scholarly journals Uncoupled Cerebral Blood Flow and Metabolism after Severe Global Ischemia in Rats

1992 ◽  
Vol 12 (5) ◽  
pp. 802-808 ◽  
Author(s):  
Narendra C. Singh ◽  
Patrick M. Kochanek ◽  
Joanne K. Schiding ◽  
John A. Melick ◽  
Edwin M. Nemoto
Keyword(s):  
Blood Flow ◽  
Cardiac Arrest ◽  
Cerebral Blood Flow ◽  
Brain Ischemia ◽  
Global Ischemia ◽  
Global Brain Ischemia ◽  
Sagittal Sinus ◽  
Postischemic Period ◽  
Baseline Values ◽  
Global Brain

In a rat model of complete global brain ischemia (neck tourniquet) lasting either 3 min or 20 min, we monitored global CBF (sagittal sinus H2 clearance) and CMRO2 for 6 h to test the hypothesis that delayed postischemic hyperemia and uncoupling of CBF and CMRO2 occur depending on the severity of the insult. Early postischemic hyperemia occurred in both the 3-min and 20-min groups ( p < 0.05 vs. baseline values) and resolved by 15 min. Hypoperfusion occurred in the 3-min group between 15 and 60 min postischemia (≈23% reduction), and in the 20-min group from 15 to 120 min postischemia (≈50% reduction) ( p < 0.05), and then resolved. CMRO2 was not significantly different from baseline at any time after ischemia in the 3-min group. After 20 min of ischemia, however, CMRO2 was decreased (≈60%) throughout the postischemic period ( p < 0.05). At 5 min after ischemia, CBF/CMRO2 was increased in both groups but returned to baseline from 60 to 120 min postischemia. In the 3-min group, CBF/CMRO2 remained at baseline throughout the rest of the experiment. However, in the 20-min group, CBF/CMRO2 once again increased (≈100%), reaching a significant level at 180 min and remaining so for the rest of the 6-h period ( p < 0.05). These data demonstrate biphasic uncoupling of CBF and CMRO2 after severe (20 min) global ischemia in rats. This relatively early reemergence of CBF/CMRO2 uncoupling after 180 min of reperfusion is similar to that observed after prolonged cardiac arrest and resuscitation in humans.

Creatine kinase isoenzymes in human cerebrospinal fluid and brain.

1984 ◽  
Vol 30 (11) ◽  
pp. 1804-1806 ◽  
Author(s):  
W L Chandler ◽  
K J Clayson ◽  
W T Longstreth ◽  
J S Fine
Keyword(s):  
Cerebrospinal Fluid ◽  
Creatine Kinase ◽  
Cardiac Arrest ◽  
Brain Ischemia ◽  
Blood Contamination ◽  
Global Brain Ischemia ◽  
Qualitative And Quantitative ◽  
Human Cerebrospinal Fluid ◽  
Brain Extracts ◽  
Global Brain

Abstract Extracts of normal brains obtained at autopsy and cerebrospinal fluid (CSF) from patients with global brain ischemia were analyzed for creatine kinase (CK; EC 2.7.3.2) isoenzymes. We used both qualitative and quantitative assays (electrophoresis and immunoinhibition). Brain extracts contained CK-BB isoenzyme and mitochondrial CK. In 54 CSF samples free of blood contamination and with total activities ranging from 7 to 2010 U/L (mean 202 U/L), virtually all of the CK activity was due to CK-BB, and none to CK-MM or CK-MB. We conclude that brain contains CK-BB and mitochondrial CK, but lacks CK-MM and CK-MB. After cardiac arrest, CK-BB is released into the CSF. Any CK-MM in the CSF is probably from blood contamination, in which case immunoinhibition with anti-CK-M antibodies accurately quantifies CK-BB.

Abstract TP43: Transient Global Brain Ischemia Induces Striatal Neuronal Death of T1-Hyperintensity without Hemorrhage: Susceptibility-Weighted Imaging Study on Cardiac Arrest Survivors

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Masayuki Fujioka ◽  
Tomoo Watanabe ◽  
Toshiaki Taoka ◽  
Kazuo Okuchi
Keyword(s):  
Cardiac Arrest ◽  
Brain Ischemia ◽  
Neuronal Death ◽  
Late Onset ◽  
Global Brain Ischemia ◽  
Dorsolateral Striatum ◽  
Selective Neuronal Death ◽  
T1 Hyperintensity ◽  
Hemoglobin Degradation ◽  
Global Brain

