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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study we examined the reactions of cerebral vessels to hypercapnia and hypoxia during the recovery period following cerebral ischemia. We used ventilated, lightly anesthetized rats and induced complete ischemia by CSF compression, incomplete ischemia by bilateral carotid occlusion combined with hypotension. After 15 min of ischemia and 60 min of recirculation the animals were rendered hypercapnic or hypoxic for 2-3 min and local CBF was then measured autoradiographically with 14C-iodoantipyrine. Following complete ischemia vascular CO2 responsiveness was abolished or attenuated in most structures analysed. However, there was a considerable interstructural heterogeneity. For example, in the cerebellum and the red nucleus flow rates were observed which approached values obtained in hypercapnic control animals, whereas CO2 responsiveness was abolished in several cortical areas and hippocampus. The response to CO2 following incomplete ("forebrain") ischemia varied considerably. In the cerebral cortices areas with low flow rates were often mixed with hyperemic zones, and in most structures that had very low flow rates during ischemia, CO2 responsiveness was lost or grossly attenuated. Structures that had suffered moderate or only mild ischemia had better retained or completely preserved CO2 response. The cerebrovascular reaction to hypoxia was found to be attenuated in most, but not abolished in any of the structures examined. In general, the vascular response to hypoxia was better preserved than that to hypercapnia. Reactivity was similar following complete and incomplete ischemia. As observed during hypercapnia, there were pronounced interstructural variations with considerable increases in flow rates e.g. in the substantia nigra and the cerebellum.
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PMID:Cerebral circulatory responses to hypercapnia and hypoxia in the recovery period following complete and incomplete cerebral ischemia in the rat. 641 51

Radiolabeled 15-microns microspheres were used to examine alterations in regional CBF and cerebrovascular resistance in response to changes in arterial PCO2. Flow measurements were obtained before and 1-3 and 24 h after 12 min of total cerebral ischemia. Striking sensitivity of blood flow in all areas of the central nervous system was shown to changes in arterial PCO2 between 24 and 50 mm Hg during the control nonischemic period. Following 12 min of total cerebral ischemia, cerebrovascular resistance increased, producing a decrease in regional blood flow when the important controlling variables for CBF were held constant. One to 3 h after total cerebral ischemia, the effect of variations in arterial PCO2 on cerebral blood flow was almost completely abolished. Within 24 h after total cerebral ischemia, the sensitivity of CBF to changes in PCO2 was almost completely restored, whereas the secondary severe neurologic deficit remained. Therapeutic interventions following global cerebral ischemia, designed to ameliorate the "no-reflow" phenomenon and minimize residual ischemic neurologic damage, must take into account this marked early post-ischemic reduction in sensitivity to normally potent cerebrovasodilatory influences.
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PMID:Total cerebral ischemia: effect of alterations in arterial PCO2 on cerebral microcirculation. 643 7

Repeated CBF-measurements can be performed after inhalation or intravenous injection of 133Xe. After the development of a bicompartmental model by Obrist et al. in 1975 atraumatic CBF-measurements became widely used but there were still some difficulties concerning the sensitivity of different flow-indices towards CBF changes in normals under test conditions or ischemia in stroke patients. Due to the "slippage phenomenon" mostly noncompartmental flow-indices are used for the detection of ischemic brain areas. In this study a scintillation camera, that is usually available in every nuclear medicine department, was used for atraumatic CBF-studies. A collimator consisting of hexagonal lead tubes (septa 0.2 mm thick; FWHM 1.7 cm in 10 cm) was constructed for this purpose. The obtained counting rate varied between 2432 and 9081 cps over the whole hemisphere and 116-1094 cps in regions of approximately 2.5 X 2.5 cm. In 31 patients with CVD CBF was measured with the intracarotid (i.c.) technique and 1 hour later after i.v. 133Xe-injection. Intravenous flow values were comparable to those obtained after i.c. 133Xe injection (fB X MFr = 0.904; p less than 0.001). In 12 of the used 13 regions also significant correlation coefficients were found. In order to estimate the reproducibility of the intravenous injection method CBF-measurements were performed in both hemispheres of 10 patients on two consecutive days. Highly significant correlation coefficients were found for hemispheric blood flow (r = 0.933; p less than 0.001) and temporal, frontotemporal, temporoparietal and praecentral regions, while in the high parietal, frontal and occipital region lower reporducibility was found. Normal CBF-values were obtained from 12 healthy volunteers (MF right hemisphere: 50.7 +/- 4.6 ml/100 g/min; MF left hemisphere: 50.6 +/- 4.6 ml/100 g/min). MF did not show any hyperfrontality, while F1 and the ISI gave highest flow values in frontal regions. The clinical status of 76 patients suffering from cerebral ischemia (68 with flow disturbances in one hemisphere, 8 with vertebrobasilar insufficiency) was estimated by a semiquantitative scorescale at time of admission and after an observation period lasting from 6 to 35 months. In each case CBF was measured twice: once in the subacute stage after onset of symptoms and once after the observation period. The duration of neurologic symptoms (TIA, RIND, CS) was compared to the obtained flow values. A significant relationship was found between the duration of symptoms and impairment of CBF, thus showing the prognostic value of intravenous CBF measurements.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Noninvasive measurement of cerebrovascular circulation with the scintillation camera. A neurologic nuclear medicine study]. 659 71

