimental studies have shown that this effect, by increasing vascular permeability causes vasogenic edema that contributes to the ischemic penumbra. In this study, after developing an experimental animal model simulating the concept of ischemic penumbra in the rat, the levels of leukotriene C and prostaglandin E2 produced in the forebrain were measured and the effects of these mediators in prolonged ischemia were investigated. The results, in the first 4 min of ischemia, showed that the arachidonic acid metabolites, particularly, leukotriene C4, reached a peak in the ischemic cerebral tissue in association with leukocyte accumulation. Later in the 15th min, significant decreases in leukotriene C4 and prostaglandin E2 levels were seen. In the 1st and 4th h, probably due to the stimulation of the relevant enzymes by free oxygen radicals in the ischemic tissue; the levels increase again, returning to control values by the 12th h. It is concluded that the use of lipoxygenase inhibitors and free radical scavengers may be helpful to limit the infarct area in the first 4 h of ischemia.
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PMID:The alterations of leukotriene C4 and prostaglandin E2 levels following different ischemic periods in rat brain tissue. 201 13


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