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

Platelet-activating factor has been implicated in a variety of disease processes including ischemic brain injury and endotoxic shock, but its effects on cerebral blood flow (CBF) and metabolism in normal brain have not been described. The effects of platelet-activating factor on global CBF (hydrogen clearance) and the global cerebral metabolic rate for oxygen (CMRO2) were studied in halothane-N2O anesthetized Wistar rats. Hexadecyl-platelet-activating factor infused into the right carotid artery (67 pmol/min) for 60 min decreased mean arterial pressure (MAP) from 122 +/- 4 (x +/- SEM) to 77 +/- 6 mm Hg and CBF from 159 +/- 12 to 116 +/- 14 ml/100 g/min (p less than 0.002). In contrast, CMRO2 increased from 9.7 +/- 0.9 to 11.7 +/- 1.1 ml/100 g/min after 15 min (p less than 0.05). In controls rendered similarly hypotensive by blood withdrawal and infused with the platelet-activating factor vehicle, CMRO2 was unchanged, whereas CBF transiently decreased then returned to baseline at 60 min. These cerebrovascular and cerebrometabolic effects of PAF are reminiscent of and may be relevant to hypoperfusion and hypermetabolism observed after global brain ischemia and in endotoxic shock.
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PMID:Cerebrovascular and cerebrometabolic effects of intracarotid infused platelet-activating factor in rats. 339 15

Using rats in which incomplete cerebral ischemia was induced, the authors evaluated the effects of halothane (H) and isoflurane (I) on neurologic outcome compared to nitrous oxide (N2O) controls. Incomplete cerebral ischemia was produced by right carotid artery occlusion combined with hemorrhagic hypotension. Neurologic outcome was evaluated using a graded deficit score from 0 to 5 (0 = normal, 5 = death associated with stroke). Two levels of cerebral ischemia were tested. At moderate ischemia with hypotension of 30 mmHg, an FIO2 of 0.3, and ischemic periods of 30 or 45 min, N2O produced a deficit of 4.7-5.0 and a mortality rate of 90-100%. In contrast, halothane (1 MAC) and isoflurane (1 MAC) resulted in similar deficit scores (H = 1.1-1.8, I = 1.4-1.6) and mortality rates (H = 17-30%, I = 17-20%). Cerebral blood flow (CBF) measured with radioactive microspheres showed a 60-65% decrease in the ischemic hemisphere at this level of hypotension. With severe ischemia with hypotension = 25 mmHg, FIO2 = 0.2, and a 30-min period of ischemia, deficit scores increased to 3.0 and 3.9 with 1 MAC halothane and 1 MAC isoflurane, respectively. Mortality rates also increased to 40% with halothane and 70% with isoflurane. Increasing the concentration of halothane or isoflurane to 2 MAC did not significantly improve outcome. Brain histology demonstrated extensive neuronal damage in striatal, hippocampal, and neocortical regions of N2O control treated rats, and less damage with little difference between H- and I-treated rats at each level of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neurologic outcome in rats following incomplete cerebral ischemia during halothane, isoflurane, or N2O. 340 68

