[Influence of combined moderate arterial hypoxaemia and moderate hypovolaemic hypotension on cerebral blood flow and cerebral oxidative and energy metabolism in the dog (author's transl)].

The influence on total cerebral blood flow, cerebral metabolic rates for oxygen, carbon dioxide, glucose, lactate and pyruvate and on cerebral grey matter content of glucose, lactate and pyruvate and high energy phosphate compounds of combined moderate reduction in cerebral perfusion pressure (CPP) and moderate arterial hypoxaemia was studied. Individually arterial hypoxaemia and arterial hypotension of the same degree would neither impair autoregulation of cerebral blood flow nor cerebral oxygen availability. Four groups of 10 dogs each were studied under control conditions (group I), with reduction of CPP to 70 mm Hg (group II), with reduction of paO2 to 45 mm Hg (group III) or with a combination of these degrees of hypotension and hypoxaemia (group IV) after steady states of 30 min duration. Cbf was elevated by 40% in group III (p less than or equal to 0.01), CMRO2 was reduced significantly in group IV (p less than or equal to 0.01, CMR lactate was raised significantly in all three experimental groups (p less than or equal to 0.01). All other data were not significantly different from values in control animals. Cerebral tissue lactate content was elevated significantly in groups II to IV as compared to controls (less than or equal to 0.05); changes in cerebral tissue content of glucose and energy rich phosphate compounds were not statistically significant. From the seemingly normal cerebral blood flow in hypotensive-hypoxaemic dogs it is concluded that autoregulation of cerebral blood flow has become ineffective because of vasodilatation consequent upon arterial hypoxaemia. Reduction of CMRO2 in this group points to metabolic insufficiency and to relative cerebral hypoperfusion, but since changes in cerebral content of high energy phosphate compounds were not significant, severe tissue hypoxia may be excluded. The increase in cerebral tissue lactate content is attributable to increased glycolytic activity known from hypotensive and hypoxaemic states. The present investigation suggests that in patients with hypoxaemia and hypotension, brain function may be endangered by a similarly marked change of circulatory and metabolic parameters.