In Vitro and in Situ Studies

We tested the hypothesis that a parenchymally derived mediator is required for arterioles to exhibit oxygen sensitivity. To that end, the parenchyma was dissected and removed from around hamster cheek pouch arterioles, and the oxygen sensitivity of these 'aparenchymal arteriolar segments' was studied, either in vitro, after cannularion, or in situ. Arteriolar segments in situ with and without parenchyma had similar oxygen sensitivities (20% constriction as Po? increased from 15 to 150 mm Hg). Arteriolar occlusion, which eliminated blood flow in the in situ aparenchymal segments, did not eliminate their oxygen sensitivity. The oxygen-induced constriction in the occluded aparenchymal segments was blunted but not eliminated by covering the segments with glass plates to prevent changes in P02 from occurring around these vessels. We hypothesized that propagation of a portion of the oxygen response might explain the persistent response in the covered and occluded arteriolar segments. Oxygen sensitivity could be shown in only 32% of the in vitro cannulated arterioles (16% mean constriction as P02 increased from 20 to 150 mm Hg). In contrast, 75% of aparenchymal arterioles were sensitive to changes in P02 in situ. These data led us to reject the hypothesis that a parenchymally derived mediator is absolutely required for arterioles to exhibit oxygen sensitivity. We infer that the oxygen sensitivity of hamster cheek pouch arterioles results partially or totally from the local action of oxygen on some component of the arteriolar wall or blood, that a portion of the oxygen response may be the result of a propagated phenomenon, and that the oxygen-sensitive component is fragile and is easily lost in preparation for in vitro measurements or in cannulation. It is emphasized that the O2 sensor need not reside in vascular smooth muscle. (Circ Res 53: 515-525, 1983)