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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Numerous reports have concluded that propofol is suitable for maintenance of anesthesia by continuous infusion. The aim of this study was to evaluate the use of propofol and fentanyl for coronary bypass surgery in patients with good left ventricular function. The effects of this anesthetic combination on quality of anesthesia, hemodynamic status, and endocrine and metabolic responses were assessed. Postoperative recovery and side effects were also noted. The effects were compared with those of a standard method using etomidate, midazolam, and fentanyl. METHODS. Twenty patients who presented for aortocoronary bypass surgery (NYHA class II-III) were randomly allocated to one of two groups: propofol-fentanyl (group A) or etomidate-midazolam-fentanyl (group B). In each patient the dosage of the drugs was adjusted to obtain the optimum responses during induction and maintenance. RESULTS. Propofol in combination with fentanyl diminished mean arterial pressure (-28.7%) and heart rate (-17.3%) when used for induction in patients with ischemic heart disease, even in low doses and with slow administration. In 5 of the 10 patients it was impossible to prevent a critical fall in coronary perfusion without active intervention. However, during maintenance anesthesia, stable circulatory parameters were obtained with both drug regimens. Clinical signs thought to reflect myocardial ischemia were not observed. In both groups reductions in basal and stimulated catecholamine secretion were demonstrated. Similarly, perioperative cortisol secretion was reduced with both techniques. Despite all the complicated metabolic inhibitory effects seen, preoperative hormonal levels were restored within 1 h of the end of anesthesia. The magnitude and duration of the metabolic changes were found to be related to the duration of surgery. There was no evidence of non-homogeneous tissue perfusion as assessed by increases in lactate concentration, cardiac ischemia, or liver dysfunction in any of the patients. There were no postoperative complications in either group, but the return of consciousness, adequate spontaneous ventilation, and psychomotor activity was more rapid in the propofol patients. CONCLUSION. In summary, it can be concluded that a propofol infusion technique positively enhances the recovery period after cardiac surgery and provides good control during anesthesia. However, the use of propofolfentanyl for induction of anesthesia in patients with limited coronary perfusion is not recommended because of its hypotensive effect.
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PMID:[Propofol for induction and maintenance of anesthesia during heart surgery. Results of pharmacological studies in man]. 203 20

The purpose of this investigation was to examine the effects of thoracic epidural anesthesia (TEA) on myocardial stunning during propofol anesthesia. Six dogs were chronically instrumented for measurement of left atrial, aortic, and left ventricular pressure, maximal rate of increase of left ventricular pressure, and myocardial wall-thickening fraction (WTF). Myocardial blood flow was determined with colored microspheres. Experiments were performed on separate days with 1) 10 min of left anterior descending artery (LAD) ischemia during propofol anesthesia without TEA, and 2) 10 min of LAD ischemia during propofol anesthesia with TEA. WTF was measured as baseline (BL) prior to propofol anesthesia and at predetermined time points until complete recovery from stunning. Propofol anesthesia caused a significant decrease of WTF in the LAD-perfused myocardium (LAD-WTF) compared to BL in awake animals. LAD ischemia led to a further significant decrease of LAD-WTF. There were no significant differences in LAD-WTF between the two experimental conditions at any of the time points measured. TEA did not change subendocardial blood flow in nonischemic myocardium. During ischemia neither the subendocardial/subepicardial nor the occluded/normal zone blood flow ratio were affected by TEA. After myocardial ischemia during propofol anesthesia TEA does not affect functional recovery of stunned myocardium in dogs.
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PMID:The effects of thoracic epidural anesthesia on functional recovery from myocardial stunning in propofol-anesthetized dogs. 908 46

