Increased flow rate and papaverine increase K+ exchange in perfused rat hind-limb skeletal muscle

1999 ◽  
Vol 77 (7) ◽  
pp. 536-543 ◽  
Author(s):  
Michael I Lindinger ◽  
Thomas J Hawke

This study tested the hypothesis that increases in perfusate flow rate result in increased rates of unidirectional and net K+ transport in rat hind-limb skeletal muscle at rest. Ten neurally and vascularly isolated hind limbs, with arterial and venous catheters placed proximal to the popliteal region, were perfused for 10-min periods at flow rates (presented in a random order) of 0.27, 0.42, 0.63, 0.84, or 1.05 mL·min-1·g-1. Potassium extraction and unidirectional K+ influx were determined using 42K, and arterial perfusion pressure was measured continuously. Increases in flow rate resulted in decreases in K+ extraction and increases in unidirectional K+ influx, unidirectional K+ efflux, and net K+ efflux. The increases in K+ flux were associated with increases in oxygen uptake, glucose uptake, and lactate release. In separate experiments (n = 5), the vasodilator papaverine (10-4 M) did not further vasodilate the vasculature of resting hind limbs, suggesting that the hind limbs in this preparation were fully vasodilated. Papaverine, at constant flow, resulted in a nearly 1.5-fold increase in K+ extraction, a doubling of unidirectional K+ influx, and increases in unidirectional K+ efflux and net K+ efflux. It is concluded that physiological increases in flow rate result in increases in K+ transport in isolated, perfused rat hind-limb skeletal muscle. Furthermore, papaverine appeared to induce an increase in skeletal muscle membrane permeability to K+.Key words: K+ transport, potassium extraction, Na-K ATPase, sarcolemma, plasma flow, vasodilator, VO2.

1978 ◽  
Vol 235 (6) ◽  
pp. E686 ◽  
Author(s):  
D Hollander ◽  
P E Ruble

beta carotene absorption in the unanesthetized rat was investigated by recirculating a micellar perfusate that contained beta-carotene through jejunal and ileal intestinal loops. Radioautography revealed extensive distribution of the provitamin throughout the layers of the small bowel. A linear relationship was found between the concentration of beta-carotene in the perfusate and its rate of absorption at perfusate concentrations of 0.5--11 mM. Increases in the perfusate hydrogen ion concentrations, additions of fatty acids of varied chain lengths and degrees of saturation, and an increase in the perfusate flow rate caused higher rates of beta-carotene absorption. Increase in the perfusate sodium taurocholate concentration above 2.5 microM did not change the absorption rate of beta-carotene. These experiments indicate that beta-carotene absorption takes place by passive diffusion. The process of diffusion can be modulated by intraluminal factors that change the physical characteristics of perfusate or stimulate the intracellular cleavage of carotene to retinal.


1995 ◽  
Vol 269 (6) ◽  
pp. E1044-E1051 ◽  
Author(s):  
H. Pilegaard ◽  
J. Bangsbo ◽  
P. Henningsen ◽  
C. Juel ◽  
E. A. Richter

The influence of blood flow on muscle lactate and H+ release as well as muscle glyconeogenesis was studied in the perfused rat hindlimb. After 2 min of supramaximal stimulation the perfusate flow rate was 7 (F7), 12 (F12), or 18 (F18) ml/min for 30 min. Perfusate samples were drawn frequently and muscle samples were obtained before stimulation, immediately after stimulation, and at 3, 10, and 30 min of recovery from soleus, white gastrocnemius (WG) and red gastrocnemius. During the first 5 min of recovery lactate release was 35-39% lower (P < 0.05) in F7 than in F12 and F18 but with no differences in total release during recovery. In F7 the concentration of lactate was higher (P < 0.05) in soleus after 10 min (18-20%) and in WG after 30 min (63-67%) than in F12 and F18. During the first 2 min of recovery H+ release was 23-34% lower (P < 0.05) in F7 than in F12 and F18. The difference between H+ and lactate release was larger (P < 0.05) in F7 than in F12 and F18 from 3 to 10 min and from 5 to 10 min of recovery, respectively. Muscle glycogen concentrations after 30 min of recovery were independent of flow in each of the muscles. The present data suggest that 1) in the range of blood flow rates from 0.61 to 0.92 ml.min-1.g-1, lactate and H+ release are independent of the flow rate, whereas at a lower flow rate (0.36 ml.min-1.g-1) release of these substances is decreased; 2) low blood flow influences lactate efflux more than H+ release; and 3) muscle glyconeogenesis from lactate is of minor importance.


