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)

Activity of protein-O-methyltransferase in synaptosomal fractions was obtained. Km values calculated for S-adenosylmethionine as substrate were 1 microM and Vmax = 4.3 pmoles/mg p/min. In the presence of gelatin (exogenous protein acceptor), activity was about 3 times higher. Without gelatin, activity of endogenous protein-O-methyltransferase decreased by about 20% under hypoxic conditions and by about 15% in ischemia. Exogenous activity under both hypoxic and ischemic conditions did not change. These results can possibly be explained by the changes in methyl acceptor proteins. In normal conditions, after inhibition methylcarboxylation by S-adenosyl-L-homocysteine, the decrease of GABA uptake and increase in the uptake of dopamine were observed. Uptake of serotonine and noradrenaline were unchanged.
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PMID:Protein-O-methyltransferase in brain synaptosomal fraction under normal, ischemic and hypoxic conditions. Possible role in neuronal function. 614 61

To investigate the relationship between flow and energy metabolism during coronary underperfusion, regional myocardial ATP content, cytosolic adenosine concentrations, and blood flow were measured during segmental coronary artery occlusion (complete ligation, n = 10) and demand ischemia (catecholamines plus atrial pacing with subtotal stenosis, n = 6) in halothane anesthetized open-chest dogs. During coronary occlusion or demand ischemia, L-homocysteine thiolactone was infused for 20 min, after which left ventricular tissue was rapidly frozen and analyzed for regional blood flow (microspheres) and content of ATP and S-adenosylhomocysteine (SAH), an index of cytosolic adenosine. In nonischemic regions, ATP and SAH contents in both groups were the same as in unstimulated control animals with intact coronary circulation (n = 7), indicating that adrenergic stimulation during unrestricted flow had no effect on ATP or cytosolic adenosine. In the ischemic regions of both groups, there were decreases in regional flow, ATP content, and systolic wall thickening, and increases in SAH content. To compare the indexes of energy metabolism in tissue regions receiving equal blood flow, tissue samples were grouped into intervals of equal blood flow (ml.min-1.g-1). At every level of flow, ATP content in demand ischemia was 25-39% higher than in coronary occlusion. Estimates of cytosolic adenosine concentrations (using a mathematical model) in the lowest flow interval averaged 5 microM in demand ischemia, approximately twice as high as in coronary occlusion. It is concluded that in tissue regions receiving equal blood flow, ATP was better maintained and cytosolic adenosine was higher in demand ischemia than in coronary occlusion. The differences in ATP content and cytosolic adenosine were not due to different blood flows but rather to more favorable energy metabolism in demand ischemia.
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PMID:Comparison of myocardial ATP, blood flow, and cytosolic adenosine in demand ischemia and coronary occlusion. 757 23

In this prospective study we report the outcome for all patients with a verified aneurysmal SAH managed at the Department of Neurosurgery at the University Hospital in Lund, Sweden during the four-year span from June 1, 1989 to May 31, 1993. A total of 275 patients were admitted during the study period. The vast majority of patients (196 individuals, i.e. 71%) was admitted within 24 h after the bleed. Mean age was 54.3 years and the female/male ratio 1.8/1. Nimodipine was administered in 231 (84%) of the 275 patients. We clipped the ruptured aneurysm in 199 patients. At follow-up 3 months after the bleed 161 patients were classified as having made a good neurological recovery (59%). The morbidity was 20% and 59 patients (21%) had died. The overwhelming cause for morbidity and mortality was damage from the initial bleed (62 patients, 23%). Notably, considering morbidity and mortality, delayed ischemia was less frequent than both surgical complications and rebleeding, respectively. Of the 275 patients, 13 (5%) patients made an unfavorable outcome due to delayed ischemic deterioration. There was a strict correlation between the initial clinical condition and final outcome. Of 51 grade V patients, only 2 made a good recovery. There was also a strict correlation between the amount of extravasated blood and outcome. There was no difference in clinical outcome between patients with arterial hypertension versus normotensive individuals. The mortality rate was worse for posterior circulation aneurysms.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Which are the major determinants for outcome in aneurysmal subarachnoid hemorrhage? A prospective total management study from a strictly unselected series. 783 9