We investigated the brain protection effects of propofol anesthesia and nitrous oxide-oxygen-isoflurane anesthesia (GOI) using forebrain ischemic model of male Sprague-Dawley rats. Propofol group (P, n = 15) was anesthetized with propofol, oxygen and nitrogen (FIO2 = 0.33), and isoflurane group (GOI, n = 15) with 66% nitrous oxide, 33% oxygen and 1.2% isoflurane under mechanical ventilation. The anesthesia was deepened until electroencephalographic burst suppression appeared in each group. The bilateral common carotid arteries were, then, occluded for 10 minutes while the blood pressure was maintained at about 40 mmHg by venesection. The venesected blood was returned at the end of ischemic period. The animals were kept and fed in cage after emergence. On the day 2, 4, and 7, five animals of each group were sacrificed and the microscopic samples were obtained. The CA-1 cells of hippocampus were then stained with hematoxylin and eosin for the delayed neuronal death (DND) and with TUNEL method for the apoptosis. Propofol reduced the apoptosis, i.e., reduced the TUNEL positive cell count (GOI = 121.2 +/- 25.2.mm-1; P = 53.8 +/- 11.4.mm-1; P < 0.01; mean +/- SD) on the day 2 after ischemia, and also reduced the delayed neuronal death (alive CA-1 cell count; GOI = 18.1 +/- 8.9.mm-1; P = 33.1 +/- 12.8.mm-1; P < 0.01) on the day 7 after ischemia. It is important to determine the recovery interval after brain ischemia in detection of DND and apoptosis. We conclude that propofol inhibits neuronal apoptosis after brain ischemia and consequently reduces the delayed neuronal death in the CA-1 pyramidal cell layer of the hippocampus.
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PMID:[Depressive effects of propofol on apoptotic injury and delayed neuronal death after forebrain ischemia in the rat--comparison with nitrous oxide-oxygen-isoflurane]. 1070 15

Excessive glutamate accumulation in extracellular space due to ischemia in the central nervous system (CNS) is believed to initiate the cascade toward irreversible neuronal damage. An intravenous general anesthetic, propofol (2,6-diisopropylphenol) has been implicated to be neuroprotective against cerebral ischemia. The purpose of this study was to test the hypothesis that intracerebroventricular propofol produced a reduction in extracellular glutamate level during global ischemia and the resultant neuroprotection. Adult male Wistar rats were anesthetized with halothane in nitrous oxide/oxygen and mechanically ventilated. Propofol (3 or 10 mg/kg), Intralipid((R)) as a vehicle for propofol, or artificial cerebrospinal fluid (aCSF) was administered into the cerebral ventricles 15 min prior to a 10-min forebrain ischemia elicited by the four-vessel occlusion. Extracellular glutamate concentration in the hippocampal CA1 was continuously monitored during the peri-ischemic period with a microdialysis biosensor. Neuronal cell loss in the hippocampal CA1 was evaluated by cresyl-violet staining of sections 7 days later. Propofol (3 and 10 mg/kg) and Intralipid, compared with aCSF, similarly reduced the extracellular glutamate accumulation during the peri-ischemic period (P<0.05), indicating that the extracellular glutamate reduction that was seen primarily reflects the effect of Intralipid. The number of intact neurons in the hippocampal CA1 in propofol 10 mg/kg-treated rats was significantly higher than that in rats treated with propofol 3 mg/kg, Intralipid, or aCSF (P<0.05). We conclude that intracerebroventricular propofol exhibits neuroprotection against transient global forebrain ischemia; however, the extracellular glutamate level during ischemia is not a major determinant of this neuroprotection.
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PMID:Intracerebroventricular propofol is neuroprotective against transient global ischemia in rats: extracellular glutamate level is not a major determinant. 1106 89

Acute brain ischemia causes neurotoxic cascades including NMDA receptors and NO. Propofol, an i.v. anesthetic, is thought to have a neuroprotective effect. We investigated the influence of propofol on NMDA/NO neurotoxicity using Shibuta's established model of primary brain cultures. Cortical neurons prepared from E16 were used after 13-14 days in culture. The neurons were exposed to various concentrations of propofol with NMDA or NO-donor. The survival rates of neurons exposed to 30 microM NMDA with or without 300 microM propofol were 12.1 +/- 2.2% and 11.9 +/- 2.2%, respectively. The survival rates exposed to 30 microM NO-donor with or without 300 microM propofol were 11.2 +/- 4.2% and 14.0 +/- 3.9%, respectively. These results suggest that neuroprotective effect of propofol is limited and propofol does not offer advantages over thiopental against NMDA/NO-induced cytotoxicity.
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PMID:The effects of propofol on NMDA- or nitric oxide-mediated neurotoxicity in vitro. 1120 38