Background: Global brain ischemia-reperfusion leads to selective neuronal death in the hippocampal CA1 area, cerebellar cortex, dorsolateral striatum, and/or neocortical layers 3, 5, and 6 in animal models and in humans. We have reported a delayed neurodegeneration of late-onset neuroimaging change in such brain areas vulnerable to ischemia (Stroke.1994;25:2091-95., Stroke.1999;30:1038-42., Stroke.1999;30:1043-46., Cerebrovasc Dis.2000;10:2-7., Ann Neurol.2003;54:732-7.). The magnetic resonance imaging (MRI) studies on patients after cardiac arrest showed 1) bilateral neurodegeneration with hyperintensity on T1-weighted MRI in the striatum, thalamus, and/or substantia nigra (Stroke.1994;25:2091-5., Neuroradiology.1994;36:605-7.), and 2) specific hippocampal atrophy in the chronic stage (MRI volumetry) (Cerebrovascular Dis.2000;10:2-7.). In the current study with susceptibility-weighted MRI (SWI), we investigated if the delayed T1-hyperintensity in the dorsolateral striatum consistently observed in cardiac arrest survivors represents minor hemorrhage (methemoglobin) or signifies selective neuronal death without bleeding reported as a specific type of ischemic neurodegeneration (Ann Neurol.2003;54:732-47.). Methods: We studied 11 patients in a vegetative state after unexpected out-of-hospital cardiac arrest who were able to undergo multiple brain MRI. We performed SWI to evaluate if the late-onset striatal T1-hyperintensity represents iron accumulation derived from hemoglobin degradation products or not. Results: In the 11 patients, serial MR images demonstrated delayed T1-hyperintesity in the bilateral striatum from one to two weeks after the onset. The SWI study showed no hypointense change in the striatal T1-hyperintensity. Conclusion: The striatal T1-hyperintensity after cardiac arrest seems to correspond to selective neuronal death and glial proliferation with paramagnetic effects but not hemoglobin degradation due to erythrocyte-extravasation.

scholarly journals Magnetic Resonance Imaging Assessment of Regional Cerebral Blood Flow after Asphyxial Cardiac Arrest in Immature Rats

2008 ◽  
Vol 29 (1) ◽  
pp. 197-205 ◽  
Author(s):  
Mioara D Manole ◽  
Lesley M Foley ◽  
T Kevin Hitchens ◽  
Patrick M Kochanek ◽  
Robert W Hickey ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Blood Flow ◽  
Cardiac Arrest ◽  
Cerebral Blood Flow ◽  
Magnetic Resonance ◽  
Resonance Imaging ◽  
Magnetic Resonance Imaging Assessment ◽  
Baseline Values ◽  
The Relationship ◽  
Asphyxial Cardiac Arrest

Cerebral blood flow (CBF) alterations after asphyxial cardiac arrest (CA) are not defined in developmental animal models or humans. We characterized regional and temporal changes in CBF from 5 to 150 mins after asphyxial CA of increasing duration (8.5, 9, 12 min) in postnatal day (PND) 17 rats using the noninvasive method of arterial spin-labeled magnetic resonance imaging (ASL-MRI). We also assessed blood-brain barrier (BBB) permeability, and evaluated the relationship between CBF and mean arterial pressure after resuscitation. After all durations of asphyxia CBF alterations were region dependent. After 8.5- and 9-min asphyxia, intense subcortical hyperemia at 5 min was followed by return of CBF to baseline values by 10 mins. After 12-min asphyxia, hyperemia was absent and hypoperfusion reached a nadir of 38% to 65% of baselines with the lowest values in the cortex. BBB was impermeable to gadoteridol 150 mins after CA. CBF in the 12-min CA group was blood pressure passive at 60 min assessed via infusion of epinephrine. ASL-MRI assessment of CBF after asphyxial Ca in PND 17 rats reveals marked duration and region-specific reperfusion patterns and identifies possible new therapeutic targets.

