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Microperfusion and free-flow micropuncture studies were performed in anesthetized rats to compare the rates of K flux in early and late segments of the distal tubule. Early distal segments were located within the initial 40% of distal tubule length, and late distal segments were located within the terminal 35% of the distal tubule. In early distal segments of control rats, significant K secretion was observed at perfusion rates of 6 and 14 nl/min. In high-K rats significant K secretion was only observed at the lower perfusion rate. Late segments of control rats secreted 70.5 +/- 8.2 at the low flow rate and 139 +/- 18.9 pmol X min-1 X mm-1 at the high flow rate. In K-adapted rats, values were 134.4 +/- 30.2 and 178 +/- 29.3 pmol X min-1 X mm-1. During free flow, we observed a K flux in control rats of 11.0 +/- 9.4 pmol X min-1 X mm-1 (NS) in early segments and a K flux of 55 +/- 6.5 pmol X min-1 X mm-1 in late segments. In K-adapted rats, values were 18.3 +/- 6.7 (P less than 0.05) in early and 123 +/- 17.2 pmol X min-1 X mm-1 in late segments. The majority of our data suggests that the distal convoluted tubule secretes K at a low rate that is not influenced by flow rate or a high-K diet.

The roles of luminal pH and flow rate in determining ammonia entry along the rat proximal tubule were examined using in vivo microperfusion. With perfusion rate constant at 15 nl/min, perfusate bicarbonate concentration was varied. Collected fluid ammonia concentration correlated with collected fluid bicarbonate concentration, consistent with nonionic diffusion (r = 0.726; P less than 0.001). Hence ammonia entry was dependent on luminal pH. With perfusate bicarbonate constant at 5 or 25 mM, perfusion rate was varied. In all groups, there was little change in collected fluid ammonia concentration with flow rate. Thus ammonia entry was also highly dependent on flow rate. With paired collections using a 25 mM bicarbonate perfusate, collected fluid bicarbonate was higher at a 30 nl/min perfusion rate than at 15 nl/min (16.8+/- 1.1 vs. 10.3+/- 1.1 mM), whereas total ammonia concentrations were similar (0.54+/- 0.1 and 0.55+/- 0.1). Thus the NH3 concentration was higher at 30 than at 15 nl/min (6.1+/- 1.2 vs. 3.4+/- 0.5 microM; P less than 0.025), a result not predicted by simple nonionic diffusion. Thus these studies demonstrate the importance of nonionic diffusion in determining ammonia entry along the proximal tubule. However, the results also demonstrate that flow rate importantly determines ammonia entry in vivo in a manner not predicted by simple nonionic diffusion of NH3. This augmentation of ammonia entry with increasing flow rate may involve flow-dependent alterations in ammonia synthesis or transport of NH+4.

We previously found, using an in vivo microperfusion pump rate of 30 nl/min, that proton secretion in the early (S1) proximal convoluted tubule (PCT) of the Munich-Wistar rat exhibited saturation kinetics. The maximal transport capacity was very high, approximately 500–600 peq.mm-1.min-1. The present studies assessed the change in early PCT acidification kinetics in response to an increase in microperfusion rate to 45 nl/min. First, bicarbonate permeability in the early PCT was measured and was found to be flow dependent. Proton secretion was then calculated using perfusate bicarbonate concentrations from 8 to 100 mM. Saturation of early proximal acidification (Vmax) still occurred at approximately 500–600 peq.mm-1.min-1, but the bicarbonate concentration effecting half-maximal acidification (apparent Km) decreased (from approximately 11 mM at 30 nl/min perfusion rate to less than 6 mM at 45 nl/min). By increasing luminal perfusion rate further to 60 nl/min at constant luminal bicarbonate concentration (25 mM), we confirmed that luminal flow rate did not affect the maximal level of acidification. Similar flow-dependent changes in acidification kinetics in the late PCT were also found, as has been previously shown. In conclusion, although an increase in luminal flow increased bicarbonate permeability and apparent affinity for substrate transport, there was no effect on maximal acidification rate in the early PCT.

The perfusion rates of the brain, intestine and heart ventricle were studied under conditions of total body perfusion. The perfusion rates were estimated by using antipyrine and D2O as reference substances. Local flow was determined from arterial curves and tissue analysis. When the total body perfusion rate was varied between 20 and 80 cc/kg/min., it was found at each rate that the perfusion rate of these organs was over three times that of the body as a whole. At the lowest flows these three organs were favored even more. Tables of perfusion rates at various sites in the brain and intestine are given. Pressure-flow curves for the brain, intestine and heart are given.

Fifty dogs have been perfused at flow rates of between 5 and 100 cc/kg/min. with complete cardio-pulmonary bypass for up to three hours using a pump-oxygenator. There was an approximately linear relationship between pressure and flow. Extrapolation to zero flow produced an intercept on the pressure axis of approximately 20 mm Hg. Calculated total systemic resistance was more uniformly related to flow than to pressure. Coronary blood flow did not correlate with perfusion pressure. There was, however, an inverse relationship between perfusion rate and the percentage of total flow passing through the coronary bed. Coronary resistance decreased with perfusion time whereas total systemic resistance rose initially and then declined. Total peripheral resistance in these open chest perfused animals was one to two times the accepted normal for the intact dog. The actual value varied with the anesthetic agent used.