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 interaction of plasma catecholamines and nitrous oxide (N2O) ventilation was examined during brain ischemia in rats. Group 1 (n = 19) was anesthetized with 50 micrograms.kg-1 x h-1 of fentanyl and ventilated with 70% nitrogen in oxygen. Group 2 (n = 19) was anesthetized with intravenous fentanyl (25 micrograms.kg-1 x h-1) and 70% N2O ventilation in oxygen. Group 3 (n = 10) received 25 micrograms.kg-1 x h-1 of fentanyl and 70% N2O ventilation and 100 micrograms/kg of dexmedetomidine, an alpha 2-adrenergic receptor agonist that decreases sympathetic activity. Incomplete brain ischemia was produced by right carotid ligation combined with hemorrhagic hypotension to 30 mm Hg for 30 min. Plasma catecholamines were measured during ischemia. Cerebral blood flow (CBF) was evaluated by using laser Doppler. Neurologic outcome was evaluated for 3 days after ischemia. Plasma epinephrine and norepinephrine and were decreased 20% and neurologic outcome was significantly worse in Group 2 ventilated with N2O compared with fentanyl-anesthetized controls (P < 0.05). Dexmedetomidine-treated rats had lower plasma catecholamines (20% of control) and larger decreases in CBF during ischemia compared with controls. Dexmedetomidine (Group 3) improved outcome from ischemia in comparison to both Groups 1 and 2 (P < 0.05). These results suggest that catecholamines play a major role in worsening ischemic outcome. N2O ventilation may increase neuronal injury by enhancing the sympathetic response to ischemia.
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PMID:Interaction of catecholamines and nitrous oxide ventilation during incomplete brain ischemia in rats. 810 26

During inhalation anesthesia using N2O, the intracuff pressure has been reported to increase due to diffusion of N2O into the cuff. The excessive intracuff pressure may produce ischemia of the tracheal mucosa. In this study, the changes in the intracuff pressure of endotracheal tube with a cuff made of a material with high N2O gas-barrier properties were compared with those of the normal endotracheal tubes. Forty adult patients (16 males and 24 females) were anesthetized with oxygen 2 l.min-1, N2O 4 l.min-1 and isoflurane under controlled ventilation and they were divided into the following three groups according to the type of the endotracheal tube used: the tube with a standard cuff made by PORTEX Co. Ltd; the tube with a profile cuff (high volume cuff) made by PORTEX Co. Ltd; the tube with gas-barrier cuff made by TERUMO Co. Ltd. The changes of each intracuff pressure were recorded continuously for 180 minutes after cuff inflation. A marked increase of the pressure was observed after inhalation of N2O in standard and profile cuff groups. In gas-barrier cuff group, there was a tendency of increasing cuff pressure without a statistically significant difference. The present study suggests that the use of a cuff with a material of high N2O gas-barrier properties would be effective to prevent increased intracuff pressure by N2O diffusion, and this would be especially useful during long anesthesia and hypotensive anesthesia.
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PMID:[The intracuff pressure changes in N2O gas-barrier cuff made of a special material]. 832 Jul 98

The potential usefulness of somatosensory evoked potential monitoring during aortic cross-clamping is slowly being realized. In addition, the protection of endangered spinal nervous tissue during aortic cross-clamping has not been sufficiently evaluated. To test the pharmacologic protective efficacy of various agents, we recorded spinal evoked somatosensory potentials (bipolar epidural catheter) in dogs under controlled conditions (N2O/O2-enflurane anesthesia) following clamping of the aorta for 1 hour. There were 5 groups of animals: those treated with different medications, such as prostaglandin E1 (PGE1), prostacyclin (PGI2), superoxide dismutase (SOD), and PGE1 plus SOD for pharmacologic protection during ischemia, and the controls. The time to recovery of evoked potentials during the reperfusion period was 36 minutes in the controls, 15.9 minutes in the SOD group (p < 0.01), 12.5 minutes in the PGE1 group (p < 0.001), 10.8 minutes in the PGI2 group (p < 0.001), and 3.8 minutes in the combination group (p < 0.001). In addition, treatment resulted in a better neurologic outcome on the seventh postoperative day when compared with the control group. While in the control group only 1 animal could walk (9%), 7 of 12 in the PGE1 group (58%), 4 of 12 in the SOD group (33.8%), 8 of 12 in the PGI2 group (66.7%), and all animals in the combination group (100%) could walk. We computed an exponential correlation that related the mean time of potential recovery during reperfusion with Tarlov scoring (grade 0 = paraplegia; grade 1 = paraplegia with little movements; grade 2 = paraparesis; grade 3 = paraparesis with some problems; grade 4 = normal motor function) in the various groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Somatosensory evoked potential, a prognostic tool for the recovery of motor function following malperfusion of the spinal cord: studies in dogs. 834 72