Isoflurane has protective properties during experimental global brain ischemia or hypoxia. However, this has not been evaluated in the more common case of focal ischemia, e.g., as caused by middle cerebral artery occlusion (MCAO). The authors therefore compared the effects of isoflurane, thiopental, and N2O/fentanyl anesthesia on neurologic and neuropathologic outcome in baboons subjected to 6 h of transorbital left MCAO. Prior to MCAO, animals were assigned to one of three groups: Group 1 (n = 7) received isoflurane (in O2/air) in concentrations sufficient to maintain deep burst suppression on the EEG (2.0% +/- 0.5% inspired, mean +/- SD); group 2 (n = 6) received thiopental (O2/air) in doses adequate to maintain similar EEG suppression (3.6 +/- 0.7 g total); and group 3 (n = 6) received 60% N2O/40% O2 and fentanyl (25 micrograms/kg load, 3 micrograms X kg-1 X h-1 infusion). Efforts were made to keep mean arterial pressure (MABP) between approximately 80 and 100 mmHg, using nitroprusside/hydralazine or phenylephrine/metaraminol, with PaCO2 at approximately 30 mmHg. The selected anesthetic was established 45 min before MCAO, was maintained until 1 h after clip removal, and in decreasing concentrations for 5 h. Neurologic status was scored for 7 days and formalin-fixed brains were later sectioned for determination of infarction volume. Six of seven group 1 (isoflurane) animals were hemiplegic, and 7/7 had verified infarctions. By contrast, 4 of 6 group 2 (thiopental) animals were normal, with 2/6 having infarctions. Outcome in group 3 (N2O/fentanyl) was intermediate between groups 1 and 2 (3/6 hemiplegic, 4/6 with infarctions). Differences in the infarction rates between groups 1 and 2 was significant (P less than 0.05), while a similar comparison of neurologic outcome scores achieved a P value of 0.055. Infarctions in group 1 were more hemorrhagic in character than in group 3 (groups 1 and 2 could not be meaningfully compared). These results must be considered in light of differences in MABP during the occlusion period; MABP in group 1 was approximately 80 mm Hg in spite of vasopressor use, while that in group 2 was approximately 100 mmHg (in spite of vasodilators). Nevertheless, they fail to demonstrate any protective value of isoflurane anesthesia, at least when compared with thiopental.
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PMID:A comparison of the cerebral protective effects of isoflurane and barbiturates during temporary focal ischemia in primates. 356 10

Coronary air embolism (CAE) can occur after heart surgery whenever air is present in the left heart or proximal aorta. When CAE occurs, its sequelae can range from electrocardiographic changes of ischemia to severe myocardial dysfunction and cardiac arrest. Since N2O has been shown to have detrimental effects in the presence of coronary obstructions, as well as the tendency to enlarge air emboli, the authors tested the hypotheses that N2O would enhance the deleterious effects of CAE, and that discontinuing N2O at the time of CAE would minimize those effects. The effects of ventilation with and without N2O on the cardiac insult due to left anterior descending CAE (0.02 ml.kg-1) were studied in 27 swine. Global cardiovascular changes that occurred after CAE included decreases in cardiac output, systemic arterial and coronary perfusion pressure, and LV dP/dt, as well as increases in LVEDP. These parameters returned towards baseline over time when N2O was discontinued at the time of CAE. Maintenance of N2O in the inspired gas after CAE occurred was uniformly fatal within 2-4 min in this model. Regional myocardial ischemia was significantly greater in animals receiving N2O, as documented by: 1) a greater incidence of elevations of epicardial ST-segments exceeding 3 mm from baseline in embolized and non-embolized coronary artery distributions, 2) a greater incidence of dysrhythmias (greater than 6 PVCs.min-1), 3) longer duration of depression of coronary blood flow, 4) longer duration of post-ischemic coronary hyperemia, and 5) larger decreases with less recovery over time of regional myocardial lactate extraction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of nitrous oxide on coronary perfusion after coronary air embolism. 368 38

A prospective evaluation of regional cerebral blood flow (rCBF) (ipsilateral middle cerebral artery distribution) was determined using a 133Xe clearance technique in 31 ASA P.S. II-III patients anesthetized with isoflurane-50% N2O in O2 for carotid endarterectomy. Each patient was monitored with 16-channel EEG throughout anesthesia and surgery. Critical rCBF was defined as that flow below which EEG signs of ischemia occurred. Critical rCBF (T1/2 method of analysis) was less than 10 ml X 100 g-1 X min-1 (mean +/- SE 5.9 +/- 1.2) in the six patients in whom transient EEG changes occurred at the time of temporary surgical carotid artery occlusion. No EEG changes occurred with occlusion in the other 25 patients; mean (+/- SE) occlusion rCBF in this group was 18.9 +/- 1.3 ml X 100 g-1 X min-1 (P less than 0.001). Preocclusion flows were not significantly different in the two groups. Critical rCBF during isoflurane anesthesia was less than that previously determined during halothane anesthesia (18-20 ml X 100 g-1 X min-1), and is compatible with the effects of isoflurane on CMRO2 and CBF.
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PMID:Correlation of regional cerebral blood flow (rCBF) with EEG changes during isoflurane anesthesia for carotid endarterectomy: critical rCBF. 382 93

