Modulation of the pathophysiology of primate focal cerebral ischaemia by indomethacin.
The effect of indomethacin (3mg/kg IA) preloading on the pathophysiology of a model of acute cerebral ischaemia has been tested. Primates anaesthetised with alpha-chloralose were used. Indomethacin reduced basal blood flow by 39% and reduced CO2 reactivity by 71%. Water content changes of the cerebral cortex and relationships between blood flow and extracellular potassium (Ke), and calcium (Cae) activities have been measured. Indomethacin infusion did not effect the water content of the left side but there was more water in all regions of the right hemisphere which were rendered ischaemic. There water increases were significant for blood flows greater than 5ml/100g/min in exposed areas. There was a significant increase in the flow thresholds for change in Ke and Cae. Possible mechanisms for these changes have been discussed.
D000818:Animals; D001834:Body Water / Q000378:metabolism; D001929:Brain Edema / Q000209:etiology / Q000517:prevention & control; D002545:Brain Ischemia / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D002118:Calcium / Q000378:metabolism; D002560:Cerebrovascular Circulation / Q000187:drug effects; D006706:Homeostasis / Q000187:drug effects; D007213:Indomethacin / Q000494:pharmacology*; D010215:Papio; D011188:Potassium / Q000378:metabolism
D011188:Potassium; D002118:Calcium; D007213:Indomethacin