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Query: UMLS:C0278134 (anesthesia)
 110,339 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A new model of transient, bilateral hemispheric ischemia in the unanesthetized rat is described. During ether anesthesia the rat's vertebral arteries were electrocauterized through the alar foramina of the first cervical vertebra and reversible clasps placed loosely around the common carotid arteries. Twenty-four hr later, the awake rats were restrained and the carotid clasps tightened to produce 4-vessel occlusion. The carotid clasps were removed after 10, 20 or 30 min of 4-vessel occlusion and the animals killed by perfusion fixation 72 hr later. Rats which convulsed during the ischemic or post-ischemic period were excluded from further study. All rats subjected to 20 or 30 min of 4-vessel occlusion demonstrated ischemic neuronal damage. The H1 and paramedian hippocampus, striatum and layers 3, 5 and 6 of the posterior neocortex were the regions most frequently damaged. The advantages of this model are the ease of preparation of large numbers of animals, a high rate of predictable ischemic neuronal damage, a low incidence of seizures and the absence of anesthesia.
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PMID:A new model of bilateral hemispheric ischemia in the unanesthetized rat. 3 14

Cortical reflectance, mean arterial blood pressuees, electroencephalograms, and cortical blood flow were continuously recorded together with fluorescence of reduced pyridine nucleotides (PN) at various carbon dioxide tensions before, during, and following middle cerebral artery occlusion in 10 squirrel monkeys receiving halothane or babiturate anesthesia. Measurements were continued through a nitrogen breathing cycle and to death produced by anoxia. The anesthetic agent produced no detectable differences in PN fluorescence in cerebral tissue during ischemia and anoxia. The known cerebral protective action of barbiturates is apparently unrelated to the intracellular redox state.
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PMID:Intracellular redox states under halothane and barbiturate anesthesia in normal, ischemic, and anoxic monkey brain. 3 37

Hemorrhage to a mean arterial pressure of 41 mm. Hg in ten dogs decreased Heidenhain pouch blood flow to 6 ml. per minute and aminopyrine clearance to 0.93 ml. per minute. Pouch oxygen consumption fell from 1.47 to 0.74 ml./min.-100 Gm. and total body oxygen consumption remained unchanged. Net ion fluxes during shock and reinfusion did not change significantly from control values of minus 89.8 muGq./30 min.-100 cm.-2 for H-+ and 88.6 muEq./30 min.-100 cm-2 for Na-+. However, PD decreased from 54 to 24 mv. in parallel with a fall in net Cl-minus flux from 56.8 to minus 11.7 muEq./30 min.-100 cm-2. Nine of ten pouches subjected to shock and instilled acid test solution (ATS) developed superficial mucosal erosions. No ulcerations were found in either seven control dogs (anesthesia + ATS) or in three dogs subjected to shock without ATS. Acid appears to be of prime importance in the production of stress ulcers during or following ischemia, even though there is no increase in mucosal ionic permeability.
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PMID:The role of acid and ischemia in production of stress ulcers during canine hemorrhagic shock. 23 95

Fifteen patients were studied to detect unrecognized intraoperative ischemia or necrosis in perioperative myocardial infarction (MI) associated with coronary bypass. Simultaneous arterial and coronary sinus blood samples were analyzed for lactate and both total and MB-CPK. Coronary sinus flow measurements were done coincident with sampling in seven patients. Five had perioperative MI diagnosed by positive pyrophosphate scan and electrocardiogram. Although normal initially (mean 19 +/- 5.0%), lactate extraction after thoracotomy, before aortic cross-clamping, became abnormal in 12 patients with more pronounced abnormality in those with perioperative MI (-19 +/- 9.0%). Net efflux of lactate was higher in perioperative MI (mean 0.6 +/- 0.2 vs 0.016 +/- 0.04 mM/L) than in non-MI patients. All patients had detectable total and MB-CPK (mean 295 and 31 IU/L, respectively) and all those with coronary disease had a positive arterial-coronary sinus gradient for MB-CPK (mean 9 IU/L). Perioperative MI patients had a higher gradient than non-MI patients (mean 25 vs 2 IU/L) and with one exception that gradient exceeded 5-7 IU/L. It is concluded that severe ischemia before aortic cross-clamping precedes perioperative MI and may contribute to release of CPK into coronary sinus blood. Improvement in the techniques of anesthesia and intraoperative myocardial preservation are suggested.
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PMID:Coronary sinus blood flow and sampling for detection of unrecognized myocardial ischemia and injury. 30 99

The relationship between long-term propranolol hydrochloride therapy and subsequent coronary bypass operation was prospectively investigated in 119 patients who were grouped three ways: propranolol therapy continued in full dosage to operation (group A), propranolol therapy discontinued or tapered 24 to 72 hours preoperatively (group B), and no preoperative propranolol therapy (control group). During preoperative hospitalization, one patient in each group A and the control group suffered an increase in anginal symptoms compared with 15 patients in group B, three of whom also had new ventricular arrhythmias. During anesthesia up to the period of cardiopulmonary bypass, 26% of group A patients showed signs of ischemia (eg, ST segment deviation or ventricular arrhythmias) as compared with 51% of the control group and 70% of group B. Hypotension and bradycardia were not more common in group A patients. No differences among groups were noted in case of emergence from bypass, need for cardiac stimulants, or mortality.
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PMID:Preoperative propranolol therapy and aortocoronary bypass operation. 30 9