A review of current techniques and results of monitoring spinal cord function by the intraoperative testing of somatosensory evoked potentials is given. The criteria for an ideal monitoring method are defined: (1) potential alterations occur before the lesion is irreversible, (2) monitoring itself does not harm the patient, (3) there are no false-positive or false-negative results, (4) warning criteria are defined by objective and quantifiable parameters. In recording and stimulation, two different approaches are applied: cortical or spinal recording and peripheral or spinal stimulation. Spinal stimulation techniques are considered more invasive, but an averaged potential is obtained quicker and more reliably by spinal methods. Failure rates in establishing useful monitoring procedures vary between 2.85 and 5%. The N2O-analgesic-relaxant-type of anesthesia is recommended. A precise definition of criteria indicating spinal cord damage has been difficult because of the natural variability of intraoperative evoked potentials. Wide ranges of physiologic, anesthesiologic, and technical and surgical factors have been found to influence intraoperative potential monitoring adversely. The so-called warning criteria drawn from evoked potential changes have so far been set arbitrarily: amplitude reductions of 30-50% for several recordings or at least 15 minutes have mostly been used. It has become clear, however, that warning criteria should be different for healthy or impaired spinal cord function and for cortical and spinal recordings. The value of a lesion-specific spinal cord potential for monitoring remains to be clarified. SEPs are sensitive for demonstrating ischemic changes to the spinal cord, but the limited experience with these lesions does not allow firm conclusions regarding the reversibility of clinical and evoked potential changes in spinal cord ischemia in man. The limited experience with multilevel recording, i.e., simultaneously recording at spinal and cortical level, indicates that epidural recordings are less variable and less failure-prone than cortical recording. Simultaneous multilevel recording also gives more information and allows easier recognition of false-positive or false-negative results. Poor preoperative SEP nearly always preclude useful monitoring. The results obtained so far point out areas where further development is necessary in order to increase the efficacy of this method. Major unsolved problems are (1) definition of warning criteria, (2) incidence of false-positive and false-negative findings, and (3) improvement of data acquisition.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Spinal cord monitoring: current status and new developments. 391 21

The influence of a new eburnamenine derivative RU 24722 [(3 beta, 14 alpha, 16 alpha)-(+/-)-14,15-dihydro-20,21-dinoreburnamenin -14-ol] on post-ischemic EEG recovery was studied in N2O anesthetized rats subjected to 1 min of global-compression cerebral ischemia. RU 24722 was compared with vincamine, dihydroergotoxine mesylate and nicergoline. Treatment with RU 24722 (2 mg/kg i.v.) significantly decreased the EEG recovery time and increased the electrocortical activity during the first phase of the post-ischemic recovery. Vincamine (2 mg/kg i.v.), dihydroergotoxine mesylate (0.5 mg/kg i.v.) and nicergoline (0.5 mg/kg i.v.) were devoid of activity. In an attempt to elucidate its mechanism of action, the influence of RU 24722 on changes in the cerebral metabolic energy reserves was studied in mouse brain after different periods of decapitation ischemia. The changes occurring during the first 10 s of ischemia were used to calculate the baseline cerebral metabolic rate (CMR). The activity of RU 24722 was compared with that of vincamine and pentobarbital. RU 24722 (10 mg/kg i.p.) significantly retarded glucose, phosphocreatine and adenosine triphosphate utilisation and lactate production. Vincamine (10 mg/kg i.p.) had no effect on cerebral energy substrates. Pentobarbital (100 mg/kg i.p.) markedly increased the tissue concentration of glucose and phosphocreatine and decreased lactate levels before and after ischemia. The improvement of EEG recovery suggests that RU 24722 may be therapeutically effective in cerebral insufficiency, and the decreased brain energy demand may be one of the mechanisms by which RU 24722 has a protective effect against cerebral ischemic damage.
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PMID:Effects of the new eburnamenine derivative RU 24722 on EEG recovery and cerebral energy metabolism after complete ischemia. 403 69

