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)

Forty-two nonhypertensive patients with a proven subarachnoid hemorrhage but normal cerebral panangiography were in vestigated. The follow-up period was 1 to 5 years, with a mean of 39.1 months. Treatment consisted of 2 weeks of bedrest and sedation, followed by progressive mobilization on the 3rd week. Thirteen patients (Group A) were treated with tranexamic acid, whereas 29 patients (Group B) received no antifibrinolytic therapy. Five patients Of Group A died of ischemia caused by cerebral vasospasm. No patient of Group B died, and there was no early rebleeding in either group. Therefore, antifibrinolytic therapy is not indicated in these patients. Only 1 of 42 patients (2.4%) experienced late rebleeding, and he again had normal cerebral panangiography. Reangiography several weeks or months after the first hemorrhage seems not to be indicated. The overall prognosis of the surviving patients was good; almost all were able to return to their previous occupations within 6 months after the hemorrhage.
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PMID:Subarachnoid hemorrhage with normal cerebral panangiography. 663 33

There have been several case reports in which various hypertension-inducing regimens have been used in the treatment of postoperative cerebral vasospasm. Regimens have included the used of metaraminal bitarate, norepinephrine with intravascular volume expansion, and high-dose dopamine with mannitol and volume expansion. Clinical response has been very favorable. Our patient improved markedly after administration of dopamine and intravascular volume expansion. Little work has been done to document vasospasm as the cause of the ischemia or to demonstrate increased cerebral blood flow following treatment. We suggest that noninvasive Doppler flow velocity studies may be an ideal tool for the further assessment of these patients.
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PMID:Correction and monitoring of postoperative cerebral vasospasm. 678 9

It was found that Fluosol-DA 20% relieves human acute cerebral ischemia resulting from vasospasm in 62% of the cases. However, several problems were encountered during the investigation. The efficacy of the solution was temporary, that is, within 24 hours. This is considered logical because perfluorochemical particles are eliminated fairly rapidly from the circulating blood. Successive administrations should be necessary until cerebral vasospasm is remitted. Another problem is that it is not clear whether the doses of the solution given in this study (10 ml/kg/day) are sufficient or not, since the depth of the cerebral ischemia is considered to vary depending on the case. It might be necessary to change the volume of the solution given in accordance with the depth of the ischemia of each patient.
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PMID:New treatment of cerebral vasospasm with Fluosol-DA 20%: protective effect on cerebral ischemia and change of cerebral blood flow (CBF). 687 74

Spinal cord stimulation (SCS) has been increasingly used in the treatment of ischemia caused by obliterative diseases in the extremities and in the cardiac circulation. The most promising effects have been obtained when physicians suspect that a major vasospastic component underlies the ischemic symptoms (e.g., as in Raynaud's disease). Despite the clinical success of this treatment method, little is known about the mechanisms underlying the pain relief it produces and its anti-ischemic effects. Most earlier experimental studies have used normal animals or animals with cerebral vasospasm induced by injection of autologal blood into the cerebrospinal fluid space. In the present study, we applied SCS in a rat model via implanted electrodes to study the effect of preemptive stimulation on the ischemia caused by vasospasm in a neurovascular flap in the groin; the vasospasm was induced by mechanical pressure applied to the feeding artery. In rats treated with SCS, delivered with parameters similar to those used clinically, the percentage of flaps recovering normal microcirculation after the spasm was significantly higher than in the untreated control group (100 and 28%, respectively; P < 0.05), and the maximal blood flow after the ischemic episode was significantly higher in the SCS group than in the control group (127 and 51 arbitrary units, respectively; P < 0.05). The percentage of animals regaining the premanipulation circulation after the provocation of a second spasm was also greater in the SCS-treated group than in the control animals (50 and 14%, respectively; P < 0.05). Pilot studies showed that this protective effect was specific to SCS given before spasm induction, an observation corroborated by clinical experiences.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Preemptive spinal cord stimulation reduces ischemia in an animal model of vasospasm. 747 78

