Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the present study, the anti-edema effect of AVS [1,2-bis (nicotineamide)-propane] was evaluated using the cat MCA occlusion model with or without recirculation. In the prolonged ischemia (PI) group, cortical edema as assessed by the changes in specific gravity, developed in those cortical areas where the mean 1-CBF was less than 25-30 ml/100 g/min during MCA occlusion (4 hours). In the recirculation group (2 hours' ischemia followed by 2 hours' recirculation: RC group), the ischemic threshold for edema development was almost the same as in the PI group. In both groups, the drop in cortical specific gravity was significantly suppressed by AVS. Regarding the time-course of 1-CBF, there was no difference between the PI-AVS-treated and PI-saline-treated groups. In the RC group, however, the postischemic hypoperfusion was significantly ameliorated by AVS. Based on the present and previous data showing the antiedema effect of AVS, the mechanism of action of AVS was discussed in relation to the pathomechanism underlying ischemic brain edema. Our new concept of ischemic brain edema is briefly stated below. Related in vitro studies have shown the followings: (i) the influx of sodium not of proteins is the principal cause of ischemic brain edema: (ii) the eicosanoid synthetic capacity of the brain microvessel (MV) is increased simultaneous to edema development (iii) an elevation in the level of hydroperoxides enhances the activities of Na+, K+-ATPase as well as the arachidonate cascade of MV. These data suggest that free fatty acids and free radicals liberated following cerebral ischemia stimulate the activity of the MV-Na+, K+-ATPase, which results in increased sodium influx across the BBB. AVS was shown to scavenge hydroxyl radicals and to inhibit the stimulatory effects of a lipid hydroperoxide (15-HPAA) on the activities of Na+, K+-ATPase and the arachidonate cascade of the MV. These actions of AVS may be linked to its antiedema effect.
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PMID:[The pathomechanism underlying ischemic brain edema: the role of Na+, K+-ATPase of the brain microvessels]. 300 17

Ten minutes of complete cerebral ischemia was produced in 18 dogs by temporary ligation of the aorta and venae cavae. Dogs were randomly assigned to one of three groups. A bolus dose of 10 micrograms kg-1 nimodipine, a dihydropyridine calcium entry blocker, followed by a constant infusion of 1 microgram kg-1 min-1 was given at 15, 30, or 60 min post ischemia. Cerebral blood flow and metabolism were measured for 2 h postischemia. Delayed treatment with nimodipine ameliorated or reversed the cerebral hypoperfusion that routinely occurs after complete ischemia. In the groups treated at 15 and 30 min, CBF remained above 60 ml min-1 100 g-1. In the group treated at 60 min, there was a progressive decline in CBF to 37 ml min-1 100 g-1. Following treatment with nimodipine, CBF immediately increased and was maintained above 50 ml min-1 100 g-1 for the remainder of the study. Once treatment with nimodipine was begun, CBF was approximately double that of an untreated group. Changes in CBF reflected changes in cerebrovascular resistance. Nimodipine had no effect on cerebral metabolism. Since the postischemic hypoperfusion state is believed to contribute to the ultimate neurologic damage following complete ischemia, treatment with nimodipine, even if delayed up to 60 min, may improve the outcome.
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PMID:Delayed treatment with nimodipine improves cerebral blood flow after complete cerebral ischemia in the dog. 308 30

Effects of hypocapnia on cerebral oxygen consumption (CMRO2) and blood flow (CBF) in cerebral ischemia were studied in 19 patients. The CMRO2 did not change significantly during hypocapnia within the whole group of patients, because 10 out of 19 cases showed a decrease (p less than 0.001) and other 9 showed an increase (p less than 0.01) of CMRO2 during hypocapnia. The first 10 showed higher resting CMRO2 (p less than 0.001) and arteriovenous differences of oxygen content (AVDO2; p less than 0.02) than the other 9. However, the resting CBF and CO2 reactivity to hypocapnia were not different between them, and clinical situations were also similar. A dissociation between flow and metabolism was suggested in the first 10 with rather preserved CMRO2, while reduced metabolic demands were suggested in the other 9. Different responses of CMRO2 to hypocapnia are expected in cerebral ischemia, i.e. in cases with rather preserved CMRO2 it decreases despite an AVDO2 increase, suggesting a capability of CMRO2 to respond to CBF reduction, while it increases in cases with more decreased CMRO2, as the AVDO2 increase exceeds the CBF reduction to maintain the decreased CMRO2 for a further CBF reduction. The vascular CO2 reactivity, therefore, might be maintained to be constant between these patients.
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PMID:Effect of hypocapnia on cerebral oxygen metabolism and blood flow in ischemic cerebrovascular disorders. 311 60

