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

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

Failure of microvascular re-perfusion, no reflow, of the brain after a period of ischemia has been proposed as the etiology of the cerebral dysfunction frequently seen in patients after resuscitation from hemorrhagic shock. For this investigation rats were stressed by subjecting them to a period of combined hypoxia and hypotension followed by resuscitation. Micro-oxygen electrodes measured brain oxygen tension, thus allowing an assessment of the distribution of cerebral blood flow, during stress and after resuscitation. After resuscitation, a hyperemic response was noted, followed by gradual return of some areas of the brain to normal perfusion, while other areas remained hyperemic for at least 2 hours post-resuscitation. On the basis of these results there appears to be no support for the no-reflow hypothesis. These data imply that therapeutic modalities aimed at increasing cerebral blood flow and oxygenation in the post-resuscitation period are insufficient in themselves for improved survival of patients sustaining a hypotensive, hypoxic episode.
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PMID:Effects of hypoxia and hypotension on oxygen delivery in the brain. 49 Jul 43

Clinical use of profound hypothermia and total circulatory arrest has been accompanied by occasional postoperative neurological abnormalities. In a series of infant baboons, surface cooling to 32 degrees C (brain) followed by perfusion cooling by cardiopulmonary bypass with a membrane oxygenator and heat exchanger to 18 degrees C was carried out, after which the circulation was stopped for 30 minutes. The animal was rewarmed to 35 degrees C. Marked alterations in the regional cerebral circulation were observed during perfusion cooling and rewarming. Regional cerebral ischemia was negatively correlated with jugular outflow (total cerebral blood flow) during rewarming, while regional hyperemia showed positive correlation both following perfusion cooling and after rewarming. A higher degree of ischemia in brain ischemic samples was found during rewarming than during cooling. These alterations in regional cerebral perfusion were associated with lactacidosis and hyperglycemia after rewarming, and may be considered potentially responsible for posthypothermic cerebral dysfunction.
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PMID:Cerebral effects of profound hypothermia (18 degrees C) and circulatory arrest. 115 33

Using autoradiography, we have measured the in vivo binding of [3H]nimodipine to brain in a rat model of reversible cerebral ischemia. Ischemia was induced by simultaneous occlusion of the middle cerebral artery (MCA) and ipsilateral common carotid artery by microaneurysm clips. Rats were studied after 15 min of ischemia (ischemic group) or after 45 min of reperfusion following 15 min of ischemia (reperfused group). Regional cerebral blood flow (CBF) was determined autoradiographically using [14C]iodoantipyrine in both ischemic (n = 6) and reperfused (n = 6) groups. During ischemia blood flow in the territory of the MCA was depressed and recovered to normal only in the distal territory of the MCA following reperfusion. [3H]Nimodipine binding in the ischemic group (n = 12) was elevated in ischemic brain regions and declined significantly (p < 0.01) in these regions in the reperfused group (n = 11). The ratio of the volume of cortex showing increased binding to the total volume of the forebrain was 0.113 +/- 0.025 (mean +/- SD) in the ischemic group and declined to 0.080 +/- 0.027 following reperfusion (p < 0.005). In general, infarct was only observed in regions showing persistent elevation of nimodipine binding following reperfusion as determined by histology performed in a separate group of rats (n = 8) after 24 h of reperfusion. We conclude that increased nimodipine binding to ischemic tissue is initially reversible with prompt reestablishment of CBF and is a sensitive indicator of early and reversible ischemia-induced cerebral dysfunction.
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PMID:Reversibility of nimodipine binding to brain in transient cerebral ischemia. 140 19