Reduced glutathinone (tau-glutamylcysteinglycine, GSH) is a scavenger for oxygen radicals and plays in important role in protection of cells from ischemia and from the harmful effects of free oxygen radicals. Free oxygen radicals due to cerebral vasospasm increase in both vasospasm and proliferative vasculopathy. This experiment was performed to determine whether GSH plays a role in cerebral vasospasm after subarachnoid hemorrhage by preventing the harmful effects of free oxygen radicals. In this study, GSH was administered intraarterially and intracisternally following vasospasm of the canine basilar artery. Less vasospasm was observed in the group treated with GSH intraarterially following subarachnoid hemorrhage than in the one treated with GSH intracisternally and in the control group. The arterial wall was investigated ultrastructurally. We evaluated the effect of the anti-oxidating substance through the activity of superoxide dismutase in the arterial wall. We compared the effect of glutathione reductase in the two groups treated with GSH intraarterially and intracisternally. Arterial degeneration was more prominent in the group in which GSH was used intracisternally, while the superoxide dismutase levels were low. In contrast, arterial degeneration was less in the other group in which GSH was used intraarterially, while the superoxide dismutase levels were high.
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PMID:Effect of GSH on cerebral vasospasm in dogs. 775 17

To examine the possible role of endothelin and vasospasm in eclamptic seizures, we studied and analyzed the electroencephalograms (EEG) of endothelin-1 (ET-1)-treated pregnant, nonpregnant and sham control (dextrose-treated) rabbits. After multiple intravenous bolus injections of ET-1 (500 pmol/kg) or 5% dextrose in the rabbits, we recorded EEG directly from the brain cortex and analyzed by Fast Fourier Transform (FFT). Water content was measured in the brain of all groups (n = 7). Repeated seizures occurred in all of the pregnant and 2 of the nonpregnant rabbits by variable doses of ET-1. FFT analysis showed remarkable changes in frequency and power arrays characterized by mild to severe form of dysrhythmia, high-voltage spikes, high-voltage fast and slow waves after ET-1 injections. Water content was increased in brain mass in ET-1-treated rabbits (p = 0.001) suggesting an ET-1-induced edema. Histologically we confirmed that ET-1 caused ischemic changes in brain tissues. However, ET-1 induced more pronounced changes in behavior, EEG, brain edema or ischemia in pregnant than in nonpregnant groups. The injections of exogenous ET-1 into the brain substances were strongly suggested by immunohistochemical study with polyclonal antiendothelin antibody in brain tissue sections. Therefore, we assume that endothelin along with other vasoactive substances causes acute cerebral vasospasm and ischemia inducing EEG changes leading to ultimate clinical convulsions in eclampsia.
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PMID:Eclampsia-like seizures and electroencephalographic changes in pregnant rabbits with endothelin-1 injections. 789 Feb 45

Many patients survive SAH with minimal neurologic deficits but are at risk for developing further neurologic insult from ischemia resulting from cerebral vasospasm. Nursing care of the patient experiencing vasospasm is challenging. The nurse who is knowledgeable about the signs and symptoms of cerebral ischemia and necessity for continually reviewing the patient's neurologic status can initiate prompt treatment to prevent further ischemic damage. Recognition of this critical problem is the first step toward combating its ominous effects.
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PMID:Cerebral vasospasm: early detection and intervention. 805 86

