Cerebral Na<sup>+</sup>, K<sup>+</sup>-ATPase Activity during Exposure to and Recovery from Acute Ischemia

MacMillan, V.

doi:10.1038/jcbfm.1982.52

Cited by 69 publications

(20 citation statements)

References 34 publications

(26 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In that study, Na +,K+ ATPase activity was reduced slightly less after 60 min than after 30 min of MCA occlusion in compar ison to the nonischemic hemispheres, even though further decreases were observed at 2 and 4 h. Nei ther water content nor cation concentrations changed at 30 min, but these values later decreased progressively from 1 to 4 h after the onset of MCA occlusion. The partial temporary recovery of ATPase activity may have been due to a transient improvement in collateral circulation or excitotoxic cell activity during ischemia (MacMillan, 1982;Strong et aI., 1983).…”

Section: Discussionmentioning

confidence: 99%

Diffusion-Weighted Magnetic Resonance Imaging of Acute Focal Cerebral Ischemia: Comparison of Signal Intensity with Changes in Brain Water and Na⁺,K⁺ -ATPase Activity

Mintorovitch

Yang

Shimizu

et al. 1994

J Cereb Blood Flow Metab

191

View full text Add to dashboard Cite

Summary: Diffusion-weighted magnetic resonance (MR) images from rats during acute cerebral ischemia induced by middle cerebral artery occlusion were analyzed for correspondence with changes in brain water, cation con centrations , and Na + ,K + -ATPase activity measured in vitro after 30 or 60 min of ischemia. In the ischemic hemi sphere, signal intensity was increased at 30 min (p < 0.05 vs contralateral hemisphere) and further increased at 60 min. Na + ,K + -ATPase activity was 34% lower in isch emic cortex and 40% lower in ischemic basal ganglia after 30 min (p < 0.05), but water content and Na + and K + concentrations were not significantly different between Diffusion-weighted magnetic resonance (MR) im aging can detect less severe and potentially revers ible cerebral ischemia much earlier than conven tional T2-weighted MR imaging (Moseley et aI., 1990; Mintorovitch et aI., 1991; Minematsu et aI., 1992; van Bruggen et aI., 1992 Abbreviations used: ADC, apparent diffusion coefficient; ANOV A, analysis of variance; MCA, middle cerebral artery; MR, magnetic resonance; TE, echo time; TR, repetition time. 332hemispheres. After 60 min , water content and Na + con centration were increased , and both Na + ,K + -ATPase activity and K + concentration were decreased in the ischemic hemisphere (p < 0.05). These findings are con sistent with the hypothesis that the early onset of signal hyperintensity in diffusion-weighted MR images may re flect cellular edema associated with impaired membrane pump function. Early in vivo detection and localization of potentially reversible ischemic cerebral edema may have important research and clinical applications.

show abstract

Section: Discussionmentioning

confidence: 99%

Diffusion-Weighted Magnetic Resonance Imaging of Acute Focal Cerebral Ischemia: Comparison of Signal Intensity with Changes in Brain Water and Na⁺,K⁺ -ATPase Activity

Mintorovitch

Yang

Shimizu

et al. 1994

J Cereb Blood Flow Metab

191

View full text Add to dashboard Cite

show abstract

“…Restoration of circulation and substrate supply are necessary for repletion of cellular ATP stores and return to normal levels of pH and ion concentrations. MacMillan (27) reported that EEG recovered in parallel with the recovery of Na-K-ATPase activity over 72 h after global ischemia in rat forebrain. Thus, although metabolic recovery is necessary for electrophysiological recovery, the two are not necessarily contemporaneous and there are numerous experimental models in which the EEG recovers more slowly than cerebral energy metabolism, as reflected by brain oxygen consumption, high-energy phosphate content, and intracellular pH (28).…”

