Coagulopathy following experimental cerebral ischemia.
In adult normothermic cats cerebral blood flow was interrupted for 1 hour by clamping the innominate and subclavian arteries. Following ischemia the brains were recirculated with blood, and the coagulation system was investigated by measuring coagulation times and blood content of fibrinogen and platelets. Ischemia induced progressive consumption coagulopathy with an increase in coagulation times and a decrease of platelets and fibrinogen by more than 40%. Coagulopathy was accompanied by a respiratory distress syndrome with a significant increase in the alveolar-arterial carbon dioxide gradient from --3.3 to --13.5 mm Hg. A correlation was found between plasma fibrinogen concentration, cerebral blood flow and electrophysiological function, indicating that a relationship exists between the severity of postischemic coagulopathy and functional recovery following prolonged cerebral ischemia.
D000818:Animals; D001772:Blood Cell Count; D001792:Blood Platelets; D001921:Brain / Q000098:blood supply* / Q000473:pathology; D002415:Cats; D002543:Cerebral Hemorrhage / Q000209:etiology; D002560:Cerebrovascular Circulation; D004211:Disseminated Intravascular Coagulation / Q000209:etiology*; D007511:Ischemia / Q000150:complications*; D010477:Perfusion; D012128:Respiratory Distress Syndrome / Q000503:physiopathology; D013566:Sympathomimetics / Q000494:pharmacology
D013566:Sympathomimetics