No-flow state following cerebral ischemia. Role of increase in potassium concentration in brain interstitial fluid.
Rats were subjected to total cerebral ischemia by occluding outflow from the heart. In control experiments and following different periods of ischemia, potassium concentration was measured in cisternal cerebrospinal fluid (CSF). It rose to 19.4 mEq/liter following 16 minutes of ischemia. Changes in cerebrovascular resistance (CVR) were also assessed by measuring the cerebral perfusion rate (CPR). Following two minutes of ischemia, CVR was decreased to half control value. After 8 and 16 minutes of ischemia, CVR was markedly increased, and "no-flow" state was approached after 16 minutes of ischemia. The CVR increased concomitantly with increase in potassium concentration in cisternal CSF. We suggest that the increase in CVR following cerebral ischemia is due to increase in potassium concentration in brain extracellular fluid and is part of a vicious circle that leads to brain death.
D000818:Animals; D002531:Cerebellum / Q000503:physiopathology; D002540:Cerebral Cortex / Q000378:metabolism / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D002712:Chlorides / Q000097:blood / Q000134:cerebrospinal fluid; D007511:Ischemia / Q000503:physiopathology*; D008297:Male; D010477:Perfusion; D011188:Potassium / Q000097:blood / Q000134:cerebrospinal fluid* / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000097:blood / Q000134:cerebrospinal fluid; D013997:Time Factors; D014316:Tritium; D014655:Vascular Resistance; D014867:Water / Q000378:metabolism
D002712:Chlorides; D014867:Water; D014316:Tritium; D012964:Sodium; D011188:Potassium