With the use of positron emission tomography (PET) and the 15O steady-state-[18F]fluorodeoxyglucose combined method, the local interrelationships between the cerebral metabolic rate for oxygen (CMRO2) and the cerebral metabolic rate for glucose ( CMRGlc ) were investigated in control subjects and in stroke patients. In addition to the classic in vivo autoradiographic approach, a kinetic method was used to measure CMRGlc because it was expected to be more reliable in cerebral ischemia. In control subjects local coupling between CBF, CMRO2, and CMRGlc was confirmed, and acceptable values for the CMRO2/ CMRGlc ratio were found; the latter, however, was lower in white matter than in gray. Uncoupling between CMRO2 and CMRGlc was observed in all stroke patients, suggesting that (1) enhanced anaerobic glycolysis occurred both in reperfused recent infarcts and in chronically ischemic tissue, and (2) substrates other than blood-borne glucose were being oxidized at the borders of recent infarcts. However, methodological uncertainties presently make such observations only tentative. Finally, a coupled depression of CMRO2 and CMRGlc was found in the contralateral cerebellum.
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PMID:Local interrelationships of cerebral oxygen consumption and glucose utilization in normal subjects and in ischemic stroke patients: a positron tomography study. 660 28

Ten minutes of complete cerebral ischemia was produced in 26 dogs by temporary ligation of the aorta and the venae cavae. Twenty dogs received nimodipine, a calcium entry blocker, 10 micrograms kg-1 i.v. 2 min after the ischemic period, followed by 1 microgram kg-1 min-1 for 2-3 h. Six dogs received only the solvent used for nimodipine. Fourteen dogs received nimodipine for 3 h and were subsequently evaluated neurologically up to 48 h postischemia. In the 12 other dogs, CBF and metabolism were followed for 2 h postischemia while either nimodipine or the solvent only was infused. The results were compared to previously published results for untreated dogs and dogs given nimodipine before the ischemic event. Nimodipine had the same effect on postischemic CBF whether started before or after the ischemic event, nearly doubling the flow when compared with untreated controls, whereas the solvent alone caused only a slight increase in CBF over control. By contrast, nimodipine initiated in the preischemic period significantly improved the neurologic outcome, but when initiated in the postischemic period the results were equivocal, such that the outcome was not significantly different from either the untreated group or the group in which nimodipine was initiated preischemia. Metabolic measurements did not give any indication of a specific effect of nimodipine, nor could the metabolic results be used as an indicator of neurologic outcome. The results are consistent with a beneficial effect of nimodipine following complete cerebral ischemia; however, evaluation of neurologic functional effects will require a more sensitive model.
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PMID:Cerebral blood flow and neurologic outcome when nimodipine is given after complete cerebral ischemia in the dog. 669 15

The effect of mannitol on focal cerebral ischemia in cynomolgus monkeys was studied. After the implantation of a snare ligature about the right middle cerebral artery (MCA) and of deep electrodes for measurement of cerebral blood flow, unanesthetized animals underwent 4-hour MCA occlusion. Ten monkeys were untreated, and 12 animals received mannitol (1.2 g/kg i.v.) 20 minutes after occlusion. The preocclusion and postocclusion deep hemispheric cerebral blood flows (mean CBFs) were similar in the treated and untreated groups. Occlusion produced an average decrease in flow of about 50% in both groups. In the mannitol-treated group the mean CBF of 30.0 fell to 15.8 ml/100 g/minute, and in the untreated group the mean CBF of 29.5 fell to 12.5 ml/100 g/minute. Several animals showed increased CBF after mannitol treatment, and there was an average 21% increase in CBF in the mannitol group after treatment, but this was not a statistically significant difference from the untreated group. With regard to clinical status, there was no significant difference between the mannitol group and the untreated group after MCA occlusion. In individual animals, mannitol treatment caused no significant improvement. Two weeks after occlusion, brains were evaluated for infarct size; there was no significant difference between the mannitol and the untreated groups. In this study, treatment with mannitol (1.2 g/kg) 20 minutes after MCA occlusion failed to modify significantly the mean hemispheric CBF, clinical status, or the pathological effects of 4-hour focal cerebral ischemia.
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PMID:Effect of mannitol on experimental focal ischemia in awake monkeys. 681 50

