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)

The mitochondrial fraction obtained from brains of animals submitted to ischemia shows a decrease of phospholipid level, especially plasmalogens in the fraction of ethanolamine phospholipids and choline phospholipids. There appears simultaneously an increase of free radical oxidation processes of unsaturated fatty acids from these phospholipids. The peroxidation processes of mitochondrial lipids are stimulated by calcium ions and, to a smaller extent, by magnesium ions. Barbiturate anesthesia inhibits the peroxidation of fatty acids and increases the antioxidant abilities of the nervous tissue. Nembutal added in vitro remains without effect on the above processes. The effect of acetylcholine and the antioxidant ability of nervous tissue under barbiturate anesthesia with respect to ischemia are discussed.
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PMID:Effect of ischemic anoxia and barbiturate anesthesia on free radical oxidation of mitochondrial phospholipids. 70 72

We report two cases of traumatic cerebral vascular disease which were treated successfully with barbiturate. The first case sustained blunt trauma to the bilateral vertebral arteries, resulting in complete occlusion of both arteries. After ligation of the injured vertebral arteries, multiple cerebral infarction appeared. Cerebral angiography revealed dissection and stenosis of the bilateral internal carotid arteries. We treated this case with barbiturate (Thiamylal) in combination with administration of heparin. The second case sustained cerebral contusion and traumatic subarachnoidal hemorrhage as a result of a motor cycle accident. This patient deteriorated and cerebral angiography showed diffuse cerebral arterial vasospasms. When this was treated with induced hypertension, he developed recurrent subarachnoid hemorrhage. In order to protect the brain from ischemia without elevating blood pressure, we employed barbiturate therapy and the patient recovered without major neurological deficit. The condition of severe head injury with cerebral ischemia is complicated. Therefore it has been hard for neurosurgeons to cure the patient with this condition. But we treated it with barbiturate successfully. Barbiturate therapy in severe head injury with cerebral ischemia may decrease the mortality in that group of patients considered difficult to treat with the usual therapeutic modalities.
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PMID:[Barbiturate therapy in traumatic cerebral vascular disease: report of two cases]. 261 99

The effect of barbiturate treatment on post-ischemic cerebral protein biosynthesis was studied in gerbils subjected to 5 min transient occlusion of carotid arteries followed by 2 h or 48 h recirculation. Ischemia induced a remarkable decline of amino acid incorporation into brain proteins in most forebrain structures. The initial inhibition recovered to near normal after 2 days recirculation in all regions except the vulnerable CA1 sector. Barbiturate treatment, which previously has been shown to prevent delayed neuronal death in CA1 sector, did not ameliorate the initial inhibition of protein synthesis but it significantly improved subsequent recovery, especially in the vulnerable CA1 sector of hippocampus. These observations indicate that delayed neuronal death in CA1 sector of hippocampus results from selective failure of post-ischemic recovery and not from selective ischemic injury of the protein synthesizing machinery. This explains that delayed neuronal death can be prevented by therapeutic interventions which are initiated during the post-ischemic recirculation phase.
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PMID:Effect of barbiturate treatment on post-ischemic protein biosynthesis in gerbil brain. 280 24

Energy depletion and lactate are at plateau levels within five minutes of complete ischemic-anoxia in the brain; however, irreversible brain injury has not occurred in this time. Brain free fatty acids (FFA) rise sharply during the first five minutes of ischemic-anoxia, but then continue to rise during the following hour without plateauing. Barbiturate anesthesia preischemia attenuates the FFA rise. Other agents which also attenuate the FFA increase include, among others, phenytoin and Innovar. The Ca2+ antagonists flunarizine and gallopamil also attenuated FFA rise, but were not as effective as pentobarbital during ischemia. Protective effects of Ca2+ antagonists may be more important during recirculation than during ischemia.
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PMID:Free fatty acid accumulation in the pathogenesis and therapy of ischemic-anoxic brain injury. 668 Jun 18

The use of barbiturates to induce coma as a means of extending the period of reversible cerebral ischemia is reviewed. Barbiturate use in patients who had had strokes or were undergoing aneurysm surgery was initially encouraging. In uncontrolled feasibility trials in patients with cardiopulmonary arrest or in deep coma, 40 patients received 10 mg/kg thiopental sodium by i.v. push followed by 20 mg/kg thiopental sodium i.v. over the next 30 minutes; 60% of these patients regained consciousness. In a subgroup of 22 patients who had ischemia normally associated with a 90% mortality rate, 14 recovered completely. In the largest clinical trial, 45 patients with severe head injury and elevated intracranial pressure received 3--5 mg/kg pentobarbital over 10--20 minutes. A serum barbiturate level of 2.5--4.0 mg/dl was maintained for 14 days, and 30% of these patients recovered but with neurologic deficits. Other results in stroke and drowning victims were not as encouraging. It is concluded that barbiturate therapy is beneficial in the lowering of intracranial pressure. Focal and global cerebral ischemia have been shown amenable to barbiturate therapy in isolated cases. The prophylactic use of barbiturates in surgical procedures requiring focal cerebral anoxia appears to be beneficial. Controlled trials of the use of barbiturate-induced coma are clearly indicated.
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PMID:Barbiturate-induced coma to protect against cerebral ischemia and increased intracranial pressure. 702 14

