The relative contribution of O2 and CO2 to the metabolic control of blood flow in long-term exercise was examined in the denervated gracilis muscle of the anesthetized dog. The data show that 1) on initiation of heavy exercise, the effluent blood PO2 and pH fall markedly and then rise slowly but remain depressed relative to control during 60 min of exercise hyperemia, while the initial increases in [K+] and osmolality rapidly approach and eventually reach preexercise levels. 2) The enhanced vasodilator activity of venous blood from exercising muscle is attenuated when effluent blood PO2 or pH is corrected to preexercise levels; it is completely abolished when both are corrected. 3) Induced reduction PO2 or pH in the arterial inflow, and thus venous outflow, of resting muscle produces a fall in resistance; simultaneous reductions of both to levels seen in heavy exercise produce a fall in resistance to near that observed during exercise. Since the enhanced vasodilator activity of venous blood from the contracting muscle was abolished by simultaneous correction of the PO2 and pH, it seems likely that these factors, acting directly or indirectly, are the principal chemicals responsible for the maintenance of the vasodilation seen in canine skeletal muscle during heavy exercise.

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Brains of methoxyflurane-anesthetized chickens were perfused from a lateral cerebral ventricle to cisterna magna with an artificial cerebrospinal fluid (CSF) containing trace quantities of radioiodinated human serum albumin (RIHSA) or inulin (1.0 mg/ml) to measure CSF bulk absorption. In addition, it contained either trace quantities of 22Na, 42K, 45Ca or [14C]creatinine; the concentrations of the latter three were varied to determine permeability coefficients (K-D's) as a function of concentration. A mass balance for the tracer molecules was calculated to determine their movement into brain or blood. K-D's for 45Ca, 42K, 22Na, and creatinine (Cr) were unaffected by perfusion time and the latter two were larger than previously reported (3). The lack of effect of time on K-D and the large values for K-D22Na and K-D-Cr are attributed to anesthetic effects on brain blood flow. K-D-Cr and K-D42K were larger than K-D22Na or K-D45Ca and K-D's for 45Ca, Cr, and 42K were independent of their inflow concentrations. An active transport process is suggested for potassium and creatinine, but one that is located at sites other than the ependymal wall. Bulk flow clearance accounted for RIHSA movement from CSF, whereas nonbulk clearance accounted for 50% of 22Na and 45Ca movement and 90% of 42K clearance. Fifty percent of 42K and 25% of 22Na and 45Ca were found in brain. The large recovery of 42K in brain supports the hypothesis that intracellular potassium serves as an exchangeable pool for the tracer.

The rate coefficients and fluxes of sodium across the outside and inside barriers of an in vitro, short-circuited frog skin preparation were determined in the presence of a uremic serum fraction to localize the site of action of an inhibitor of sodium transport. In unpaired studies, the mean depression of short-circuit current (SCC) resulting from the addition of the uremic serum fraction (21.9 ± 2.2%) was significantly greater than the decrease in SCC resulting from either frog Ringer’s wash or normal serum fractions. Paired studies comparing active and inactive uremic serum fractions indicated that the reduction in net sodium transport, whether calculated from changes in SCC ( – 0.55 ± 0.12 µEq/h) or changes in unidirectional ²⁴Na fluxes (? 0.56 ± 0.15 µEq/h) was significantly greater in hemi-skins treated with the active fraction. The depression in sodium transport was associated with a significant decrease of sodium movement from the skin to the inside compartment, Φ22 (-0.62 ± 0.2 µEq/h). The results of these studies suggest that the inhibition of sodium transport ascribed to the uremic serum fraction is due to an inhibition of the active transport mechanism located at the serosal barrier.