The aim of these studies is to elucidate the mechanisms of reactive hyperemia and other local regulatory phenomena. According to current concepts reactive hyperemia is due to loss of myogenic tone of the arterioles and to metabolic factors, i.e. drop in tissue PO2, and accumulation of metabolic bi-products. However, the time course of reactive hyperemia typically requires 5-10 seconds to attain peak flow in skeletal muscle. The prolonged rising phase suggests that an additional mechanism may be involved. It seems quite possible that the latent period for restoration of myogenic tone is different from the time course for the washout of vasodilator metabolites. Therefore the pattern of return to control flow levels may depend importantly upon the relative strength of these factors. In earlier studies of reactive hyperemia in single capillaries of skeletal muscle we have noticed that flow in some capillaries returns gradually to control while in others it returns very quickly and flow may drop to zero for a time. We propose to study this phenomena by lowering arterial pressure to varying levels for varying durations in order to differentially effect the metabolic and myogenic factors. We will also monitor tissue PO2 in the vicinity of arterioles while measuring flow in the vessel to determine whether this factor seems to be regulated. Also tissue PO2 will be altered by application of suffusing solution. Micro-occlusions of arterioles and capillaries are also planned.
NIH ExPorter
NIH ExPorter