Barbiturate administration for protection from focal ischemia was evaluated in baboons. All animals were monitored for 96 hours in an intensive care unit during various regimens of pentobarbital administration. Intermittent bolus injections of barbiturate yielded inconsistent electroencephalographic responses and produced the most cardiovascular instability. Continuous barbiturate infusion safely allowed the greatest amount of barbiturate to be employed with the most stable electrophysiological and cardiovascular response.
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PMID:Management of prolonged therapeutic barbiturate coma. 725 31

A decrease in myofilament sensitivity to Ca2+ has been proposed as a mechanism for reversible contractile dysfunction after ischemia and reperfusion. The direct actions of intracoronary myofilament Ca2+ sensitizers on stunned myocardium have not been examined. Barbiturate-anesthetized dogs (n = 9) were instrumented for measurement of left ventricular (LV) and aortic blood pressure, cardiac output, left anterior descending coronary artery (LAD) blood flow velocity, and subendocardial segment length (percent segment shortening [%SS]). Dogs were subjected to five 5-min LAD occlusions interspersed by 5-min reperfusions. Three hours after the final reperfusion, levosimendan (1.5, 3, 6, and 12 microg/min) was administered via an intracoronary catheter. Hemodynamic effects and regional myocardial function were determined under control conditions, during each LAD occlusion and reperfusion, 3 h after final reperfusion, and after 10 min equilibration at each dose of levosimendan. Three hours after the final reperfusion, %SS and the ratio of effective to total regional work were significantly (P < 0.05) decreased, and postsystolic shortening area was increased, consistent with myocardial stunning. In stunned myocardium, intracoronary levosimendan caused dose-dependent increases in %SS (2 +/- 1 at 3 h after reperfusion to 13% +/- 2% during 12 microg/min), abolished postsystolic shortening area, and restored the ratio of effective to total regional work while producing minimum systemic hemodynamic effects.
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PMID:Intracoronary levosimendan enhances contractile function of stunned myocardium. 921 17

Recently, we reported that exogenous administration of Met(5)-enkephalin (ME) for 24 h reduces infarct size after ischemia-reperfusion in rabbits. In the present study, we tested whether ME-induced cardioprotection is exhibited in murine hearts and whether chronic infusion of this peptide can render hearts tolerant to ischemia. Barbiturate-anesthetized open-chest mice (C57BL/6J) were subjected to regional myocardial ischemia-reperfusion (45 min of occlusion and 20 min of reperfusion). Mice received saline vehicle or ME for 24 h or 2 wk before undergoing regional myocardial ischemia-reperfusion or for 24 h followed by a 24-h delay before regional myocardial ischemia-reperfusion. Infarct size was measured with propidium iodide and is expressed as a percentage of the area at risk. Infarcts were smaller after infusion of ME for 24 h than with vehicle control: 49.2 +/- 9.0% vs. 22.2 +/- 3.2% (P < 0.01). In contrast, administration of ME for 2 wk failed to elicit cardioprotection: 36.5 +/- 9.1% and 41.4 +/- 8.2% for control and ME, respectively (P = not significant). When a 24-h delay was imposed between the end of drug treatment and the onset of the ischemic insult, cardioprotection was lost: 38.5 +/- 6.1% and 42.8 +/- 6.6% for control and ME, respectively (P = not significant). Chronic sustained exogenous infusion of the endogenously produced opioid peptide ME is associated with loss of the cardioprotection that is observed with 24 h of infusion. Furthermore, in this in vivo murine model, ME failed to induce delayed tolerance to myocardial ischemia-reperfusion.
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PMID:Long-term infusion of Met5-enkephalin fails to protect murine hearts against ischemia-reperfusion injury. 1555 May 29

The selective phosphodiesterase type 5 inhibitor sildenafil has been demonstrated to produce cardioprotection; however, diabetes is known to abolish cardioprotective signaling. We tested the hypothesis that sildenafil-induced cGMP-dependent protein kinase-I (PKG-I) expression and cardioprotection are attenuated by diabetes. Barbiturate-anesthetized dogs (n = 38) were instrumented for measurement of hemodynamics and subjected to 60-minute occlusion of the left anterior descending coronary artery and 3-hour reperfusion. Dogs were randomly assigned to receive 0.9% saline (control) or intravenous sildenafil (0.7 or 1.4 mg/kg) in the absence or presence of diabetes (3 weeks after administration of alloxan and streptozotocin). No differences in hemodynamics or coronary collateral blood flow (radioactive microspheres) were observed between groups before and during ischemia and reperfusion, except that infusion of sildenafil produced transient decreases in left ventricle systolic pressure. Sildenafil significantly (P < 0.05) reduced infarct size (16 +/- 2% of the left ventricular area at risk; triphenyltetrazolium staining) as compared to control (31 +/- 39%). Diabetes alone did not alter infarct size (31 +/- 2%) but abolished the protective effect of sildenafil (0.7 mg/kg: 26 +/- 3%; 1.4 mg/kg: 26 +/- 3%). Sildenafil increased PKG-I expression (immunohistochemistry and Western blotting) in the absence but not the presence of diabetes. The results indicate that diabetes abolishes cardioprotection by sildenafil and implicates PKG-I in the signal transduction pathway activated by this drug.
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PMID:Diabetes abolishes sildenafil-induced cGMP-dependent protein kinase-I expression and cardioprotection. 1809 84