Cerebral ischemia was induced in normothermic, artificially ventilated rats, anesthetized with 70% N2O or 150 mg/kg of phenobarbitone, by bilateral occlusion of the common carotid arteries and by simultaneous depression of the mean arterial blood pressure to 50 mm Hg. The levels of tyrosine, dopamine (DA), noradrenaline (NA), tryptophan, 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were measured after 15 min of ischemia as well as after 30 min of recirculation. In separate experiments (70% N2O) the rate of accumulation of DOPA and 5-hydroxytryptophan (5-HTP) was determined in three different brain regions (striatum, limbic forebrain and hemispheres) during recirculation. During ischemia, the monoamine pattern was unaffected. Following recirculation, increases in DA, 5-HIAA, tyrosine and tryptophan were found irrespective of the type of anesthesia used. Pronounced postischemic decreases in NA and 5-HT were observed in animals anesthetized with nitrous oxide but not in those given phenobarbitone. During recirculation the rate of tyrosine hydroxylation increased in all three brain regions while tryptophan hydroxylation was reduced. It is tentatively concluded that following transient, global cerebral ischemia, neuronal activity is low or eliminated in dopaminergic and serotoninergic neurons and high in noradrenergic neurons.
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PMID:Influence of transient ischemia on monoamine metabolism in the rat brain during nitrous oxide and phenobarbitone anaesthesia. 30 81

71 patients undergo myocardial revascularisation for Prinzmetal's angina; among them, 50 p. cent are operated upon in emergency according to three ways of anaesthesia: neuroleptanalgesia, analgesic anaesthesia, combined anaesthesia. The authors lay stress on the importance of per- and post-operative complications: electrocardiographic ischemia in 22 p. cent of the cases, severe ventricular excitability perturbations were observed in 21 p. cent, myocardial necrosis in 14 p. cent, cardiovascular collapse in 21 p. cent and hypertensions in 22 p cent. These complications are often associated. In the discussion, the authors underline anesthetic induction as a cause of Prinzmetal's angina in 50 p. cent of the cases. They put the accent on the severity of peroperative crisis followed in 50 p. cent of the cases by serious ventricular excitability perturbations. In 25 p. cent of the cases myocardial necrosis is a complication of the spasm of a coronary artery. In this field, posterior necrosis are more frequent and correspond to the spasm of the right coronary artery. All the patients of this series, except one, develop necrosis in the spastic area (by-passed or not). Per-operative hypertension has no incidence on the occurrence of post-operative complications. Lastly, continuous per-operative infusions of nitroglycerine has been performed in several patients in order to reduce morbidity of this type of surgery.
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PMID:[Prinzmetal's angina during myocardial revascularisation. Cardiovascular complications in 71 patients (author's transl)]. 31 82

Time-compressed Fourier analysis of the electroencephalogram has proven to be a useful analytical procedure during anesthesia and surgery which simplifies data interpretation by presenting the EEG in a time-compressed frequency domain rather than the conventional time domain. This method of data analysis graphically accentuates the electroencephalographic correlates of ischemia-induced cerebral dysfunction and other cerebral oxygen consumption abnormalities. The ability to accentuate trends in frequency and power is derived from sequential plotting of spectra to produce a graph with three dimensional axes of frequency, time, and power. In carotid endarterectomies the system has proven more useful than the conventional EEG in assessing the need for a vascular shunt to maintain internal carotid flow during endarterectomy. In open-heart surgery time-compressed EEG spectral analysis has allowed early recognition of cerebral ischemia resulting from arterial hypotension and venous hypertension. Five cases are presented which demonstrate the ability of our system to reflect developing cerebral ischemia.
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PMID:Monitoring of cerebral perfusion during anesthesia by time-compressed Fourier analysis of the electroencephalogram. 32 37

In 22 elderly patients haemodynamic alterations after epidural anaesthesia with Carticain 2% (Ultracain) with epinephrine (1:200 000) were compared to those after Lidocaine 2% with epinephrine. There were no differences to be found in these agents, and a less pronounced depressing effect of Carticain on circulation could not be confirmed. Unlike young people elderly patients only develop slight and short rises of heart rate and cardiac output after epidural anaesthesia, which are not sufficient to compensate for the distinct fall of mean arterial pressure up to the 15th minute. In our study mean arterial pressure decreased to critical values which might lead to cerebral and coronary ischemia in these patients. Adequate prophylactic and therapeutic measures are discussed.
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PMID:[Haemodynamic alterations after epidural anaesthesia in geriatric patients (author's transl)]. 41 59

The capacity of delayed barbiturate administration to limit brain damage after unilateralcerebral ischemia was examined histologically in gerbils. The right common carotid artery was occluded in 50 animals under brief (3-minute) halothane anesthesia; 18 animals (36%) developed motor abnormalities consistent with stroke. The arterial clasps were removed after 1 hour and the abnormal animals were divided into treatment and placebo groups. Treated gerbils received sodium pentobarbital (70 mg/kg) intarperitoneally 1 hour after clasp removal and a smaller dose (50 mg/kg) 2 hours later; these animals lost corneal reflexes but retained spontaneous respiration and were kept normothermic. Animals in the placebo group received equivalent volumes of normal saline. Except for the period of anesthesia, both groups had similar postischemic motor behavior. Neuropathological examination of animals killed by perfusion-fixation after 24 hours revealed fewer pentobarbital-treated animals with shift of midline structures and with ipsilateral ischemic damage (including infarction). Compared with the placebo group, there was less extensive neuronal ischemic cell change in five regions of the ipsilateral cerebral hemispheres of the pentobarbital-treated animals (p less than 0.05). The results suggest that barbiturates administered as long as 1 hour after the end of an ischemic insult can still limit brain damage.
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PMID:Delayed pentobarbital administration limits ischemic brain damage in gerbils. 42 68


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