No abstract

No abstract

No abstract

Determinations of acid monoamine metabolites, such as homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA), in cerebrospinal fluid (CSF) give valid information on the metabolism of the corresponding amines in the brain tissue (Moir et al., 1970; Roos, 1970). The monoamine metabolites in the CSF are related to age. The concentrations of HVA and 5-HIAA increase with age (Gottfries et al., 1971). Probenecid blocks the elimination of HVA and 5-HIAA from brain tissue to blood (Neff et al., 1964, 1967; Werdinius, 1966) and from CSF to blood (Guldberg et al., 1966; Olsson and Roos, 1968). Probenecid thus normally induces an increase in the concentrations of the acid monoamine metabolites in the CSF, which is related to the turnover of monoamines in the brain tissue.

KJALLQUIST, A., M. NARDINI and B. K. SIESJO. T h e effect of acetazolamide u p o n tissue concentrations of bicarbonate, lactate, and pyruuate in the rat brain. Acta physiol. scand. 1969. 77. 241-251. The effect of various doses of acetazolamide upon acid-base parameters in brain tissue, cisternal CSF and arterial plasma was studied in rats, anesthetized with phenobarbital or nitrous oxide. The results confirmed older findings that carbonic anhydrase inhibition increases the CSF /plasma ratio for bicarbonate, and decreases the corresponding chloride ratio, and showed that the CSF p H remains unchanged during at least 6 hrs in spite of a marked plasma acidosis. The tissue bicarbonate was found to be significantly, but transiently, increased, and since the CSF bicarbonate was essentially unchanged, the increase in bicarbonate must have occurred in the intracellular phase, i.e. an alkaline shift in the cells. However, both the lactate and the pyruvate concentrations in the tissue were decreased after acetazolamide, suggesting a n acidosis. It is discussed if these controversial findings indicate that cai bonk anhydrase inhibition gives rise to a carbonic acid acidosis in the brain.The effects of carbonic anhydrase inhibition on secretory functions and on ion transport in several different organs are well known (see review by Maren 1967), and as the occurrence of carbonic anhydrase in glial cells in the brain has been established (Giacobini 1962), it has been assumed that carbonic anhydrase-catalyzed reactions are involved in hydrogen ion transport in the brain. However, since a study of the acid-base metabolism of a tissue requires that the tissue COZ tension is known, and since carbonic anhydrase inhibitors like acetazolamide lead to a disequilibrium in the COZ buffer systems of the organism, precluding accurate assessment of blood COZ tensions, the effect of carbonic anhydrase inhibition on tissue acid-base parameters is poorly understood.Recently we reported measurements of blood and brain tissue C 0 2 tensions in rats and cats given various doses of acetazolamide (Brzezihski, Kjallquist and Siesjo 1967). The tissue CO, tension were either measured directly with a surface CO-1 0 n leave of absence from the