alpha 2-Adrenergic agonists decrease sympathetic activity and improve outcome from brain ischemia. We evaluated whether changes in alpha 2-adrenergic receptor binding activity may be important in the sympathetic depressant and cerebral protective effects of halothane (1.1% inspired) or isoflurane (1.4% inspired) compared to fentanyl/nitrous oxide (N2O) anesthesia. Brain alpha 2-adrenergic receptor binding was measured using [3H]-clonidine in each of four treatment conditions: 1, unanesthetized; 2, anesthetized (fentanyl/N2O, halothane, or isoflurane): 3, anesthetized with ischemia; 4, after 4 h recovery from ischemia. Ischemia was produced by right carotid artery ligation combined with hemorrhagic hypotension to 30 mm Hg for 30 min. Both halothane and isoflurane decreased alpha 2-adrenergic receptor density 20% compared to unanesthetized values (P < 0.01). This decrease was attenuated in ischemic tissue. There were no consistent changes in receptor affinity. These results suggest that inhaled anesthetics decrease the number of alpha 2-adrenergic receptors. This decrease appears to be unrelated to plasma catecholamine concentrations but may be influenced by the degree of ischemia.
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PMID:Brain alpha 2-adrenergic receptor binding during incomplete cerebral ischemia in the rat. 838 Sep 57

The relation between sympathetic activity and neurologic outcome was evaluated during fentanyl/nitrous oxide (N2O) (25 micrograms.kg-1.min-1 plus 70% N2O in oxygen), halothane (1.1% inspired), and isoflurane (1.4% anesthesia in a rat model of incomplete cerebral ischemia. Ischemia was produced by right carotid ligation combined with hemorrhagic hypotension to 30 mm Hg for 30 min. Plasma catecholamines were measured during ischemia. Neurologic outcome was measured for 3 days following incomplete ischemia. Both halothane and isoflurane decreased plasma catecholamines 50-80% and improved ischemic outcome compared to fentanyl/N2O anesthesia (P < 0.05). These results indicate a relation between the ability of inhaled anesthetics to decrease sympathetic activity and to improve outcome from incomplete cerebral ischemia.
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PMID:The effect of halothane and isoflurane on neurologic outcome following incomplete cerebral ischemia in the rat. 842 3

Recently, attention has been focused on the degradation of cytoskeletal proteins in animal models of cerebral ischemia, as the collapse of cytoskeletal proteins may be closely related to cytoskeletal disintegration and ultimate neuronal cell death. Among these proteins, microtubule-associated protein 2 (MAP2) has been shown to be highly vulnerable to ischemic injuries. To determine the degree of anesthetic effect on the collapse of cytoskeletal proteins, we compared the effect of three inhalation anesthetics; isoflurane, halothane, and nitrous oxide (N2O), on MAP2 degradation during 20 min of forebrain ischemia in the rat. Under equipotent anesthesia, forebrain ischemia was induced by the occlusion of the bilateral common carotid artery (CCA) combined with a lowering of mean arterial pressure (mAP) to 50 mmHg. After 20 min of ischemia, three regions of the brain, the frontoparietal cortex, brainstem, and hippocampus, were removed and separately homogenized. Subsequently, MAP2 of each region was measured using an enzyme-linked immunosorbent assay (ELISA). In the frontoparietal cortex and hippocampus, MAP2 was significantly protected from degradation when isoflurane was used combined with nitrogen (N2). However, the protective effects of isoflurane were drastically reduced when N2O was given instead of N2. These results suggest that the use of N2O should be discontinued when severe cerebral ischemia is accidentally incurred during anesthetic management.
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PMID:Nitrous oxide attenuates the protective effect of isoflurane on microtubule-associated protein2 degradation during forebrain ischemia in the rat. 932 46