Sedatives continue to be used on a routine basis in critically ill patients. Although many agents are available and some approach an ideal, none are perfect. Patients require continuous reassessment of their pain and need for sedation. Pathophysiologic abnormalities that cause agitation, confusion, or delirium must be identified and treated before unilateral administration of potent sedative agents that may mask potentially lethal insufficiencies. The routine use of standardized and validated sedation scales and monitors is needed. It is hoped that reliable objective monitors of patients' level of consciousness and comfort will be forthcoming. Each sedative agent discussed in this article seems to have a place in the ICU pharmacologic armamentarium to ensure the safe and comfortable delivery of care. Etomidate is an attractive agent for short-term use to provide the rapid onset and offset of sedation in critically ill patients who are at risk for hemodynamic instability but seem to need sedation or anesthesia to perform a procedure or manipulate the airway. Ketamine administered through intramuscular injection or intravenous infusion provides quick, intense analgesia and anesthesia and allows patients to tolerate limited but painful procedures. The risk/benefit ratio associated with the use of this neuroleptic agent must be weighed carefully. Ketamine is contraindicated in patients who lack normal intracranial compliance or who have significant myocardial ischemia. Barbiturates are reserved mainly to induce coma in patients at risk for severe CNS ischemia, which frequently is associated with refractory intracranial hypertension, or in patients with status epilepticus. When administered in high doses, these drugs have prolonged sedative and depressant effects. Judicious hemodynamic monitoring is required when barbiturate coma is induced. Haloperidol is indicated in the treatment of delirium. Patients should be monitored for extrapyramidal side effects and, when they require higher doses, for potential electrocardiographic prolongation of the QT interval. Dexmedetomidine may evolve into an agent with qualities comparable with midazolam and propofol, and it may even become a drug of choice in select patients. Further study is required, however. Propofol has many of the qualities of an ideal sedative agent. Benzodiazepines and narcotics often are used in concert with propofol to provide reliable amnesia and to relieve pain, respectively. Propofol frequently causes hypotension when administered as a bolus or infusion, particularly in patients with limited cardiac reserve or hypovolemia. More data must be obtained to identify potential deleterious effects of hypertriglyceridemia, and further evaluation of the potential benefits in certain patient populations, such as neurosurgical patients, is needed.
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PMID:Use of propofol and other nonbenzodiazepine sedatives in the intensive care unit. 1176 65

Propofol has cerebral vascular and metabolic effects similar to those of barbiturates, and it is used to maintain neurosurgical anesthesia because it reduces cerebral metabolic rate, cerebral blood flow, and intracranial pressure. Although the use of propofol as a cerebral protectant during certain neurosurgical procedures has been advocated, consensus has not been reached as to a protective effect of propofol on cerebral ischemia. In this study we observed the neuroprotective effects of propofol during global cerebral ischemia-reperfusion injury by the use of four-vessel occlusion method in a rat model. We measured the levels of malondialdehyde as a marker of lipid peroxidation in ischemic tissue, and the results indicate that propofol plays a role in the inhibition of neuronal death induced by brain ischemia.
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PMID:Neuroprotective effects of propofol following global cerebral ischemia in rats. 1195 72