Regional cerebral blood flow (rCBF), sensory evoked potentials (SEP), and intracranial pressure (ICP) were investigated in dogs with focal cerebral ischemia produced by a silicone cylinder embolus in the middle cerebral artery (MCA) trunk as compared to that produced by trapping the same vessel. These variables were measured at intervals of 1 hour for a period of 6 hours after MCA occlusion. In the embolized animals, rCBF decreased most extensively at the basal ganglia, from a control level of 53.9 +/- 3.9 (mean +/- SE) to 21.5 +/- 2.7 ml/100 gm/min at the 6th hour. Sensory evoked potentials decreased progressively from the resting level of 100% to 53.0% +/- 7.2% at the 3rd hour. Intracranial pressure, measured by epidural pressure on the occluded side, increased rapidly during the first 3 hours, from 10.6 +/- 0.3 to about 30 cm H2O. In the animals with trapping, the decreases in rCBF and declines of SEP were significantly less than those in the embolized animals, and no evident brain swelling was observed. This study demonstrates that MCA trunk occlusion by silicone cylinder embolization produces a more marked decrease in deep CBF, with diminution of SEP and increase in ICP, than that produced by trapping.
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PMID:Regional cerebral blood flow, sensory evoked potentials, and intracranial pressure in dogs with MCA occlusion by embolization or trapping. 682 46

Focal incomplete cerebral ischemia was created in 20 adult cats by retro-orbital middle cerebral artery (MCA) occlusion under halothane anesthesia. Arterial blood flow (CBF), bilateral electroencephalographic (EEG) recordings, and systemic arterial blood pressure (SABP) were monitored for the 1st hour of occlusion. Ten animals were treated with 10 mg/kg of naloxone within 10 minutes of MCA clipping, followed by a continuous infusion of naloxone at 2 mg/kg/hr for the duration of the occlusion (8 hours). Ten animals were treated in a similar fashion with physiological saline (control). Blood flow was restored after 8 hours. The brains were examined at the time of death or 7 days after the occlusion period. There was no difference between the two groups regarding cerebral infarction size or distribution, neurological outcome, SABP, PaCO2, or CBF. Minor changes in EEG amplitude observed in the naloxone-treated group appear to represent interaction of the drug with halothane after prolonged administration. The authors conclude that naloxone did not modify the outcome of focal cerebral ischemia in the cat.
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PMID:Failure of naloxone to affect focal incomplete cerebral ischemia and collateral blood flow in cats. 686 89

Severe incomplete cerebral ischemia of 30 min duration with CBF below 5% of normal was induced in rats by clamping both carotids and lowering BP. One group of rats were fasting (f-rats), while the other was infused with glucose before induction of the ischemia (g-rats). In f-rats the lactate accumulating in the cerebral cortex was about 15 mumol . g-1, whereas in g-rats it rose to about 35 mumol . g-1. In f-rats considerable recovery of the energy state and electrical activity occurred during recirculation, whereas in g-rats the energy failure persisted with no electrical activity reappearing. In f-rats the structural alterations were of minor severity, but in g-rats extensive progressive tissue damage was seen. The data indicate that the degree of tissue lactic acidosis has pronounced effects on the development of irreversible ischemic nerve cells injury.
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PMID:The role of lactic acidosis in the ischemic nerve cell injury. 693 34

Progressive brain damage after transient cerebral ischemia may be related to changes in postischemic cerebral blood flow and metabolism. Regional cerebral blood flow (rCBF) and cerebral glucose utilization (rCGU) were measured in adult rats prior to, during (only rCBF), and serially after transient forebrain ischemia. Animals were subjected to 30 minutes of forebrain ischemia by occluding both common carotid arteries 24 hours after cauterizing the vertebral arteries. Regional CBF was measured by the indicator-fractionation technique using 4-iodo-[14C]-antipyrine. Regional CGU was measured by the 2-[14C]deoxyglucose method. The results were correlated with the distribution and progression of ischemic neuronal damage in animals subjected to an identical ischemic insult. Cerebral blood flow to forebrain after 30 minutes of moderate to severe ischemia (less than 10% control CBF) was characterized by 5 to 15 minutes of hyperemia; rCBF then fell below normal and remained low for as long as 24 hours. Post-ischemic glucose utilization in the forebrain, except in the hippocampus, was depressed below control values at 1 hour and either remained low (neocortex, striatum) or gradually rose to normal (white matter) by 48 hours. In the hippocampus, glucose utilization equaled the control value at 1 hour and fell below control between 24 and 48 hours. The appearance of moderate to severe morphological damage in striatum and hippocampus coincided with a late rise of rCBF above normal and with a fall of rCGU; the late depression of rCGU was usually preceded by a period during which metabolism was increased relative to adjacent tissue. Further refinement of these studies may help identify salvageable brain after ischemia and define ways to manipulate CBF and metabolism in the treatment of stroke.
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PMID:Regional cerebral blood flow and glucose metabolism following transient forebrain ischemia. 710 26


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