The possibility of measuring cerebral blood flow by mobile bedside units with the intravenous 133-Xenon technique increased the interest to monitor haemodynamic changes after head injury and subarachnoid haemorrhage in intensive care. Time course of resting CBF after trauma is variable (reduced CBF, hyperemia) and there is no strong correlation to clinical outcome. Additional studies of CBF/CO2 reactivity show normal and impaired CO2 response in the acute stage after trauma (day 1-8). A permanently impaired CO2 reactivity correlates with severe brain damage and bad outcome (GOS 1,2). A normal or improving CO2 reactivity indicates a favourable outcome (GOS 3-5). There was no significant correlation between CBF and ICP, nor between CBF and CPP. A CPP of more than 70 mmHg did not guarantee a sufficient CBF in every case indicating the variability of the limits of autoregulation. As therapeutic hyperventilation may lead to ischemia, mannitol was preferred to reduce ICP and increased low CBF to normal values. This fact should be considered in the treatment of patients with low CBF and normal CO2 reactivity. Delayed ischemic neurological deficits ("vasospasm") are well-known as significant complications of the clinical course following SAH. Immediately postoperatively performed CBF measurements enable to detect ischemia and allow to start early antiischemic therapy. During "vasospasm" CBF showed a better correlation to the neurological status than blood flow velocity in the basal arteries measured by transcranial doppler sonography. Furthermore hyperemia after SAH could only be verified by CBF measurements.
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PMID:Xenon 133--CBF measurements in severe head injury and subarachnoid haemorrhage. 790 78

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

The purpose of this study was to determine the effects of homocysteine, which consumes intracellular adenosine via formation of S-adenosylhomocysteine, on interstitial fluid (ISF) adenosine and cerebral blood flow (CBF) before, during, and after cerebral ischemia. Microdialysis probes, used to measure local CBF (H2 clearance) and to sample ISF, were implanted bilaterally into the caudate nucleus of halothane-anesthetized rats (n = 8). L-Homocysteine thiolactone was administered locally via one of the probes. Animals were exposed to 20 min of ischemia, induced by bilateral carotid occlusion plus hemorrhage to an arterial blood pressure of 50 mm Hg, followed by 60 min of reperfusion. Before ischemia, CBF and dialysate adenosine were decreased with homocysteine. During ischemia and early reperfusion, dialysate purine metabolites increased on both sides of the brain; however, the ischemia-induced increase in adenosine was attenuated on the side of local homocysteine. CBF was lower on the side of homocysteine throughout reperfusion. These data demonstrate that homocysteine (a) decreases basal ISF adenosine and CBF, (b) attenuates the increase in dialysate adenosine during ischemia, and (c) reduces hyperemia during early reperfusion.
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PMID:Attenuation of ischemia-induced extracellular adenosine accumulation by homocysteine. 843 12

Adenosine outflow and adenosine and adenine nucleotide content of hippocampal slices were evaluated under two different experimental conditions: ischemia-like conditions and electrical stimulation (10 Hz). Five minutes of ischemia-like conditions brought about an 8-fold increase in adenosine outflow in the following 5 min during reperfusion, and a 2-fold increase in adenosine content, a 43% decrease in ATP, a 72% increase in AMP and a 30% decrease in energy charge (EC) at the end of the ischemic period. After 10 min of reperfusion ATP, AMP and EC returned to control values, while the adenosine content was further increased. Five minutes of electrical stimulation brought about an 8-fold increase in adenosine outflow that peaked 5 min after the end of stimulation, a 4-fold increase in adenosine content and an 18% decrease in tissue EC at the end of stimulation. After 10 min of rest conditions the adenosine content and EC returned to basal values. The origin of extracellular adenosine from S-adenosylhomocysteine (SAH) was examined under the two different experimental conditions. The SAH hydrolase inhibitor, adenosine-2,3-dialdehyde (10 microM), does not significantly modify the adenosine outflow evoked by electrical stimulation or ischemia-like conditions. This finding excludes a significant contribution by the transmethylation pathway to adenosine extracellular accumulation evoked by an electrical or ischemic stimulus, and confirms that the most likely source of adenosine is from AMP dephosphorylation.
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PMID:The source of brain adenosine outflow during ischemia and electrical stimulation. 852 Apr 62

Adenosine outflow and adenosine and adenine nucleotide content of hippocampal slices were evaluated under two different experimental conditions: ischemia-like conditions and electrical stimulation (10 Hz). Five minutes of ischemia-like conditions brought about an 8-fold increase in adenosine outflow in the following 5 min during reperfusion, and a 2-fold increase in adenosine content, a 43% decrease in ATP, a 72% increase in AMP and a 30% decrease in energy charge (E.C.) at the end of the ischemic period. After 10 min of reperfusion ATP, AMP and E.C. returned to control values, while the adenosine content was further increased. Five minutes of electrical stimulation brought about an 8-fold increase in adenosine outflow that peaked 5 min after the end of stimulation, a 4-fold increase in adenosine content and an 18% decrease in tissue E.C. at the end of stimulation. After 10 min of rest conditions the adenosine content and E.C. returned to basal values. The origin of extracellular adenosine from S-adenosylhomocysteine (SAH) was examined under the two different experimental conditions. The SAH hydrolase inhibitor, adenosine-2,3-dialdehyde (10 microM), does not significantly modify the adenosine outflow evoked by electrical stimulation or ischemia-like conditions. This finding excludes a significant contribution by the transmethylation pathway to adenosine extracellular accumulation evoked by an electrical or ischemic stimulus, and confirms that the most likely source of adenosine is from AMP dephosphorylation.
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PMID:The source of brain adenosine outflow during ischemia and electrical stimulation. 874 71

