Effect of Ischemia

Maker, Howard S.; Lehrer, Gerard M.

doi:10.1007/978-1-4615-7175-9_10

Cited by 9 publications

(3 citation statements)

References 132 publications

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“…This is also due to the fact that prolonged tissue hypoxia leads to a decrease in the sum of the adenine nucleotides, a finding which the present study has confirmed (LJUNGGREN et al 1974). This is possibly due to deamination ofAMP to inosine monophosphate (IMP) (MAKER & LEHRER 1970). It is conceivable then that restitution from anoxia could be accompanied by a low ATP concentration despite a normal ECP.…”

Section: Discussionsupporting

confidence: 76%

Brain Energy Metabolism During the Process of Dying and After Cardiopulmonary Resuscitation

Nilsson

Busto

1976

Acta Anaesthesiol Scand

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In order to study the problem of how fast and to what degree severe hypoxic brain tissue changes are reversed after reoxygenation, we challenged the viability of the brain by exposing experimental animals to anoxia of such a duration that cardiopulmonary resuscitation was just possible. The brain tissue concentrations of glucose, lactate, pyruvate and of ATP, ADP, AMP and phosphocreatine were determined. Two series of experiments were carried out. In the first, groups of rats deprived of oxygen for 1, 2, 4 and 6 min were studied in order to show brain tissue changes in the period of impending death as well as the changes coinciding with the onset of clinical death (blood pressure zero). In addition, one group maintained at a rectal temperature of 37 +/- 0.5 degrees C and ventilated for 60 min with an oxygen free gas mixture was included aimed at representing a state of irreversibility. In the second series, restitution after 6 min of no oxygen supply was studied 10 min, 1/2 h, 1 h, and 2 h after cardiopulmonary resuscitation. Attempts were also made to correlate biochemical changes to EEG status and to clinical recovery. The restitution study showed that oxidative phosphorylation of the brain tissue was rapidly resumed with normalization of the adenylate energy charge in all animals in which the pump function of the heart could be restored by our artificial means. However, there was a strikingly poor correlation between recovery of mitochondrial function and restitution of EEG or clinical recovery. Thus, it seems likely that a delayed functional restitution is not due to energy failure but to other biochemical changes or to biophysical alterations not revealed by the present type of study.

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Section: Discussionsupporting

confidence: 76%

Brain Energy Metabolism During the Process of Dying and After Cardiopulmonary Resuscitation

Nilsson

Busto

1976

Acta Anaesthesiol Scand

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“…In rats, histochemical methods revealed that glia contribute to the increase in brain LD post ischemia (Yap and Spector, 1965). The lack of damage and enzyme decrease in cerebral white matter, compared with the extensive damage and enzyme decrease in neocortex, may relate to re gional differences in cerebral blood flow (Kagstrom et aI., 1983;Wolfson et aI., 1988) and metabolism (Maker and Lehrer, 1971 ) after global brain insults.…”

Section: Morphologic Changesmentioning

confidence: 99%

“…In the hippocampus, however, normal CK concentration was lower. If this indicates lower metabolic activity than in the other regions, the "selective vulnera bility" of certain neurons in the hippocampus post arrest, and the decrease in enzyme activities, may be related to other differences peculiar to the hip pocampus, such as blood supply (Maker and Lehrer, 1971;Myers, 1979;Graham, 1985) or cal cium-and neurotransmitter-related hyperexcitabil ity (Siesj6 and Wieloch, 1985).…”

Section: Morphologic Changesmentioning

confidence: 99%

Brain Enzyme Levels in CSF after Cardiac Arrest and Resuscitation in Dogs: Markers of Damage and Predictors of Outcome

Vaagenes

Šafář

Diven

et al. 1988

J Cereb Blood Flow Metab

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Summary: Levels of brain creatine kinase (CK), aspar tate aminotransferase (ASAT), and lactate dehydroge nase (LD) in CSF after cardiac arrest were studied in dog models. Ventricular fibrillation cardiac arrest lasting 10 min or asphyxiation cardiac arrest lasting 0-10 min was followed by cardiopulmonary resuscitation and 96-h in tensive care. Outcome was scored as neurologic deficit (0% = normal, 100% = brain death) and overall perfor mance category (1 = normal,S = death). Both measures correlated with EEG return time after asphyxiation car diac arrest, but not after ventricular fibrillation cardiac arrest. Peak activity of enzymes in CSF at 48-72 h post arrest correlated with outcome, and CK was the best pre dictor. Brain histopathologic damage score at autopsy 96 h post arrest correlated with CK level in CSF (r = 0.79, n = 39) and neurologic deficit (r = 0.70, n = 50). Ischemic neuronal changes occurred after ventricular fibrillation cardiac arrest of 10 min, and neuronal changes plus miAdvanced cardiopulmonary-cerebral resuscita tion (Safar and Bircher, 1988) has made cardiac ar rest (complete temporary global brain ischemia) of longer than 5 min reversible to complete recovery (Abramson et aI., 1986;Safar, 1986 262croinfarcts occurred after asphyxiation cardiac arrest of 1.5-10 min. Brain enzymes were decreased at 6 h post arrest in regions with worst histologic damage (gray matter of neocortex, hippocampus, caudate nucleus, cer ebellum). Brain CK decreased further, ASAT remained low, and LD increased at 72 h after arrest. The temporal changes in CK level paralleled the temporal ischemic neuronal changes in the brain, and time to peak activity was unaffected by the severity of the ischemic insult. Peak activity of individual enzymes in CSF was deter mined predominantly by the brain concentration, but was also influenced by rate of decomposition. This "chemical brain biopsy method" represents a useful adjunctive tool to predict permanent, severe brain damage during coma tose states after cardiac arrest and resuscitation.

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Ryanodine Perfusion Decreases Cardiac Mechanical Function Without Affecting Homogenate Sarcoplasmic Reticulum Ca2+Uptake: Comparison with the Stunned Heart

1996

Journal of Molecular and Cellular Cardiology

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Effect of Ischemia

Cited by 9 publications

References 132 publications

Brain Energy Metabolism During the Process of Dying and After Cardiopulmonary Resuscitation

Brain Energy Metabolism During the Process of Dying and After Cardiopulmonary Resuscitation

Brain Enzyme Levels in CSF after Cardiac Arrest and Resuscitation in Dogs: Markers of Damage and Predictors of Outcome

Ryanodine Perfusion Decreases Cardiac Mechanical Function Without Affecting Homogenate Sarcoplasmic Reticulum Ca2+Uptake: Comparison with the Stunned Heart

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