The purpose of this study was to examine the effect of extracorporal collateral circulation (ECCC) between the femoral and the external artery (ECA) on the cerebral circulation, in experimentally induced ischaemia, in rabbits. The animals were divided in four groups. Seven animals (Group A) were used to determine the injection pressure (150-160 mmHg) at the ECA, necessary to achieve collateral circulation between ECA and internal carotid artery (ICA), after occlusion of ICA. Group B (8 rabbits) was the control group for establishing cerebral ischaemia (CI) by a) ligating the common carotid artery bilaterally, b) coagulating the right vertebral artery and c) exsanguinating the animal (removing 28-30 ml of blood). The induced ischaemia was studied by BP and PCO2 monitoring, CBF measurement, videomicroscopy of surface cerebral vessels, and finally macroscopic and microscopic examination of brain sections. In group C (8 animals)-moderate degree of CI-brain circulation improved in all animals after the application of the ECCC, installed at 135 min after the onset of CI. In 10 animals (group D) with severe and prolonged (225 min) CI, ECCC enhanced the brain circulation in eight animals to a variable degree.
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PMID:Improvement of cerebral circulation by extracorporal collateral between the femoral and the external carotid artery in experimentally induced ischaemia. 312 12

Cerebral rCBF, rOEF, rCMRO2, and rCBV in moyamoya disease were studied by means of positron emmission tomography (PET), using 15O as a tracer. Steady-state methods with C15O2 and 15O2 were used to obtain the functional images of rCBF, rCMRO2, and rOEF. The 15O single-inhalation method was used to obtain the rCBV image. Five children (two boys and three girls) with mean age of 11 years and eight normal volunteers with mean age of 31 years were included in the study. The symptoms of moyamoya disease were due to cerebral ischemia, such as transient ischemic attack (TIA), reversible ischemic neurological deficit (RIND), and minor stroke. The interval between the latest ictus and PET scan ranged from 3 days to 3 years 6 months. Physiological parameters (rCBF, rCMRO2 etc.) in cerebral gray matter, cerebral white matter and basal ganglia were calculated from the single functional images. Any, low density areas appearing in X-ray-CT performed just prior to the PET study were carefully excluded from the analysis. The parameters of moyamoya disease were statistically compared with normal control parameters. Though the value of rCBF was slightly higher in moyamoya disease, this difference was not statistically significant. On the other hand, in moyamoya disease rCBV increased significantly in gray matter, white matter, and basal ganglia. The ratio of CBF to CBV is considered to be the index of perfusion pressure and reciprocal of cerebral mean transit time under the normal autoregulation of CBF. This ratio was calculated and compared with the normal value for each tissue.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebral circulation and oxygen metabolism in moyamoya disease of ischemic type in children. 326 63

Cerebral hemodynamic and metabolic changes, occurring during delayed hypoperfusion following transient cerebral ischemia, and the influence of treatment with almitrine plus raubasine were studied in mongrel dogs. 10 min of transient cerebral ischemia was induced by bilateral clamping of both carotid and vertebral arteries. After declamping, the mean time necessary until cerebral venous PO2 (cvPO2) reached a value of 3.6 kPa, threshold for tissue hypoxia, was 80 min. At this time (T0), venous cerebral blood flow (vCBF) and cerebral perfusion pressure (Perf P) were below (60 and 20%, respectively) preischemic values, while cerebral vascular resistance (CVR) and oxygen and glucose extraction rates increased despite a normal cerebral oxygen consumption (CMRO2). At T0 ventilatory assistance without (control group) or with (treated group) intravenous infusion of almitrine plus raubasine was applied for 110 min. Between T0 and T110 min, 2 dogs died in the control group. During this period vCBF decreased by more than 60% in the control group while it slightly increased in the treated group. A strong decrease in Perf P (40%) and increase in CVR (140%) was observed in the control group while in the treated group Perf P and CVR slightly decreased (14 and 35%, respectively). CMRO2 decreased by 60% in the control group but remained within the normal range in the treated group. The fact that cvPO2 remained constantly below the initial value of 3.6 kPa in the control group and, on contrary, above this value in the group infused with raubasine plus almitrine indicates that the vCBF improvement leads to an increase in oxygen supply and is involved in the keeping of the adequacy between flow and metabolism. Our results support the hypothesis that the post-ischemic syndrome may play an important role in the acute prognosis of stroke. They clearly indicate that early cerebral resuscitation by infusion of almitrine plus raubasine, maintaining oxygen availability and CBF above initial thresholds, should improve the long-term neurological outcome.
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PMID:Curative effect of an almitrine-raubasine combination in the postischemic syndrome following transient cerebral ischemia in dogs. 336 2