Effects of ischemia on brain blood flow and oxygen consumption of newborn pigs

1989 ◽  
Vol 257 (6) ◽  
pp. H1917-H1926 ◽  
Author(s):  
C. W. Leffler ◽  
D. W. Busija ◽  
R. Mirro ◽  
W. M. Armstead ◽  
D. G. Beasley
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Brain Ischemia ◽  
Reactive Hyperemia ◽  
Brain Blood Flow ◽  
Global Brain Ischemia ◽  
Total Brain ◽  
Newborn Pigs ◽  
Global Brain ◽  
The Brain

Brain circulation after 20 min of total brain ischemia was examined in unanesthetized newborn pigs. Except in the cerebrum, reactive hyperemia was observed throughout the brain, peaking by 5 min and subsiding by 20 min of reperfusion. Brain blood flow after 15 min of reperfusion matched the control. Blood flow to the cerebrum then decreased at 40 and 90 min reperfusion, while the rest of the brain was unaffected. Blood flow to the cerebrum returned to control by 24 h. Cerebral vascular resistance doubled by 15 min reperfusion, remained elevated at 90 min reperfusion, but returned to control by 24 h. Cerebral oxygen consumption followed a pattern similar to blood flow. Ninety minutes postischemia, hypercapnia-induced hyperemia was greatly attenuated in the cerebrum, reduced modestly in the diencephalon-mesencephalon, but unaffected in the rest of the brain. Thus 20 min of global brain ischemia in piglets does not produce reactive hyperemia in the cerebrum that is detectable at 5 min reperfusion but does in the remainder of the brain. Subsequent hemodynamic abnormalities apparently are confined to the cerebrum. Blood flow throughout the brain returns to normal by 24 h. Thus cerebral hemodynamic effects of total global ischemia are regionally dependent.

scholarly journals Changes in N-Acetyl-Aspartate Content during Focal and Global Brain Ischemia of the Rat

1995 ◽  
Vol 15 (4) ◽  
pp. 639-646 ◽  
Author(s):  
Thomas Nikolaj Sager ◽  
Henning Laursen ◽  
Anker Jon Hansen
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Brain Ischemia ◽  
Focal Ischemia ◽  
Artery Occlusion ◽  
Global Ischemia ◽  
Global Brain Ischemia ◽  
Global Brain ◽  
Cerebral Artery Occlusion

N-Acetyl-aspartate (NAA) is almost exclusively localized in neurons in the mature brain and might be used as a neuronal marker. It has been reported that the NAA content in human brain is decreased in neurodegenerative diseases and in stroke. Since the NAA content can be determined by nuclear magnetic resonance techniques, it has potential as a diagnostic and prognostic marker. The objective of this study was to examine the change of NAA content and related substances following cerebral ischemia and compare the results to the damage of the tissue. We used rats to study the changes of NAA, N-acetyl-aspartyl-glutamate (NAAG), glutamate, and aspartate contents over a time course of 24 h in brain regions affected by either permanent middle cerebral artery occlusion (focal ischemia) or decapitation (global ischemia). The decreases of NAA and NAAG contents following global brain ischemia were linear over time but significant only after 4 and 2 h, respectively. After 24 h, the levels of NAA and NAAG were 24 and 44% of control values, respectively. The concentration of glutamate did not change, whereas the aspartate content increased at a rate comparable with the rate of decrease of NAA content. This is consistent with NAA being preferentially degraded by the enzyme amidohydrolase II in global ischemia. In focal ischemia, there was a rapid decline of NAA within the first 8 h of ischemia followed by a slower rate of reduction. The reductions of NAA and NAAG contents in focal ischemia were significant after 4 and 24 h, respectively. After 24 h, the NAA and NAAG contents were 33 and 64% of control values, respectively. Also, the glutamate and aspartate contents exhibited significant decreases in focal ischemic tissue. Our studies show that NAA decreases during brain ischemia, the initial rate being faster in focal ischemia than in global ischemia. In rat transient focal ischemia, others have shown that a middle cerebral artery occlusion of 2- to 3-h duration is sufficient to produce an infarct that is similar in size to that following permanent occlusion for 24 h. The fact that we observed only a 10% decrease of NAA content 2 h after occlusion demonstrates that the NAA content of the tissue does not reflect neuronal viability. Thus, the incompetence with which ischemic/infarcted tissue removes NAA will lead to overestimation of the number of viable neurons in acute situations. Only when steady state prevails may [NAA] be used as a marker of viable nerve cells.

Post-ischemic gene transfer of IL-10 protects against global brain ischemia

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S507-S507 ◽  
Author(s):  
Takashi Shichita ◽  
Hiroaki Ooboshi ◽  
Yasuhiro Kumai ◽  
Masahiro Kumai ◽  
Junichi Takada ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Brain Ischemia ◽  
Global Brain Ischemia ◽  
Global Brain
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