Relative importance of tissue oxygenation and vascular smooth muscle hypoxia in determining arteriolar responses to occlusion in the hamster cheek pouch.

Cheek pouches of anesthetized hamsters were suffused with solutions with low, medium, and high oxygen tension, and arteriolar diameter changes were measured during and after occlusions of either single arterioles or the whole vascular bed. PO 2 was measured with microelectrodes on arteriolar walls and at surrounding tissue sites to indicate oxygen availability to the vascular smooth muscle and parenchymal cells, respectively. In each suffusion solution, whole pouch occlusion (WPO) and microvessel occlusion (MVO) induced quantitatively similar changes in tissue and periarteriolar PO 2 ; however, WPO resulted in larger diameter increases and longer recovery times than MVO. High suffusion solution PO 2 attenuated the reduction in tissue and periarteriolar PO 2 during occlusion (WPO and MVO), reduced the dilation during occlusion (WPO and MVO), and was associated with faster recovery of arteriolar diameters following release of WPO. Postocclusion recovery of periarteriolar PO 2 and tissue PO 2 in low oxygen suffusion was significantly faster than that of arteriolar diameters (WPO and MVO). Following WPO, periarteriolar PO 2 often had fully recovered while diameter was at its peak value. During intermediate and high PO 2 suffusion, arteriolar dilation occurred despite relatively high periarteriolar oxygen tensions. The evidence suggests that arteriolar responses to occlusion are determined primarily by indirect mechanisms, i.e., those mediated through parenchymal cell metabolites, rather than by the direct effects of oxygen deficiency on the vascular smooth muscle cells of the arteriolar media.