Brain cortex tissue Ca, Mg, Fe, Na, and K following resuscitation from cardiac arrest in dogs

Hoehner, Thomas; Garritano, Ann Marie; Dilorenzo, Robert A.; O’Neil, Brian J.; Kumar, Kusum; Koehler, John E.; Nayini, Narsimha R; Huang, Ran; Krause, Gary S.; Aust, Steven D.; White, Blaine C.

doi:10.1016/0735-6757(87)90283-x

Cited by 14 publications

(1 citation statement)

References 23 publications

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“…22 When measurements of conjugated dienes are used as evidence of lipid peroxidation, investigators have demonstrated only limited elevation during reperfusion from global ischemia. 23 There also appears to be both regional 21 and species 24 variations for the amount of lipid peroxidation that is produced during reperfusion from ischemia.…”

Section: Discussionmentioning

confidence: 99%

Tirilazad mesylate does not improve early cerebral metabolic recovery following compression ischemia in dogs.

Helfaer

Kirsch

Hurn

et al. 1992

Stroke

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Background and Purpose: Tirilazad mesylate (U74006F) has been reported to improve recovery following cerebral ischemia. We conducted a randomized blinded study to determine if the drug would improve immediate metabolic recovery after complete cerebral compression ischemia.Methods: Mongrel dogs were anesthetized with pentobarbital and fentanyl and treated with either vehicle (citrate buffer, n=8) or tirilazad (1.5 mg/kg i.v. plus 0.18 mg/kg/hr, n=8). Normothermic complete cerebral compression ischemia was produced for 12 minutes by lateral ventricular fluid infusion to raise intracranial pressure above systolic arterial pressure. Cerebral high-energy phosphate concentrations and intracellular pH were measured by phosphorus magnetic resonance spectroscopy. Cerebral blood flow was measured with radiolabeled microspheres, and oxygen consumption was calculated from sagittal sinus blood samples. Somatosensory evoked potentials were measured throughout the experiment.Results: During ischemia, both groups demonstrated complete loss of high-energy phosphates and a fall in intracellular pH (vehicle, 5.76±0.23; tirilazad, 5.79±0.26; mean±SEM). At 180 minutes of reperfusion, there were no differences between groups in recovery of intracellular pH (vehicle, 6.89±0.07; tirilazad, 6.88±0.18), phosphocreatine concentration (vehicle, 89±16%; tirilazad, 94±24% of baseline value), oxygen consumption (vehicle, 2.6±0.2 ml/min/100 g; tirilazad, 1.8+0.5 ml/min/100 g), or somatosensory evoked potential amplitude (vehicle, 11±6%; tirilazad, 7±4% of baseline value). Forebrain blood flow fell below baseline levels at 180 minutes of reperfusion in the tirilazad-treated animals but not in the vehicle-treated dogs (vehicle, 28±4 ml/min/100 g; tirilazad, 18±5 ml/min/100 g).Conclusions: We conclude that tirilazad pretreatment does not improve immediate metabolic recovery 3 hours following 12 minutes of normothermic complete ischemia produced by cerebral compression.

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Section: Discussionmentioning

confidence: 99%

Tirilazad mesylate does not improve early cerebral metabolic recovery following compression ischemia in dogs.

Helfaer

Kirsch

Hurn

et al. 1992

Stroke

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Simultaneous ³¹P NMR spectroscopy and laser doppler flowmetry of rat brain during global ischemia and reperfusion

et al. 1993

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The relationship between blood flow and metabolism was studied in halothane-anaesthetized, normothermic rats submitted to 30 min global ischemia by four-vessel occlusion. Phosphocreatine (PCr), ATP, intracellular pH and intracellular magnesium (pMg) were measured by 31P NMR spectroscopy, and blood flow by laser Doppler flowmetry. Prior to ischemia the PCr/ATP ratio of fully relaxed spectra was 2.4 +/- 0.3, intracellular pH was 7.26 +/- 0.15 and pMg was 3.26 +/- 0.13. Vascular occlusion led to complete cessation of blood flow in four out of eight rats, and to incomplete ischaemia (< 10% of control) in the other four animals. During vascular occlusion EEG flattened and energy metabolism broke down in all but one animal with a residual blood flow of 8% of control. pH declined to 6.70 +/- 0.08. The speed of electrophysiological and metabolic recovery after 30 min ischemia varied considerably from animal to animal. Variability depended mainly on the recirculation delay (i.e., the interval from vascular release to normalization of blood flow) but was independent of residual blood flow during ischemia, pre-ischemic glucose, ischemic or post-ischemic acidosis, or the degree of post-ischemic hypoperfusion. After 3 h recirculation PCr and intracellular pH returned to normal but pMg was slightly increased, and ATP was reduced by up to 50% in all animals except the rat with incomplete breakdown of energy metabolism during ischemia. The dissociation between PCr and ATP is attributed to a loss of total adenylate, the severity of which depends on the quality of post-ischemic recirculation.(ABSTRACT TRUNCATED AT 250 WORDS)

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Biochemical Changes and Secondary Tissue Injury After Brain and Spinal Cord Ischemia

Faden

Weinstein

Bakshi

et al. 1992

Neurochemical Correlates of Cerebral Ischemia

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Brain cortex tissue Ca, Mg, Fe, Na, and K following resuscitation from cardiac arrest in dogs

Cited by 14 publications

References 23 publications

Tirilazad mesylate does not improve early cerebral metabolic recovery following compression ischemia in dogs.

Tirilazad mesylate does not improve early cerebral metabolic recovery following compression ischemia in dogs.

Simultaneous ³¹P NMR spectroscopy and laser doppler flowmetry of rat brain during global ischemia and reperfusion

Biochemical Changes and Secondary Tissue Injury After Brain and Spinal Cord Ischemia

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Brain cortex tissue Ca, Mg, Fe, Na, and K following resuscitation from cardiac arrest in dogs

Cited by 14 publications

References 23 publications

Tirilazad mesylate does not improve early cerebral metabolic recovery following compression ischemia in dogs.

Tirilazad mesylate does not improve early cerebral metabolic recovery following compression ischemia in dogs.

Simultaneous 31P NMR spectroscopy and laser doppler flowmetry of rat brain during global ischemia and reperfusion

Biochemical Changes and Secondary Tissue Injury After Brain and Spinal Cord Ischemia

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Simultaneous ³¹P NMR spectroscopy and laser doppler flowmetry of rat brain during global ischemia and reperfusion