
doi: 10.1007/bf01400588
pmid: 1595393
Post-ischemic reperfusion impairment, ("no-reflow phenomenon"), was studied in rats subjected to 8-30 minutes of global brain ischemia. During ischemia, rapid and complete loss of cerebral blood flow, EEG and 31P-high energy phosphates (ATP/PCr) was observed. Brain intravascular perfusion defects were examined by injecting carbon black intravenously in a group of rats with stable cardiopulmonary function and in another group subjected to rapid thoracotomy and intraarterial infusion of the carbon marker. Results indicate that global brain ischemic or non-ischemic control rats given intraarterial carbon black after thoracotomy had varying degrees of vessel filling defects in brain resulting in "pale tissue areas" suggestive of impaired perfusion (no-reflow). All rats given carbon black intravenously whether global brain ischemic or not, showed normal cerebrovascular filling of the carbon black and absence of "pale tissue areas". In addition, post-ischemic cerebral reperfusion following 8-30 minutes global brain ischemia can reverse neuroelectric, energy metabolite and cerebral blood flow loss in rats whose cardiopulmonary function is not compromised. These findings indicate that the "no-reflow phenomenon" is an agonal or post-mortem artifact observed in the presence of cardiopulmonary failure.
Cerebral Cortex, Male, Phosphocreatine, Brain, Rats, Inbred Strains, Cerebral Arteries, Brain Ischemia, Rats, Adenosine Triphosphate, Cerebrovascular Circulation, Postmortem Changes, Reperfusion Injury, Animals, Brain Damage, Chronic, Artifacts
Cerebral Cortex, Male, Phosphocreatine, Brain, Rats, Inbred Strains, Cerebral Arteries, Brain Ischemia, Rats, Adenosine Triphosphate, Cerebrovascular Circulation, Postmortem Changes, Reperfusion Injury, Animals, Brain Damage, Chronic, Artifacts
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