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British Journal of Anaesthesia, 1992, Vol. 69, No. 6 615-620
© 1992 The Board of Management and Trustees of the British Journal of Anaesthesia

research-article

MODULATION BY CARBON DIOXIDE AND pH OF THE CONTRACTILE RESPONSES TO POTASSIUM AND PROSTAGLANDIN F2a IN ISOLATED HUMAN PIAL ARTERIES

P. REINSTRUP, M.D.*, T. USKI, M.D., PH.D. and K. MESSETER, M.D., PH.D.

Department of Clinical Pharmacology, Neurosurgery and Anesthesiology, University Hospital Lund, Sweden

* Present address, for correspondence: Department of Anesthesiology, University Hospital, DK-2600 Glostrup, Denmark.

Variation of PCO2 with concomitant changes in extracellular pH (pH0) may modulate cerebrovascular resistance, but the direct actions of carbon dioxide and pH0 on human cerebral arteries are unknown. In this study, we have evaluated the effects of different carbon dioxide tensions (2.7, 4.2 and 7.2 kPa) with either fixed (pH0 = 7.44) or concomitant changes in pH0 on contractions induced by depolarization (potassium) or receptor stimulation (prostaglandin F2x. in isolated human pial arteries. Isolated changes in PCO2 had no significant effect on either potency (unchanged EC50 value) or the maximum response (Emax) in potassium–contracted arteries. Hypercapnia with uncompensated pH0 significantly decreased both EC50 and Emax values, whereas uncompensated hypocapnia significantly increased the EC50 value without any effect on Emax. Concentration–response curves induced by prostaglandin (PG) F2x were shifted significantly to the right (increased EC50 = decreased potency) during both hypo– and hypercapnia, independent of changes in pH0. The maximal responses were enhanced significantly during hypocapnia (Emax =110 (SEM2)%), but this enhancement was converted into a slight attenuation when pH0 was compensated (Emax = 92 (4) %). Hypercapnia, with or without compensation of pH0 decreased the Emax values to 69 (16)% and 73 (9) %, respectively. We conclude that hypocapnia increases contractility in human pial arteries–an effect which is reversed by compensation of pH0. In contrast, the hypercapnic decrease of PGF2x –induced contractions appears to be independent of pH0. The results confirm a relationship between contractility and pH0 but do not exclude a direct action of carbon dioxide in receptor–stimulated arteries.


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