Changes in Microvascular Diameter and Oxygen Tension Induced by Carbon Dioxide

Abstract

Microvascular diameters in the hamster cheek pouch were measured with a Vickers image-shearing eyepiece, and oxygen tension (Po 2 ) was measured amperometrically with 2-6µ microcathodes. Perivascular Po 2 was dependent on both the type of microvessel observed and the composition of the solution bathing the tissue. During application of a solution with a mean Po 2 of 17 mm Hg and a Pco 2 of 0 mm Hg, a longitudinal gradient in perivascular Po 2 was observed: Po 2 decreased from 44 ± 2 ( SE ) mm Hg at the large arterioles to 18 ± 2 mm Hg at the capillary origin. Tissue Po 2 was 10 ± 1 mm Hg. Suffusion of the cheek pouch with a solution with approximately the same Po 2 and a Pco 2 of 32 mm Hg resulted in an elevation of perivascular Po 2 at all sites. Large arteriolar Po 2 under these circumstances was 47 ± 2 mm Hg, capillary origin Po 2 was 29 ± 3 mm Hg, and tissue Po 2 was 17 ± 3 mm Hg. CO 2 also produced vasodilation: the average vascular diameter increased 18 ± 7% when the solution Pco 2 was increased from 0 to 32 mm Hg. The tissue showed evidence of regulation of tissue O 2 supply both with and without CO 2 in the suffusion solution. The effects of CO 2 on the distribution of O 2 were compared with the effects of other vasodilators, and it was found that the tissue Po 2 was not consistently changed by the application of the vasodilators, whereas it was elevated 70% by CO 2 . This difference is attributed in part to the effect of CO 2 on the oxyhemoglobin dissociation curve.