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

Varying degrees of cerebral ischemia were produced in adult Wistar rats by clipping of bilateral common carotid arteries with or without induced hypotension. Local cerebral blood flow was measured from bilateral caudate nuclei and parietal cortices using the hydrogen clearance method. EEG was recorded from the same electrode as used for the hydrogen clearance method. The delta power of EEG increased along with decreasing local cerebral blood flow. There was an inverse correlation between the delta power of EEG and local CBF values, ranging from normal to extremely low (10 ml/100 g/min). When local CBF was reduced below 6-8 ml/100 g/min, EEG became isoelectric. Continuous EEG recording might contribute to predict rCBF value in the ischemic lesion.
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PMID:[Correlation between local cerebral blood flow and EEG in experimental cerebral ischemia]. 711 95

A major factor determining the severity of neurological deficits caused by cerebral ischemia is the ability of the vasculature to provide collateral circulation to the ischemic areas. By establishing a major conduit by means of extracranial-intracranial anastomosis, the increased perfusion pressure through the collateral arterioles may reduce morbidity in these patients. Twenty-seven patients were selected for superficial temporal artery to middle cerebral artery (STA-MCA) anastomosis based on clinical and angiographic evidence of lesions of the internal carotid arterial system. Cerebral blood flows (CBF's) were determined by the xenon-133 inhalation method using 16 symmetrically placed scintillator probes; two-compartment analysis was used to compute a mean flow for the compartment. An average mean flow was computed for each hemisphere, and for four regions with the lowest mean CBF in each hemisphere. The CBF was measured preoperatively and within 8 weeks postoperatively. The average mean flow was 29 ml/100 mg/min in the symptomatic hemisphere, and 30 ml/100 gm/min in the asymptomatic hemisphere. In 11 patients, the mean flow for the symptomatic hemisphere increased by 24% postoperatively, and for the asymptomatic hemisphere by 23%. Regions with lowest CBF showed an increase of 32% in the symptomatic hemisphere, and of 35% in the asymptomatic hemisphere. The low-flow regions differed from the total hemisphere (symptomatic: p less than 0.02; asymptomatic: p less than 0.05). Areas of lowest blood flow preoperatively had the greatest increase in flow postoperatively. Postoperative elevation of CBF in the contralateral hemisphere is consistent with an "intracerebral steal" before surgery. The postoperative elevation of flow in the asymptomatic hemisphere is related to improved perfusion pressure in the symptomatic hemisphere.
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PMID:Reversal of intracerebral steal by STA-MCA anastomosis. 713 Oct 62

Air embolization of the brain produces cerebral ischemia that can be focal and reversible. The method has previously been hampered by (1) lack of selective arterial injection of the embolus, (2) disruption of local hemodynamic relationships by ligation of major arterial channels, (3) excessive volume of the air embolus, and (4) uncontrolled bubble size. To minimize these factors, a technique was devised in the rat whereby a fine catheter was advanced through a branch of the external carotid artery into the internal carotid artery. Air emboli of 5 microliters were found to arrest blood flow and to attenuate electrical activity in the ipsilateral cerebral hemisphere for seconds to a couple of minutes. The duration of ischemia varied from region to region, and it tended to be prolonged by arterial hypotension. In the nonembolized hemisphere, CBF never declined abruptly (indicating no cross-over of air) although electrical activity was suppressed in two-thirds of the animals.
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PMID:Experimental air embolism of the brain: an analysis of the technique in the rat. 714 3

Regional cerebral blood flow (r-CBF) in anesthetized dogs was measured by the H2 clearance method. Cerebral ischemia was induced by permanent ligation of bilateral vertebral arteries (VA) and a 10 min occlusion of bilateral common carotid arteries (CCA). Under normal conditions, dilazep (100 and 300 micrograms/kg i.v.) increased r-CBF dose-dependently without affecting arterial PO2, PCO2 and pH. r-CBF was reduced by 40% during cerebral ischemia. Relative r-CBF rates, as compared with pre-ischemic rates, were 85%, 80%, 77% and 75% at 30, 60, 90 and 120 min after cerebral ischemia, respectively, indicating development of recirculation impairment. Dilazep (100 and 300 micrograms/kg i.v. 30 min before CCA occlusion) did not affect r-CBF reduction during the state of cerebral ischemia, whereas it prevented re-circulation impairment after cerebral ischemia. Papaverine (300 micrograms/kg i.v. 30 min before CCA occlusion) exerted similar effects. These results suggest that dilazep is a potentially effective drug for treating cerebrovascular disorders.
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PMID:[Effects of dilazep on cerebral blood flow under normal conditions and recirculation impairment after cerebral ischemia (author's transl)]. 723 62