1999 ◽  
Vol 77 (11) ◽  
pp. 835-843 ◽  
Author(s):  
Thomas J Hawke ◽  
Robert G Willmets ◽  
Michael I Lindinger

This study tested the hypothesis that paraxanthine, a caffeine metabolite, stimulates skeletal muscle potassium (K+) transport by an increase in Na+-K+ ATPase activity. The unidirectional transport of K+ into muscle (JinK) was studied using a perfused rat hind limb technique. Using 12 hind limbs, we examined the response to 20 min of paraxanthine perfusion (0.1 mM), followed by 20 min perfusion with 0.1 mM paraxanthine and 5 mM ouabain (n = 5) to irreversibly inhibit Na+-K+ ATPase activity. Paraxanthine stimulated JinK by 23 ± 5% within 20 min. Ouabain abolished the paraxanthine-induced stimulation of JinK, suggesting the increase in K+ uptake was due to activation of the Na+-K+ ATPase. To confirm the role of the Na+-K+ ATPase, 14 hind limbs were perfused for 20 min with 5 mM ouabain prior to 20 min perfusion with 0.1 mM paraxanthine and 5 mM ouabain (n = 6). Ouabain alone resulted in a 41 ± 7% decrease in JinK within 15 min. Inhibition of ouabain-sensitive JinK prevented the paraxanthine-induced increase in JinK. Hind limbs (n = 3) were also perfused with 0.1 mM paraxanthine for 60 min to examine the response to longer duration paraxanthine perfusion. The paraxanthine-induced increase in JinK continued for the entire 60 min. In another series, hind limbs were perfused with 0.01 (n = 9), 0.1 (n = 9), or 0.5 (n = 6) mM paraxanthine for 15 min. There was no concentration-dependent relationship between JinK and paraxanthine concentration, and 0.01, 0.1, and 0.5 mM paraxanthine increased JinK similarly (25 ± 5, 22 ± 4, and 27 ± 6%, respectively). The effect of paraxanthine on JinK could not be reversed by subsequent perfusion with paraxanthine-free perfusate. Caffeine (0.05-1.0 mM) had no effect on K+ transport. It is concluded that paraxanthine increases JinK in resting skeletal muscle by stimulating ouabain-sensitive Na+-K+ ATPase activity.Key words: caffeine, methylxanthine, ouabain, potassium transport, sodium pump, Na-K ATPase, VO2, glycolysis.


1959 ◽  
Vol 197 (4) ◽  
pp. 853-855 ◽  
Author(s):  
Lerner B. Hinshaw ◽  
Henry M. Ballin ◽  
Stacey B. Day ◽  
Curtis H. Carlson

Experiments were performed on isolated dog kidneys alternately perfused with homologous blood and dextran. Renal artery pressure, tissue pressure, perfusate flow rate and vascular volume changes were measured as arterial pressures were progressively elevated. Marked increases in overall vascular resistance RA/F occurred in all dextran- and blood-perfused kidneys throughout the autoregulatory range. Results indicate that autoregulation of flow occurs in both blood- and dextran-perfused kidneys concurrent with increases in tissue pressure. Dextran- and blood-perfused kidneys show similar degrees of autoregulation when values are expressed in terms of increase in flow per unit rise of arterial pressure and compared to preautoregulation values.


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