The feline infusion model of brain edema was used to evaluate the role of bradykinin in the etiology and pathophysiology of vasogenic brain edema. Bradykinin (3 or 90 ug in 600 microL saline) did not alter normocapnic regional cerebral blood flow (rCBF) nor induce specific changes in either the somatosensory (SEP) or motor (MEP) evoked potentials. The mean increases in ICP (from 4.5 to 16.1 mmHg) and peri-infusion white matter water content (from 69.4 to 79.8 ml/100 g tissue), mean decrease in lumped craniospinal compliance (from 0.040 to 0.014 ml/mmHg) and local histological changes were all similar to those after 600 microL saline infusion. The interstitial bradykinin infusion caused focal blood-brain-barrier (BBB) opening to Evans Blue dye and was chemotaxic for granulocytes. After the infusion there was a global loss of rCBF CO2 reactivity but there was no ischemia at normocapnia. These results show that bradykinin in brain edema fluid, at concentrations greater than those found in neuropathological conditions, can open the BBB of normal cerebral parenchymal capillaries and cause vascular dysregulation. In neuropathological conditions bradykinin may therefore potentiate formation of vasogenic brain edema but does not contribute to perilesional brain dysfunction.
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PMID:The role of bradykinin in the etiology of vasogenic brain edema and perilesional brain dysfunction. 159 96

Effects of S-adenosyl-L-methionine on Ca accumulation as well as the changes of electrolytes contents and glucose metabolism after transient ischemia were investigated. In the 4-vessel occlusion model of rats, brain Ca content increased to 200-250% of that in sham operated rats 1 day after 60 min transient ischemia. The change in the striatum was more severe than that in the cortex or hippocampus. Na content increased and K content decreased, and glucose, pyruvate and lactate contents increased significantly in the striatum 1 day after transient ischemia. SAM (100 mg/kg, i.p.) was injected at the end of occlusion and every hour for 5 hr thereafter. Treatment with SAM reduced Ca accumulation, decrease of K, and increase of lactate and pyruvate in the striatum significantly. The present results suggest that the inhibition of Ca accumulation might partly explain the beneficial effects of SAM on the cerebral dysfunction following ischemia.
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PMID:S-adenosyl-L-methionine improves the changes of calcium content and glucose metabolism after transient ischemia in the rat. 272 73

Serial measurements of a marker of brain ischemia, creatine kinase isoenzyme BB, were performed in arterial and internal jugular venous blood from 20 infants younger than 1 year of age before and during the first 20 hours after deep hypothermic total circulatory arrest procedures. A two-site monoclonal method was used, and the results were analyzed in relation to age, size, type of cardiac lesion, hemoglobin level, blood glucose level, pH, and duration of the total circulatory arrest. The creatine kinase BB concentrations increased after the arrest, more so in venous than in arterial blood, from 3.2 +/- 0.5 ng/ml to 17.5 +/- 4.5 in arterial blood and from 3.5 +/- 0.5 ng/ml to 18.1 +/- 5.8 in venous blood. Arterial-venous concentration differences correlated with venous concentrations (r = 0.92, p less than 0.01). The duration of the arrest correlated with creatine kinase BB concentrations during reperfusion with correlation coefficients between 0.50 to 0.90 depending of what sequence of the 20-hour sampling period was analyzed. The best correlation was obtained during the first 4 hours of reperfusion. Age, size of the child, and preoperative cyanosis correlated with postoperative creatine kinase BB but were less important than the arrest time, blood glucose level (r = 0.62, p less than 0.01), pH (r = -0.78, p less than 0.01), and hemoglobin level (r = 0.76, p less than 0.01) during reperfusion. It is suggested that a different control of blood glucose level and pH during reperfusion may be of importance to reduce biochemical signs of cerebral dysfunction after deep hypothermic total circulatory arrest procedures.
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PMID:Elective deep hypothermia with total circulatory arrest: changes in plasma creatine kinase BB, blood glucose, and clinical variables. 291 Nov 96