Section: Discussionmentioning

confidence: 99%

Relationship Between Blood Pressure, Cerebral Electrical Activity, Cerebral Fractional Oxygen Extraction, and Peripheral Blood Flow in Very Low Birth Weight Newborn Infants

et al. 2006

View full text Add to dashboard Cite

There is uncertainty about the level of systemic blood pressure required to maintain adequate cerebral oxygen delivery and organ integrity. This prospective, observational study on 35 very low birth weight infants aimed to determine the mean blood pressure (MBP) below which cerebral electrical activity, peripheral blood flow (PBF), and cerebral fractional oxygen extraction (CFOE) are abnormal. Digital EEG, recorded every day on the first 4 d after birth, were analyzed a) by automatic spectral analysis, b) by manual measurement of interburst interval, and c) qualitatively. CFOE and PBF measurements were performed using near-infrared spectroscopy and venous occlusion. MBP was measured using arterial catheters. The median (range) of MBP recorded was 32 mm . The EEG became abnormal at MBP levels below 23 mm Hg: a) the relative power of the delta (0.5-3.5 Hz) frequency band was decreased, b) interburst intervals were prolonged, and c) all four qualitatively abnormal EEG (low amplitude and prolonged interburst intervals) from four different patients were recorded below this MBP level. The only abnormally high CFOE was measured at MBP of 20 mm Hg. PBF decreased at MBP levels between 23 and 33 mm Hg. None of the infants in this study developed cystic periventricular leukomalacia. One infant (MBP, 22 mm Hg) developed ventricular dilatation after intraventricular hemorrhage. The EEG and CFOE remained normal at MBP levels above 23 mm Hg. It would appear that cerebral perfusion is probably maintained at MBP levels above 23 mm Hg. (Pediatr Res 59: 314-319, 2006) S everal authors have described an association between systemic hypotension in premature infants and neurologic morbidity (1-3), and, in some centers, clinical practice is to support blood pressure by inotropes and volume expanders when the MBP level falls below 30 mm Hg. The likely mechanism by which hypotension causes neurologic damage is by diminished oxygen delivery through decreased cerebral perfusion. However, the relationship between MBP and cerebral blood flow is unclear in premature infants (4 -8). Some authors have argued that cerebral blood flow is pressure passive and dependent on MBP in infants between 28 and 39 wk gestation (5,7). Others, who have studied infants between 24 and 34 wk gestation, observed that cerebral blood flow is independent of MBP (4,8). Furthermore, the critical level of MBP at which cerebral perfusion becomes compromised has not been clearly determined.In spite of a lack of evidence linking systemic hypotension to brain damage in very low birth weight infants, it is well known that older subjects lose consciousness when MBP falls to a seriously low level. A change in the level of consciousness may not be recognized in sick newborn infants who are heavily sedated while being ventilated, but it may be associated with recognizable changes in the EEG pattern. Using a cerebral function monitor, Greisen et al. (9) showed that reduced blood flow to the neonatal brain correlated with decreased amplitude of the EEG. There have bee...

show abstract

“…8 Using the four-vessel occlusion model, MacMillan 12 failed to observe a significant increase in cortical peroxide level for up to 72 hours of recirculation. These data disagree with our findings.…”

mentioning

confidence: 99%

Increased lipid peroxidation in vulnerable brain regions after transient forebrain ischemia in rats.