Cerebral blood volume, hemoglobin saturation and the cytochrome a, a3 redox state were monitored simultaneously by using three wavelengths of light in the near infrared portion of the spectrum for transillumination of the intact skull of rats. The changes in these parameters following incomplete cerebral ischemia were assessed in Wistar and Long-Evans rats submitted to carotid ligation. Another group of Wistar rats was submitted to vertebral + carotid occlusion. The experiments, performed under N2O/O2 anesthesia, showed that in all three groups carotid occlusion induced a decrease in blood volume, Hb saturation and a reduction of cyt. a, a3. However, the cytochrome redox state tended to normalize during ischemia as a consequence of higher O2 extraction from blood. The primary finding of this study was the marked hyperoxidation of cyt. a, a3 which occurred after reestablishing of the carotid blood supply, in spite of a secondary post-ischemic hypoperfusion of the brain. Although uncoupling of oxidative phosphorylation cannot be excluded the dissociation between blood supply and metabolism could well be due to ischemia-induced hypermetabolism of the central nervous tissue. In view of the marked oxidation of cyt. a, a3 during the reperfusion period as compared with the small extent of its reduction during the ischemic episode, the data also support the hypothesis that under steady state conditions in vivo, cytochrome oxidase is mainly reduced.
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PMID:Incomplete cerebral ischemia in the rat: vascular and metabolic changes as measured by infrared transillumination in vivo. 631 78

This study is a therapeutic evaluation of prolonged immobilization and controlled intermittent positive-pressure ventilation (IPPV) after global brain ischemia (GBI) in pigtailed monkeys. Sixteen min of GBI was produced with a high-pressure neck cuff, while the lungs were being continuously ventilated. Normotension was restored within 2 min postischemia (PI). The control group of 13 monkeys was weaned from IPPV 4 to 6 h PI. The treatment group of 18 animals was paralyzed and ventilated with a 50:50 nitrous oxide-oxygen mixture for 48 h PI. Intensive care was maintained for 96 h PI. In the control group, 8 of 10 animals were awake at 96 h PI compared to 7 of 11 in the treatment group. Neurologic deficit scores for the survivors in the 2 groups were also not significantly different. Histologic examination supported this conclusion. Paralysis/IPPV for 48 h post-GBI with 50% N2O facilitates control of blood gases and blood pressure, but does not improve the neurologic outcome over that achieved with only 4 to 6 h controlled ventilation.
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PMID:Prolonged immobilization and controlled ventilation do not improve outcome after global brain ischemia in monkeys. 636 55

A model is described in which transient ischemia is induced in rats anaesthetized with N2O:O2 (70:30) by bilateral carotid artery clamping combined with a lowering of mean arterial blood pressure to 50 mm Hg, the latter being achieved by bleeding, or by bleeding supplemented with administration of trimetaphan or phentolamine. By the use of intubation, muscle paralysis with suxamethonium chloride, and insertion of tail arterial and venous catheters, it was possible to induce reversible ischemia for long-term recovery studies. Autoradiographic measurements of local CBF showed that the procedure reduced CBF in neocortical areas, hippocampus, and caudoputamen to near-zero values, flow rates in a number of subcortical areas being variable. Administration of trimethaphane or phentolamine did not affect ischemic and postischemic flow rates, nor did they alter recovery of EEG and sensory-evoked responses, but trimetaphan blunted the changes in plasma concentrations of adrenaline and noradrenaline. Recovery experiments showed that 10 min of ischemia gave rise to clear signs of permanent brain damage, with a small number of animals developing postischemic seizures that led to the death of the animals in status epilepticus. After 15 min of ischemia, such alterations were more pronounced, and the majority of animals died. It is concluded that the short revival times noted are explained by the fact that the model induces near-complete ischemia, and that recovery following forebrain ischemia is critically dependent on residual flow rates during the period of ischemia.
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PMID:Models for studying long-term recovery following forebrain ischemia in the rat. 2. A 2-vessel occlusion model. 646 70


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