Impairment of intestinal nutritive perfusion and accumulation of inflammatory cells in the intestinal microvasculature are well-known sequelae of mesenteric ischemia/reperfusion, sepsis, and shock. However, the molecular mechanisms underlying these alterations are still not fully understood. The mouse is particularly suitable for the study of these mechanisms since in this species the involvement of, for example, adhesion receptors or pro-/anti-adhesive mediators can be selectively investigated by the use of monoclonal antibodies or gene-targeted strains. The aim of our present study was, therefore, to establish a model to investigate the microcirculation in the mouse small intestine. Under anesthesia by inhalation of isoflurane-N2O, Balb/c mice (n = 16) were laparotomized, and a segment of the jejunum was exteriorized for intrvital fluorescence microscopy. Using FITC-dextran (MW 150,000) as a plasma marker, functional capillary density (FCD) of both the intestinal mucosa and muscle layer was analyzed. Nutritive perfusion was homogeneous in both compartments with values for FCD of 512 +/- 15 cm-1 in mucosa and 226 +/- 21 cm-1 in the muscle layer. No significant changes were observed throughout the observation period of 2 h (FCD values at the end of the observation period: 524 +/- 31 cm-1 and 207 +/- 7 cm-1 in mucosa and muscle, respectively). Besides capillary perfusion, leukocyte-endothelial cell interaction was analyzed in postcapillary venules of the intestinal submucosa using rhodamine-6G as an in vivo leukocyte stain. Under physiological conditions only a few white blood cells were found rolling along or firmly adherent to the microvascular endothelium (number of rolling leukocytes 1 +/- 0.2 cells/mm per second; number of adherent leukocytes: 18 +/- 7 cells/mm2). In a separate group rhodamine-6G-labeled syngeneic platelets were infused to analyze platelet-endothelial cell interactions quantitatively in vivo. Platelets rolled along or attached to the endothelium in a manner similar to leukocytes. However, in contrast to leukocytes the interactions were not restricted to venules, but were also observed in small arterioles. The newly established model allows for the visualization and quantitative assessment of both nutritive perfusion and platelet/leukocytendothelial cell interactions within the distinct layers of the mouse small intestine. Using this model in combination with gene-targeted mice or monoclonal antibodies it is possible to investigate the molecular mechanisms of intestinal inflammation reactions.
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PMID:Quantitative analysis of small intestinal microcirculation in the mouse. 970 67

Continuous measurement of somatosensory evoked potentials (SEP) by means of characteristic changes in the signal pattern makes it possible to identify cerebral or spinal cord ischemia during critical phases of the operative procedure. A correct interpretation of the measurements is only possible, however, if the influence of drugs acting on the central nervous system is known. The authors were able to show that inhaled anesthetics have an impact on latencies and response amplitudes. This study examined the influence of various concentrations of desflurane on the conduction of SEP of the Median nerve. In addition, the authors determined how the supplementation of nitrous oxide (N2O) influences the stimulus response of the medianus nerve's SEP. Desflurane has been shown to produce dose-dependent increases in SEP latency (data in part for latency N2O: 0.5 minimum alveolar concentration [MAC] = 20.8 +/- 0.9; 1.5 MAC = 22.2 +/- 1.5; 1.5 MAC/N2O= 23.8 +/- 1.5) and decreases in amplitude, whereas cervically recorded subcortical SEP components are minimally influenced by desflurane. When nitrous oxide is added, there were marked reductions in amplitude (p<0.01) of the cortical stimulus response (1.5 MAC = 2.4 +/- 0.9; 1.5 MAC/N2O = 1.1 +/- 1). It can therefore be recommended that supplementation with N2O should be avoided in the presence of low initial amplitudes. Based on the study's results, the use of desflurane (up to 1.0 MAC) seems to be compatible with intraoperative monitoring of median somatosensory evoked potentials.
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PMID:Modulation of somatosensory evoked potentials under various concentrations of desflurane with and without nitrous oxide. 979 5