Bromont

Marie

Bralet

1989

Stroke

217

View full text Add to dashboard Cite

We examined cerebral lipid peroxidation, estimated by a thiobarbituric acid test, in rat brain regions after 30 minutes of severe forebrain ischemia and at recirculation periods of up to 72 hours. The lipid peroxide levels remained unaltered in all brain regions during ischemia and during the first hour of recirculation but were selectively increased between 8 and 72 hours of recirculation in the ischemia-sensitive regions of the hippocampus, striatum, and cortex. The most pronounced increases (30-37%) were seen at 48 hours of recirculation. In contrast, lipid peroxide levels were unchanged in infarcted brain regions 24 hours after intracarotid injection of microspheres, indicating that reoxygenation of the ischemic brain is a prerequisite for lipid peroxidation. We assessed the lipid peroxidation capacity of cerebral homogenates obtained from rats subjected to ischemia and recirculation by measuring the production of lipid peroxides after aerobic incubation. The homogenates from rats exposed to 30 minutes of ischemia or to 1 hour of recirculation were not more susceptible to peroxidation. However, the production of lipid peroxides was selectively increased in the hippocampus, striatum, and cortex at 8-48 hours of recirculation, suggesting a loss of efficacy of the antioxidant systems. These results, showing a delayed and long-lasting increase in lipid peroxidation that occurs in ischemia-sensitive brain regions and parallels the development of neuronal necrosis, support the hypothesis that free radical processes participate in postischemic neuronal damage. (Stroke 1989;20:918-924) I t has been suggested that cellular damage in cerebral ischemia is at least partly due to oxidative damage, notably that caused by free radical formation and lipid peroxidation.1 However, definitive proof of its occurrence is still controversial. Several laboratories have provided evidence that lipid peroxidation occurs in vivo either during or after brain ischemia and reperfusion, 2 -8 but other data have failed to support the hypothesis.9 -12 The controversy derives from the different methods that have been used for the detection and analysis of lipid peroxidation or from the use of different models of brain ischemia.In our study, we investigated lipid peroxidation using the four-vessel occlusion model of transient ischemia, 13 which produces severe forebrain ischemia and leads to delayed neuronal necrosis in 17 Regional blood flow was therefore measured during and after vascular occlusion to record precisely the ischemic conditions. We assessed the extent of lipid peroxidation by measuring the level of thiobarbituric acidreactive substances (TBARS) in various cerebral structures at different times after the induction of ischemia. Simultaneously, we investigated the capacity of cerebral lipid peroxidation by measuring the accumulation of TBARS in brain homogenates incubated under aerobic conditions. Materials and MethodsWe performed the study with the four-vessel occlusion model on 98 male Wistar rats (Iffa Credo, France), wei...

show abstract

Cerebral Na⁺, K⁺-ATPase Activity during Exposure to and Recovery from Acute Ischemia

Cited by 69 publications

References 34 publications

Diffusion-Weighted Magnetic Resonance Imaging of Acute Focal Cerebral Ischemia: Comparison of Signal Intensity with Changes in Brain Water and Na⁺,K⁺ -ATPase Activity

Diffusion-Weighted Magnetic Resonance Imaging of Acute Focal Cerebral Ischemia: Comparison of Signal Intensity with Changes in Brain Water and Na⁺,K⁺ -ATPase Activity

Relationship Between Blood Pressure, Cerebral Electrical Activity, Cerebral Fractional Oxygen Extraction, and Peripheral Blood Flow in Very Low Birth Weight Newborn Infants

Increased lipid peroxidation in vulnerable brain regions after transient forebrain ischemia in rats.

Contact Info

Product

Resources

About

Cerebral Na+, K+-ATPase Activity during Exposure to and Recovery from Acute Ischemia

Cited by 69 publications

References 34 publications

Diffusion-Weighted Magnetic Resonance Imaging of Acute Focal Cerebral Ischemia: Comparison of Signal Intensity with Changes in Brain Water and Na+,K+ -ATPase Activity

Diffusion-Weighted Magnetic Resonance Imaging of Acute Focal Cerebral Ischemia: Comparison of Signal Intensity with Changes in Brain Water and Na+,K+ -ATPase Activity

Relationship Between Blood Pressure, Cerebral Electrical Activity, Cerebral Fractional Oxygen Extraction, and Peripheral Blood Flow in Very Low Birth Weight Newborn Infants

Increased lipid peroxidation in vulnerable brain regions after transient forebrain ischemia in rats.

Contact Info

Product

Resources

About

Cerebral Na⁺, K⁺-ATPase Activity during Exposure to and Recovery from Acute Ischemia

Diffusion-Weighted Magnetic Resonance Imaging of Acute Focal Cerebral Ischemia: Comparison of Signal Intensity with Changes in Brain Water and Na⁺,K⁺ -ATPase Activity

Diffusion-Weighted Magnetic Resonance Imaging of Acute Focal Cerebral Ischemia: Comparison of Signal Intensity with Changes in Brain Water and Na⁺,K⁺ -ATPase Activity