Acute cerebral ischemia is associated with an increased extracellular dopamine accumulation. Attenuation or prevention of excessive dopamine accumulation alleviates the cerebral ischemic damage. Propofol, an intravenous anesthetic, has been suggested to have neuroprotective properties. The effect of propofol on dopaminergic neurotransmitters is unclear. The in vivo microdialysis technique was used in this study to examine the effect of propofol on infarct size and striatal dopamine accumulation in rat model of temporary middle cerebral artery occlusion. Sixteen rats were fitted with a right striatal microdialysis probe. Ischemia was induced by inserting a 4-0 monofilament nylon suture into the middle cerebral artery. Propofol was intravenously infused in eight rats during ischemia (60 min) and reperfusion (60 min) at an average dose of 36 mg/kg/h. Control rats (n=8) received vehicle infusion. The infarct size was determined at the end of the experiment. Propofol significantly reduced infarct size, the median (interquatile range) value was 6.84% (7.68%), significantly lower than that in the control group, which was 28.04% (32.28%) (p<0.01). The middle cerebral artery occlusion significantly increased dopamine accumulation in the striatum. Propofol infusion significantly attenuated this middle cerebral artery occlusion-induced dopamine accumulation. The data demonstrate that propofol, when administered during ischemia and reperfusion, provides neuroprotection in our middle cerebral artery occlusion in rat model. The data also suggest that attenuated dopamine accumulation may be one of the factors contributing to the neuroprotective property of propofol.
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PMID:Propofol reduces infarct size and striatal dopamine accumulation following transient middle cerebral artery occlusion: a microdialysis study. 1235 71

The purpose of this study was to investigate whether propofol has a neuroprotective effect on the fetal brain after intrauterine ischemia-reperfusion (I/R) injury in the rat fetus. Fetal brain ischemia was induced by clamping the utero-ovarian artery bilaterally for 30 min and reperfusion was achieved by removing the clamps for 2 h. A 40-mg/kg single dose of propofol was administered intraperitoneally 15 min before I/R injury. Lipid peroxidation in the brain tissue was determined as the concentration of thiobarbituric acid reactive substances (TBARS) for each fetal rat. Results showed that lipid peroxidation byproducts increased after I/R injury. Maternal treatment with propofol reduced TBARS compared to the I/R group. Propofol has been shown to have neuroprotective effects in intrauterine I/R-induced fetal brain damage in rats.
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PMID:Maternal treatment with propofol attenuates lipid peroxidation after transient intrauterine ischemia in the neonatal rat brain. 1470 28

The neuroprotective potency of anesthetics such as propofol compared to mild hypothermia remains undefined. Therefore, we determined whether propofol at two clinically relevant concentrations is as effective as mild hypothermia in preventing delayed neuron death in hippocampal slice cultures (HSC). Survival of neurons was assessed 2 and 3 days after 1 h oxygen and glucose deprivation (OGD) either at 37 degrees C (with or without 10 or 100 microM propofol) or at an average temperature of 35 degrees C during OGD (mild hypothermia). Cell death in CA1, CA3, and dentate neurons in each slice was measured with propidium iodide fluorescence. Mild hypothermia eliminated death in CA1, CA3, and dentate neurons but propofol protected dentate neurons only at a concentration of 10 microM; the more ischemia vulnerable CA1 and CA3 neurons were not protected by either 10 microM or 100 microM propofol. In slice cultures, the toxicity of 100 muM N-methyl-D-aspartate (NMDA), 500 microM glutamate, and 20 microM alpha-amino-5-methyl-4-isoxazole propionic acid (AMPA) was not reduced by 100 microM propofol. Because propofol neuroprotection may involve gamma-aminobutyric acid (GABA)-mediated indirect inhibition of glutamate receptors (GluRs), the effects of propofol on GluR activity (calcium influx induced by GluR agonists) were studied in CA1 neurons in HSC, in isolated CA1 neurons, and in cortical brain slices. Propofol (100 and 200 microM, approximate burst suppression concentrations) decreased glutamate-mediated [Ca2+]i increases (Delta[Ca2+]i) responses by 25%-35% in isolated CA1 neurons and reduced glutamate and NMDA Delta[Ca2+]i in acute and cultured hippocampal slices by 35%-50%. In both CA1 neurons and cortical slices, blocking GABAA receptors with picrotoxin reduced the inhibition of GluRs substantially. We conclude that mild hypothermia, but not propofol, protects CA1 and CA3 neurons in hippocampal slice cultures subjected to oxygen and glucose deprivation. Propofol was not neuroprotective at concentrations that reduce glutamate and NMDA receptor responses in cortical and hippocampal neurons.
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PMID:Mild hypothermia, but not propofol, is neuroprotective in organotypic hippocampal cultures. 1561 81


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