The most important premise for a successful surgical treatment of epilepsy lies in an accurate diagnosis of the focus location. The hitherto employed methods for this purpose are meticulous analysis of seizure contents and scalp EEGs, but spatial localization of the focus sites is far beyond the capacity of these diagnostic measures. With the advent of positron emission tomography (PET), in vivo observation of human brain metabolism has become possible. The indices of brain metabolism such as cerebral blood flow (rCBF), cerebral metabolic rate of glucose or oxygen (CMRG, CMRO2) are noninvasively measured by PET offering priceless information for diagnosing brain dysfunction such as ischemia, degeneration, psychosis, or epilepsy. Kuhl et al. first employed PET in assessment of epileptic foci, in which interictal foci were beautifully detected as discrete "hypometabolic zones". Many researchers have confirmed this invaluable finding, and nowadays PET seems to have acquired the citizenship as one of the most capable diagnostic measures in focus localization. We have hitherto applied PET study in 72 epileptic patients. The main contents of their seizures consists of complex partial in 32, elementary partial in 32, generalized in 6, and others in 3 cases. We administered perorally 10 mCi glucose labeled with C11 produced in the JSW Baby Cyclotron for the study of CMRG. The continuous inhalation method of CO2 and O2 labeled with O15 produced in the same cyclotron was also employed for measurement of rCBF and CMRO2. In both studies, epileptic foci were shown as well demarcated hypometabolic zones with decreased CMRG, rCBF or CMRO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Surgical treatment of convexity focal epilepsy--based on diagnosis of PET and subdural EEG]. 310 88

The effects of cytidine 5'-diphosphocholine (CDP-choline) on neurologic deficits and cerebral glucose metabolism were studied in a rat model of transient cerebral ischemia. Cerebral ischemia was induced by occluding both common carotid arteries for 20 or 30 minutes 24 hours after the vertebral arteries were permanently occluded by electrocautery. CDP-choline was administered intraperitoneally twice daily for 4 days after reestablishing carotid blood flow. CDP-choline at two dosages (50 and 250 mg/kg) shortened the time required for recovery of spontaneous motor activity in a dose-related manner; recovery time was measured early after reperfusion. Neurologic signs were observed for 10 days. High-dose CDP-choline improved neurologic signs in the rats within 20-30 minutes of ischemia. When cerebral glucose metabolism was assessed on Day 4, increases in the levels of glucose and pyruvate were accompanied by decreases in the synthesis of labeled acetylcholine from uniformly labeled [14C]glucose measured in the cerebral cortex of rats with 30 minutes of ischemia. High-dose CDP-choline also attenuated changes in these variables. CDP-[1,2-14C]choline injected intravenously 10 minutes after reperfusion was used for membrane lipid biosynthesis. These results indicate that CDP-choline has beneficial effects on brain dysfunction induced by cerebral ischemia, which may be due in part to the restorative effects of CDP-choline on disturbed cerebral glucose metabolism, probably by stimulating phospholipid biosynthesis.
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PMID:Effects of CDP-choline on neurologic deficits and cerebral glucose metabolism in a rat model of cerebral ischemia. 334 38

The recovery of the EEG and somatosensory evoked responses (SER) as compared with recovery of the cerebral energy state was studied in rats during recirculation following different degrees of brain ischemia with varying tissue lactic acidosis. Reversible complete and incomplete ischemia was induced either by increasing the intracranial pressure (compression ischemia) or by carotid artery clamping combined with arterial hypotension. In incomplete ischemia the degree of tissue lactic acidosis was varied by manipulations of blood and brain glucose levels. Animals with an increase in brain lactate to about 25 mumol X g-1 (whole brain wet weight) during ischemia showed persistent failure of both cerebral energy metabolism and neurophysiologic restitution during the recirculation phase; if less than 20 mumol X g-1 metabolic recovery was almost complete. Despite a similar restitution of tissue energy metabolism in these animals, neurophysiologic recovery was inversely proportional to brain lactate concentrations during ischemia. At similar levels of ischemic tissue lactic acidosis, and despite a similar recovery of cortical energy state, the neurophysiologic restitution was clearly inferior after complete ischemia to that following incomplete ischemia. Three conclusions were drawn: (i) neurophysiologic variables were more sensitive indicators of postischemic persistent cerebral dysfunction than the cerebral energy state; (ii) the degree to which lactate accumulated in the ischemic brain influenced neurophysiologic restitution even if concentrations critical for metabolic recovery were not attained; and (iii) incomplete ischemia was less harmful than complete ischemia provided that tissue lactic acidosis was not excessive.
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PMID:Effect of different degrees of brain ischemia and tissue lactic acidosis on the short-term recovery of neurophysiologic and metabolic variables. 397 49


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