Endothelin-1, a peptide exhibiting extremely potent cerebral vasoactive properties, is elevated in the cerebrospinal fluid after hemorrhagic stroke and implicated in cerebral vasospasm. The purpose of this study was to determine changes in endothelin in ischemic rat brain by assaying endothelin tissue and extracellular levels. Immunoreactive endothelin levels in ischemic brain tissue following permanent or transient focal ischemia produced by middle cerebral artery occlusion was determined. In addition, endothelin levels were assayed in striatal extracellular fluid collected by microdialysis before, during, and after global ischemia produced by two-vessel occlusion combined with hypotension. Twenty-four hours after the onset of permanent middle cerebral artery occlusion, the ischemic cortex level (0.58 +/- 0.27 fmol/mg protein) of immunoreactive endothelin was significantly (p < 0.05) increased, by 100%, over that in the nonischemic cortex (0.29 +/- 0.13 fmol/mg protein). Transient artery occlusion for 80 min with reperfusion for 24 h also resulted in a similar significant (p < 0.05) increase, 78%, in immunoreactive endothelin in the ischemic zone. Global forebrain ischemia significantly (p < 0.05) increased the level of immunoreactive endothelin collected in striatal microdialysis perfusate, from a basal level of 14.6 +/- 6.7 to 26.5 +/- 7.7 and 26.2 +/- 7.4 amol/microliters (i.e. 82 and 79%). These changes reflect the relative picomolar extracellular concentration increases during ischemia and following reperfusion, respectively. This is the first demonstration of elevated levels of endothelin in focal ischemic tissue and in the extracellular fluid in global ischemia and suggests a role of the peptide in ischemic and postischemic derangements of cerebral vascular function and tissue injury.
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PMID:Endothelin levels increase in rat focal and global ischemia. 811 29

Dose-response effects of acute ethanol infusions were studied, noninvasively, in the unopened brain to examine the hypothesis that ethanol can induce stroke-like events as a consequence of cerebral vasospasm and tissue ischemia. By using a single sending and receiving fiber, an optical backscatter measurement (500-800 nm) was used to monitor the levels of deoxyhemoglobin (DH), reduced cytochrome oxidase (rCO), and relative tissue blood content in a closed cranium preparation. Anesthetized rats were prepared by cannulating a branch of the internal carotid artery and subjected to either bolus infusions (1.25 or 2.5 microM ethanol in Ringers/g tissue) or to constant infusions of 5 or 10% ethanol at various rates (0.30-2.92 microM/g/min). To facilitate optical penetration, a portion of the left parietal cranium was shaved to a translucent appearance. Results showed that low, bolus doses of ethanol typically produced a slight increase (5-10%) in the oxyhemoglobin signal, indicating that vasodilation had probably occurred. Higher doses, however, produced a prompt and significant reduction in the hemoglobin signal, increased levels of DH, and a rise in rCO suggesting a vasoconstrictor response leading to ischemia had occurred, followed by recovery within 3-5 min. Constant infusions of ethanol produced a similar cerebral vascular response, in a dose-related manner, but of a more sustained nature. At levels of 50-60% of the maximum bolus dose, the effect was more pronounced, accompanied by an increase in the levels of rCO (by 50-90%). Control experiments using identical volumes/flow rates of Ringers solution produced no significant alterations in the optical spectrum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Optical spectroscopy and cerebral vascular effects of alcohol in the intact brain: effects on tissue deoxyhemoglobin, blood content, and reduced cytochrome oxidase. 811 49

The effect of high dose nicardipine on delayed cerebral vasospasm was studied in 33 patients with aneurysmal subarachnoid hemorrhage (SAH). Intravenous infusion of nicardipine started before or immediately after early operation. The dosage was from 4 to 10 mg/h with an average of 7.4 mg/h. The duration was from 2 to 17 days with an average of 12.3 days. Symptomatic vasospasm was observed in only one (3%) out of 33 patients. The remaining 32 patients (97%) showed neither ischemic symptoms nor low-density areas on computed tomography. Severe angiographical vasospasm was diagnosed in 3 patients, who entered hospital on day 3 to 5 after initial attacks. They were operated upon on day 4 to 6 under the administration of nicardipine before or immediately after the operation. No patients showed symptomatic vasospasm and angiographical vasospasm was improved markedly. The present study demonstrated that high dose nicardipine appeared to prevent both brain ischemia and angiographical vasospasm after aneurysmal SAH.
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PMID:[High dose nicardipine therapy for delayed cerebral vasospasm after aneurysmal subarachnoid hemorrhage]. 825 88


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