Temporal and site correlation of local cerebral blood flow (1-CBF), tissue redox state, energy metabolism, tissue pH, and cerebral electrophysiological activity in induced cerebral ischemia was performed in rats in an effort to obtain helpful clues for the management of occlusive cerebrovascular disease. CBF decreased acutely in both the embolized and nonembolized hemispheres but returned toward normal in 5 minutes. However, total cerebral oxidative metabolism remained depressed throughout the 30-minute observation period despite improved perfusion. The change in CBF correlated with the development and resolution of tissue acidosis, which was maximal 3 minutes after embolization but became alkaline after 30 minutes, possibly due to accumulation of sodium lactate. Oxidized form of nicotinamide-adenine dinucleotide and cytochrome a,a3 quickly became reduced in the ischemic core, but a tardyspontaneous postischemic tissue perfusion resulted in their hyperoxidation. The CBF-metabolism uncoupling as well as postischemic hyperoxidation of the electron transport system, which is associated with accumulation of pyruvate and lactate, probably resulted from stagnation of electron flow at the entrance to the mitochondrial respiratory processes. Seizures could not account for these results, as paroxysmal changes in the EEG usually appeared only in the nonembolized hemisphere and were not dependent upon lack of energy. These studies confirm that metabolic failure may persist in ischemic tissue despite adequate reperfusion, which may, in fact, contribute to tissue damage through hyperoxidation.
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PMID:The dissociation of cerebral blood flow, metabolism, and function in the early stages of developing cerebral infarction. 743 71

Neurologically critically ill patients, more often than others, are unable to communicate and, for a crucial period of time, have the vital functions of their brains hidden in the "black box" of the cranial vault behind a curtain of ambiguity and immobility. Customarily--and naively--we have relied upon beside clinical observations to pierce these barriers. Recent insights lead us to conclude that these "neurochecks" no longer suffice. This article has surveyed four major monitoring systems relied upon by neurointensivists to evaluate the pathophysiology of their patients. Of these, ICPM has the longest clinical track record. It provides a quantitative measure of the brain's capacity to withstand ICP and helps us monitor interventions to reduce it. To utilize this information intelligently requires an understanding of the principles of ICC, CPP, ICP wave morphology, and the hardware available. NICU-CEEG is a more recent introduction but, in principle, it transfers from the laboratory and operating suite to the ICU bedside, established correlations among electrophysiology, CBF, and CM. Digital EEG has allowed us to overcome significant logistical barriers and made NICU-CEEG a practical ICU tool. Early but impressive data suggest that NICU-CEEG has a significant clinical impact in patients with ACI, uncontrolled seizures, or coma. It also has revealed that NICU patients have a surprisingly high incidence of NCS, which may adversely affect their outcome. TCD has contributed greatly to diagnosis and management of SAH vasospasm. It also can be applied with benefit to patients with increased ICP, and has promising value in patients with ACI. It may prove beneficial in monitoring unstable cerebral embolization. Several bedside methods for monitoring CBF are available, but they require refinement to become true monitoring systems. These methods have revealed clinically important insights in patients with head trauma, SAH vasospasm, and ACI. Methods for directly monitoring CM and CMRo2 are improving our understanding of the brain's responses to injury, and becoming increasingly relevant to bedside management. SjvO2 can detect cerebral ischemia caused by overzealous hyperventilation and accelerated ICP. ICO holds promise as a noninvasive transcranial method for assessing Scvo2. We soon may see a scalp array of such detectors, similar to an EEG "montage," that allows us to assess multiregional Scvo2. To be useful, a clinical method should raise questions for further investigation. If the neurophysiologic monitoring systems described here provide us with some answers and lead us to ask useful new questions, they will prove their benefit to our patients.
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PMID:Neurophysiologic monitoring in the neuroscience intensive care unit. 747 20

Middle cerebral artery occlusion was performed in rats while the animals were inside the nuclear magnetic resonance (NMR) tomograph. Successful occlusion was confirmed by the collapse of amplitude on an electrocorticogram. The ultrafast NMR imaging technique UFLARE was used to measure the apparent diffusion coefficient (ADC) immediately after the induction of cerebral ischemia. ADC values of normal cortex and caudate-putamen were 726 +/- 22 x 10(-6) mm2/s and 659 +/- 17 x 10(-6) mm2/s, respectively. Within minutes of occlusion, a large territory with reduced ADC became visible in the ipsilateral hemisphere. Over the 2 h observation period, this area grew continuously. Quantitative analysis of the ADC reduction in this region showed a gradual ADC decrease from the periphery to the core, the lowest ADC value amounting to about 60% of control. Two hours after the onset of occlusion, the regional distribution of ATP and tissue pH were determined with bioluminescence and fluorescence techniques, respectively. There was a depletion of ATP in the core of the ischemic territory (32 +/- 20% of the hemisphere) and an area of tissue acidosis (57 +/- 19% of the hemisphere) spreading beyond that of ATP depletion. Regional CBF (rCBF) was measured autoradiographically with the iodo[14C]antipyrine method. CBF gradually decreased from the periphery to the ischemic core, where it declined to values as low as 5 ml 100 g-1. When reductions in CBF and in ADC were matched to the corresponding areas of energy breakdown and of tissue acidosis, the region of energy depletion corresponded to a threshold in rCBF of 18 +/- 14 ml 100 g-1 min-1 and to an ADC reduction to 77 +/- 3% of control. Tissue acidosis corresponded to a flow value below 31 +/- 11 ml 100 g-1 min-1 and to an ADC value below 90 +/- 4% of control. Thus, the quantification of ADC in the ischemic territory allows the distinction between a core region with total breakdown of energy metabolism and a corona with normal energy balance but severe tissue acidosis.
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PMID:Evolution of regional changes in apparent diffusion coefficient during focal ischemia of rat brain: the relationship of quantitative diffusion NMR imaging to reduction in cerebral blood flow and metabolic disturbances. 759 32