The effect of age on outcome after induced cerebral ischemia was tested in rats. Cerebral ischemia was produced by unilateral carotid ligation and hemorrhagic hypotension to 30 mm Hg (moderate ischemia) or 25 mm Hg (severe ischemia) in young (6 month) and old (26-28 month) rats anesthetized with 1 MAC halothane. Young rats had significantly better neurologic outcomes than old rats after similar ischemic challenges. This advantage disappears, however, when the inspired oxygen tension is altered to produce similar PaO2 in both age groups during ischemia. Measures of regional CBF with radioactive microspheres showed a 70% decrease in cortical blood flow in the ischemic cerebral hemisphere in both young and old rats. Plasma glucose concentrations increased from 150 to 250 mg/100 mL during ischemia in both age groups. Histologically, the brains showed similar signs of focal ischemic damage in striatum, hippocampus, and cortex in young and old rats. These results indicate that when blood pressure and respiratory factors are controlled experimentally during ischemia, young and aged rats have similar neurologic outcomes after cerebral ischemia.
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PMID:Neurologic outcome in aged rats after incomplete cerebral ischemia. 338 41

The authors have reported on the prognostic value of continuous monitoring of somatosensory evoked potentials (SEP) in a survey of 25 patients who underwent carotid surgery. SEP recordings were correlated with the EEG, stump pressure (SP) values and clinical outcome. A non-cephalic reference was used for SEP recordings to allow the analysis of both subcortical and cortical components. During surgery the conduction time between SEP peaks relating to the subcortical components remained stable or showed minimum variations in all patients. During carotid clamping, SEP variations were observed in 9 out of 25 cases (36%). The application of an intraluminal shunt was accompanied by the return to normal values in 7 out of 9 patients. In the remaining two cases SEP abnormalities continued post-operatively and were accompanied by new neurological deficits. EEG changes during carotid clamping were associated with SEP modifications in 6 out of 7 cases, although they were not always correlated. Results confirm that SEP recordings provide useful data concerning the function of the CNS in anaesthetized patients and that, being sensitive to CBF changes, SEP monitoring acts as an indicator of cerebral ischaemia.
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PMID:Prognostic value of early somatosensory evoked potentials during carotid surgery: relationship with electroencephalogram, stump pressure and clinical outcome. 343 37

Recently lidocaine (Ld) has been reported to have beneficial effects on neural suppression caused by experimental cerebral ischemia or spinal cord injury. In this paper, the effects of Ld on brain edema, local cerebral blood flow (lCBF), and neural function in the thalamocortical and cortical structures were experimentally studied. Vasogenic brain edema was induced by exposure of the cat's cerebral surface to the air in the manner of Prados et al. The dura mater over the left cerebral hemisphere was resected, and the brain was exposed to room air for 12 hours. The animals were divided into two groups. In the control group of 31 cats, Ld was not administered. In the treated group of 8 cats, Ld (4.5 mg/kg) was given intravenously immediately after the beginning of the air-exposure and thereafter administered as a drip infusion at the rate of 2 mg/kg/hour. In the untreated group, 12 hours after exposure, the cerebral water content measured by gravimetry in the cortex, white matter and thalamus increased by approximately 1.9, 4.1, 0.7%, respectively, compared to the control values. Local CBF measured by the hydrogen clearance method decreased to about 71, 57 and 56% of the control value, respectively. The latency of the N1 component of the somatosensory evoked response (SER) was prolonged significantly 6 hours after air-exposure. The amplitude of the direct cortical response (DCR) decreased significantly 6 hours after air-exposure, and became approximately 50% of the control 12 hours after exposure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effect of lidocaine on brain edema and neural function]. 343 87

Regional CBF (rCBF) and regional cerebral blood volume (rCBV) were evaluated by N,N,N'-trimethyl-N'-(2)-hydroxy-3-methyl-5-[123I]iodobenzyl-1, 3-propanediamine-2 HCl- and 99mTC-labeled red blood cells, respectively, and single-photon emission computerized tomography (SPECT) in a patient with focal cerebral ischemia. Sequential transmission computerized tomography (TCT) and SPECT functional data were compared with clinical findings to monitor the pathophysiological events occurring in stroke. A lack of correlation between rCBF-rCBV distributions and blood-brain barrier (BBB) breakdown was found in the acute phase. In the face of more prolonged alteration of BBB, as seen by TCT enhancement, a rapid evolution of transient phenomena such as luxury perfusion was shown by SPECT studies. Follow-up of the patient demonstrated a correlation between the neurological recovery and a parallel relative improvement of the cerebral perfusion.
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PMID:Sequential assessment of regional cerebral blood flow, regional cerebral blood volume, and blood-brain barrier in focal cerebral ischemia: a case report. 348 73


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