The effect of dextran and streptokinase on cerebral function and blood flow after cardiac arrest. An experimental study on the dog.
EEG activity and regional cerebral blood flow were studied during 5 h of maintenance following 12-16 min of cardiac arrest in 33 anesthetized dogs. Group I received no treatment. Group II received dextran 40. Group III were given both dextran 40 and streptokinase. In Group III the duration of flat EEG was significantly shorter than in Group I or II (P less than 0.002 and less than 0.008). The EEG score at 3 h had already reached a significant level as compared to Group I (P less than 0.005 at 3 h and P less than 0.002 at 5 h). The blood flow in the grey matter and hippocampus was greater in Group III than in Groups I and II. After 3 h the flow in Group III had already reached a significant level (P less than 0.0002, both grey matter and hippocampus) as compared to that in Group I. The findings suggest that impaired cerebral perfusion and function after cardiac arrest are most likely secondary to a combination of hemoconcentration, hyperviscosity, microthrombi formation, and edema at the microcirculatory level. Thus postischemic encephalopathy is in part due to perfusion abnormalities present after arrest, and is therefore amenable to therapy.
D000818:Animals; D001921:Brain / Q000187:drug effects*; D002560:Cerebrovascular Circulation / Q000187:drug effects; D003911:Dextrans / Q000494:pharmacology*; D004285:Dogs; D004569:Electroencephalography; D006323:Heart Arrest / Q000503:physiopathology*; D013300:Streptokinase / Q000494:pharmacology*
D003911:Dextrans; D013300:Streptokinase