We tested the hypothesis that fentanyl would worsen ischemia-induced brain damage. In two sequential protocols forty rats were physiologically monitored and controlled. In protocol 1, rats were randomized (n=10/group) to 30 min of control (N2O plus 0.4% halothane), low dose fentanyl (loading dose [LD] 50 micrograms kg-1, maintenance dose [MD] 2 micrograms kg-1 min-1), or high-dose fentanyl (LD 800 micrograms kg-1, MD 32 micrograms kg-1 min-1). After 15 min of fentanyl or sham infusion trimethaphan 0.5 mg was given i.v. and 3 min later bilateral carotid artery occlusion and blood withdrawal-induced hypotension were maintained for 12 min. At 18 h postischemia rats underwent cerebral perfusion fixation. Brain areas were graded from 0 (normal) to 5. In addition to analysis of specific regions, neuropathologic scores were also summated over all brain regions and analyzed to compute a summed neuropathologic score. In protocol 2, five control and five high-dose fentanyl rats were treated identically except that post-ischemic oxygenation was maintained for 6 h and cerebral perfusion-fixation was performed 6 h post-ischemia. Only the caudate/putamen was examined in protocol 2. Fentanyl worsened lesions in both fentanyl groups' summed neuropathologic scores (P=0.002) in protocol 1 and specifically, in the caudate/putamen (P<0.01) in both protocols. Fentanyl in both high and low doses can exacerbate incomplete forebrain ischemia in rats.
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PMID:Opioid neurotoxicity: fentanyl-induced exacerbation of cerebral ischemia in rats. 1008 18

Global cerebral ischemia and subsequent reperfusion induce early impairment of the vasodilator responses to hypercapnia and vasoactive substances. Nitric oxide (NO) is involved in the regulation of cerebral blood flow (CBF) in both health and disease. The present study was designed to assess possible changes in the cerebrovascular reactivity to NO donors induced by cerebral ischemia-reperfusion in goats. Female goats (n = 9) were subjected to 20 min global cerebral ischemia under halothane/N2O anesthesia. Sixteen additional goats were sham-operated as a control group. One week later the effects of ischemia-reperfusion on relaxations to NO donors sodium nitroprusside (SNP), diethylamine/NO (DEA/NO), diethylenetriamine/NO (DETA/NO), and spermine/NO (SPER/NO) were studied in rings of middle cerebral artery (MCA) isolated in an organ bath for isometric tension recording. SNP, DEA/NO, DETA/NO, and SPER/NO induced concentration-dependent relaxations of MCA precontracted with KCl (DEA/NO > SPER/NO > SNP > DETA/NO) or with endothelin-1 (DEA/NO > SNP > SPER/NO > DETA/NO). Relaxations were always higher in endothelin-1-precontracted arteries. One week after cerebral ischemia concentration-response curves to SNP and DEA/NO were displaced to the right, indicating a reduction in relaxant potency of NO donors. The classical nitrovasodilator SNP and NONOates induce relaxation of isolated goat MCA which is partially inhibited by arterial depolarization. Global cerebral ischemia followed by reperfusion induces delayed impairment of the relaxant effects of NO on cerebrovascular smooth muscle, which results in reduced vasodilatory potency of NO donors in large cerebral arteries.
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PMID:Relaxant effects of sodium nitroprusside and NONOates in goat middle cerebral artery: delayed impairment by global ischemia-reperfusion. 1035 99


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