[Changes in cerebral blood flow and oxidative cerebral metabolism after extensive acute head trauma (author's transl)].
Total cerebral blood flow and oxidative cerebral metabolism were measured at normal pCO2, hypocapnia and hypercapnia in 15 unconscious patients in the acute phase after head trauma. In the basal position (normal CO2) measurements were within normal limits and did not correspond to the severity of the clinical picture. But on altering arterial pCO2 there were market changes in oxidative cerebral metabolism, which suggests an abnormal cerebral regulatory mechanism. Measurement of the same functions 14 days later indicated, on the one hand, persistence of changes, but, on the other, a return to normal of previously markedly elevated cerebral glucose uptake. Comparing cerebral blood flow and metabolism between patients who survived and those who died in the acute phase after brain damage, there were no significant differences.
D000328:Adult; D001158:Arteries; D001921:Brain / Q000378:metabolism*; D001930:Brain Injuries / Q000150:complications / Q000378:metabolism*; D002245:Carbon Dioxide / Q000097:blood; D002560:Cerebrovascular Circulation; D002561:Cerebrovascular Disorders / Q000150:complications; D005947:Glucose / Q000378:metabolism; D006801:Humans; D010084:Oxidation-Reduction; D010313:Partial Pressure; D013997:Time Factors
D002245:Carbon Dioxide; D005947:Glucose
Veränderungen der Hirndurchblutung und des oxidativen Hirnstoffwechsels bei akuten substaniellen traumatischen Hirnschäden