Two hundred seventy-three Patients with acute SAH were treated within the last 46 months (1.4.1991 to 31.1.1995). Diagnosis was made upon visible SAH on CT-scans or bloody spinal tap regardless of a negative CT-scan. These patients harbored 194 aneurysms, 25 AVM and cavernomas. Within the same time-period we treated 27 Patients without SAH but harboring vascular malformations (17 aneurysms, 10 AVM and cavernomas). In 30 patients (11%) no bleeding source was detectable. Fourteen of these patients (5.1%) had blood concentrated within the perimesencephalic cisterns on the CT-scans. On admission all of these 14 patients (8 men, 6 female, aged 30 to 63 years) were awake and without mentionable neurological deficit, equalling Hunt & Hess grade 1 (11 patients) and 2 (3 patients). Neither the initial nor control angiography revealed a vascular malformation as a bleeding source. MRI-scans performed for 11 patients did not reveal further etiological clues. During a follow-up interval of 3 to 48 months, none of these patients suffered a rebleeding. Vasospasm was not or only slightly present, no ischemia leading to neurological deficit. GOS reached 5 and Karnofsky-scale was 100 for all of these patients. We conclude that the perimesencephalic SAH is a homogeneous entity with a different natural course than the common aneurysmatic SAH. Probably leakage within the capillary or venous circulation causes this form of SAH with a benign clinical course. Further experience is required to determine whether control angiography is mandatory in these patents with a distinct CT appearance.
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PMID:[Perimesencephalic subarachnoid hemorrhage--an independent clinical picture of non-aneurysmatic subarachnoid hemorrhage with a benign course]. 877 69

Intraoperative rupture of an aneurysm can lead to disastrous results when the rupture occurs at the neck. The authors have encountered eight cases (5%) of intraoperative rupture in a series of 155 patients. All patients were operated on in the acute stage by one of the authors of this paper (T.Y.). In six cases, the aneurysm ruptured at the dome and in two, at the neck. We report these two patients with intraoperative rupture at the neck. The first case, a 50-year-old female, developed SAH, but a 4-vessel study failed to show an aneurysm. The second series of angiograms obtained ten days later showed a broad-based, left proximal A1 aneurysm. It was decided to employ a right pterional approach. The aneurysm was arising from the right A1 segment just proximal to the anterior communicating artery. The neck was wide, with thin walls. Thus, it seemed better to apply a clip parallel to the A1 segment axis than to apply it from a direction perpendicular to the A1 segment axis. However, the right pterional approach precluded a parallel clipping, so the blades of a clip were applied perpendicularly. The clip seemed not to be completely across the neck of the aneurysm. After applying a temporary clip to the A1 segment proximal to the aneurysm, the clip blades were opened and advanced just when bursting of the sac at the base occurred and microvascular suture repair was required to control the bleeding. The second case, a 57-year-old female, underwent clipping of a right IC-PC aneurysm. However, two years postoperatively, the patient again suffered SAH. Cerebral angiography at this time revealed a relatively large recurrent IC-PC aneurysm in which the old clip was situated on the dome of the aneurysm. Aneurysmal clipping was performed on the day of rupture. Tough granular tissue was removed from the ICA, PcomA, aneurysmal neck, and the old clip. After the true neck was identified, a straight clip was applied to the neck parallel to the ICA. Soon after the clipping, arterial bleeding occurred near the neck. The ruptured aneurysm was trapped using two temporary clips. A curved clip was applied to the ruptured neck, including the wall of the ICA, to control the bleeding. This clipping caused a substantial stenosis of the ICA. Both patients demonstrated postoperative neurological deficits due to ischemia caused by temporary clipping. These encounters dramatically demonstrated that a very thin-walled aneurysm or a recurrent aneurysm has a fragile neck. In surgical treatment of these unusual aneurysms, a clip should be placed on the neck parallel to the parent artery. Furthermore, temporary clipping is advisable when dissecting the neck or applying the clip to the neck to reduce the damage to the neck.
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PMID:[Intraoperative aneurysmal rupture at the neck]. 905 36


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