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

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Abstract
Cheek pouches of anesthetized hamsters were suffused with solutions with low, medium and high O2 tension and arteriolar diameter changes were measured during and after occlusions of either single arterioles or the whole vascular bed. PO2 [partial O2 pressure] was measured with microelectrodes on arteriolar walls and at surrounding tissue sites to indicate O2 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 PO2. WPO resulted in larger diameter increases and longer recovery times than MVO. High suffusion solution PO2 attenuated the reduction in tissue and periarteriolar PO2 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 PO2 and tissue PO2 in low O2 suffusion was significantly faster than that of arteriolar diameters (WPO and MVO). Following WPO, periarteriolar PO2 often had fully recovered while diameter was at its peak value. During intermediate and high PO2 suffusion arteriolar dilation occurred despite relatively high periarteriolar O2 tensions. Arteriolar responses to occlusion are apparently determined primarily by indirect mechanisms, i.e., those mediated through parenchymal cell metabolites rather than by the direct effects of O2 deficiency on the vascular smooth muscle cells of the arteriolar media.