Cerebral oxidative metabolism in essential hypertension: a meta-analysis.

Abstract

To investigate oxidative metabolism in the brain in essential hypertension, by analysing the cerebral respiratory exchange ratio. For any organ, this value (usually designated 'respiratory quotient') is the ratio of carbon dioxide produced to oxygen consumed. Its value depends mainly on the (one or more) fuel supplying energy. Despite the inaccuracies inevitable in measurements of cerebral respiratory quotient, such measurements might provide a new line of attack on the yet unsolved problem of increased central neurogenic activity in essential hypertension. Although values for cerebral respiratory quotient have very rarely been provided in raw data tables, individual values for arterial and jugular venous blood oxygen and carbon dioxide contents were often published between 1948 and 1961 in papers in which Kety's method of measuring cerebral blood flow was used. This enabled me to calculate reasonably large samples of cerebral respiratory quotients in hypertensive as well as in normal subjects. Such information cannot be obtained from positron emission studies of brain metabolism. The respiratory quotient of the brain is normally between 0.98 and 0.99. This is compatible with current views that the brain uses almost exclusively glucose as its metabolic fuel. In the presence of essential hypertension the respiratory quotient is significantly lower (approximately 0.91). This indicates that the pattern of oxidative metabolism in the brain must be different. Although the cerebral respiratory quotient probably declines slightly with increasing age, the low value in essential hypertension is not explicable by age differences. Although other explanations are possible, the present results suggest that borderline, low-grade or intermittent cerebral ischaemia in essential hypertension may have caused a change in cerebral metabolism, or in access of glucose to brain cells. Even lower cerebral respiratory quotients have been reported in the presence of symptomatic cerebrovascular disease. It is possible that changes in cerebral oxidative metabolism may exert neurogenic or perhaps hormonal influences on long-term blood pressure regulation.