Using online in vivo chemiluminescence (CL), we studied for the first time continuously the production of reactive oxygen species (ROS) after global cerebral ischemia and the relationship of ROS production to CBF. In anesthetized rats equipped with a closed cranial window, the CL enhancer, lucigenin (1 mM), was superfused onto the brain topically. CL was measured through the cranial window with a cooled photomultiplier, and CBF was measured simultaneously with laser-Doppler flowmetry. Reperfusion after 10 min (n = 8) of global cerebral ischemia led to a CL peak to 188 +/- 77% (baseline = 100%) within 10 +/- 4 min. After 2 h of reperfusion, CL had returned to 102 +/- 28%. Reperfusion after 20 min (n = 8) of ischemia increased CL to 225 +/- 48% within 12 +/- 3 min. After 2 h, CL was still increased (150 +/- 44%, p < 0.05 compared with 10 min of ischemia). CL after 10 min of ischemia was neither affected by brain topical free CuZn-superoxide dismutase (SOD) (100 U/ml, n = 3) nor by i.v. administration of free CuZn-SOD (104 U/kg, followed by 104 U/kg/h, n = 3). The CBF hyperfusion peak on reperfusion preceded the CL peak in all experiments by several minutes. In additional in vitro experiments we investigated the source of CL: Intracellular loading of lucigenin was demonstrated in cultured CNS cells, and a very similar pattern of CL as in the in vivo preparation after ischemia developed in rat brain slices after 15 min of hypoxia, which was unaffected by free CuZn-SOD (100 U/ml) but strongly attenuated by liposome-entrapped CuZn-SOD. We conclude that lucigenin-enhanced CL is a promising tool to study ROS production continuously from the in vivo brain of experimental animals and brain slices, and that the CL signal most likely derives from the intracellular production of superoxide. The production of ROS is preceded by reperfusion, is burst-like, and is dependent on the duration of the ischemic interval.
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PMID:Global cerebral ischemia in the rat: online monitoring of oxygen free radical production using chemiluminescence in vivo. 759 53

To evaluate the course of cerebral tissue perfusion in patients with acute focal cerebral ischemia of the supratentorial compartment regional cerebral blood flow (rCBF) was measured on day 0, 7, 14, 21, and 28 in 132 patients using the 133 Xenon stationary inhalation technique. Ischemic events of the brainstem and hemorrhagic complications were excluded. The clinical status was evaluated using a modified Mathew score. In 34 patients no hemodilution, anti-edema therapy, or Ca(++)-antagonists were used but otherwise best medical therapy was applied. These patients represented the so called "natural course" of cerebral ischemia. In 30/34 patients on day 0 (within 16 hours after onset of symptoms) focal flow abnormalities were found in the involved side. In 9 of these 30 patients and in 1 of the remaining ischemia was observed in the contralateral side. rCBF above normal (relative luxury perfusion) despite pathologic neurologic findings was observed in 8/34 patients on day 3-7. Eight patients presented on day 3-7 with normal flow which later became ischemic again without evidence of another symptomatic episode. Correlation between severity of clinical findings and actual rCBF was low from day 3 to 7 but close on day 0. From day 14-21 hemispheric CBF correlated well with the total neurologic score but focal clinical findings had a lower correlation with focal flow as compared to day 0 and day 28. Contralateral ischemia was never found after day 14. In 5 other cases with "natural course" described above, a transitory decrease of rCBF below the initial ischemia level was found between day 3 and 14.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blood flow and clinical course in patients with ischemic stroke without cerebrospecific therapy. 767 77

The effects of a novel opioid kappa-receptor agonist U-50488H on Na(+)-K(+)-adenosine triphosphatase (ATPase) activity and regional cerebral blood flow (rCBF) were studied in the acute ischemic brain of rats after middle cerebral artery (MCA) occlusion. Administration of U-50488H 15 minutes prior to MCA occlusion attenuated ischemic reduction in Na(+)-K(+)-ATPase activity 15 minutes after MCA occlusion. The effect was statistically significant at a dosage of 30 mg/kg, but not at lower doses (0.3 and 3 mg/kg). There was no effect on rCBF before MCA occlusion, and the decreased flow after occlusion was enhanced with a significant fall in systemic blood pressure at a dosage of 30 mg/kg. These results indicate that U-50488H has therapeutic potential in cerebral ischemia by mechanisms other than improvement in CBF.
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PMID:Potential protection by a specific kappa-opiate agonist U-50488H against membrane failure in acute ischemic brain. 768 18


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