Interpretation of current-voltage relationships for “active” ion transport systems: II. Nonsteady-state reaction kinetic analysis of class-I mechanisms with one slow time-constant

1983 ◽  
Vol 75 (2) ◽  
pp. 141-169 ◽  
Author(s):  
U. -P. Hansen ◽  
J. Tittor ◽  
D. Gradmann
Keyword(s):  
Ion Transport ◽  
Kinetic Analysis ◽  
Time Constant ◽  
Reaction Kinetic ◽  
Transport Systems ◽  
Slow Time ◽  
Current Voltage ◽  
Nonsteady State ◽  
Active Ion Transport ◽  
Slow Time Constant

Comparative effects of vasodilator drugs on flow distribution and venous return

1985 ◽  
Vol 63 (11) ◽  
pp. 1345-1355 ◽  
Author(s):  
R. I. Ogilvie
Keyword(s):  
Blood Flow ◽  
Blood Volume ◽  
Time Constant ◽  
Venous Return ◽  
Flow Distribution ◽  
Fast Time ◽  
Central Blood Volume ◽  
Slow Time ◽  
Arterial Resistance ◽  
Slow Time Constant

Systemic vascular effects of hydralazine, prazosin, captopril, and nifedipine were studied in 115 anesthetized dogs. Blood flow [Formula: see text] and right atrial pressure (Pra) were independently controlled by a right heart bypass. Transient changes in central blood volume after an acute reduction in Pra at a constant [Formula: see text] showed that blood was draining from two vascular compartments with different time constants, one fast and the other slow. At three dose levels producing comparable reductions in systemic arterial pressure (30–40% at the highest dose), these drugs had different effects on flow distribution and venous return. Hydralazine and prazosin had parallel and balanced effects on arterial resistance of the two vascular compartments, and flow distribution was unaltered. Captopril preferentially reduced arterial resistance of the compartment with a slow time constant for venous return (−26 ± 6%, −30 ± 6%, −50 ± 5% at 0.02, 0.10, and 0.50 mg∙kg−1∙h−1, respectively; [Formula: see text]) without altering arterial resistance of the fast time-constant compartment. Blood flow to the slow time-constant compartment was increased 43 ± 14% at the highest dose, and central blood volume was reduced 108 ± 15 mL. In contrast, nifedipine had a balanced effect on arterial resistance with the lowest dose (0.025 mg/kg) but caused a preferential reduction in arterial resistance of the fast time-constant compartment at higher doses (−38 ± 4% and −55 ± 2% at 0.05 and 0.10 mg/kg, respectively). Blood flow to the slow time-constant compartment was reduced 36 ± 5% at the highest dose of nifedipine, and central blood volume was increased 66 ± 12 mL. Total systemic venous compliance was unaltered or slightly reduced by each of the four drugs. These results add further evidence to the hypothesis that peripheral blood flow distribution is a major determinant of venous return to the heart.

Analysis of venous flow transients for estimation of vascular resistance, compliance, and blood flow distribution

1987 ◽  
Vol 65 (9) ◽  
pp. 1884-1890 ◽  
Author(s):  
Richard I. Ogilvie ◽  
Danuta Zborowska-Sluis
Keyword(s):  
Time Constant ◽  
Venous Return ◽  
Fast Time ◽  
Slow Time ◽  
Venous Outflow ◽  
Venous Flow ◽  
Time Constants ◽  
Slow Time Constant ◽  
Over Time ◽  
Flow Transients

We analysed venous flow transients using a long venous circuit and right heart bypass in 17 dogs after a rapid decrease in atrial pressure. A biphase curve was obtained which we decomposed into a two-compartmental model, one with a fast time constant for venous return (0.069 min) and 52% of total circulating flow [Formula: see text], and one with a slower time constant (0.456 min) and 48% of [Formula: see text]. Subsequently, separate drainage from splanchnic and peripheral beds (with the renal venous return in the peripheral bed drainage) allowed comparison of time constants and venous outflow in these beds. The sum of the venous outflow volumes over time during separate drainage was indistinguishable from the single biphasic venous outflow volume curve over time observed with a long circuit and single reservoir. The fast time constant of the biphasic curve was not different from that determined by separate drainage from the peripheral circulation. The slow time constant of the single biphasic curve of 0.456 min was hybrid of two time constants, 0.216 min in the splanchnic bed and 0.862 min in the peripheral bed. Separate drainage from peripheral and splanchnic vascular beds demonstrated that the peripheral bed constituted 70% of venous outflow in the fast time constant compartment using Caldini's technique, whereas the splanchnic bed constituted 63% of venous outflow in the slow time constant compartment. It is concluded that, although Caldini's technique demonstrates biphasic venous flow transients, neither the fast nor the slow time constant compartments resolved from this analysis represent a particular anatomical region or vascular bed.

Passive and active ion transport by the urinary bladder of a euryhaline flounder

1984 ◽  
Vol 246 (4) ◽  
pp. F402-F408 ◽  
Author(s):  
J. R. Demarest ◽  
T. E. Machen
Keyword(s):  
Ion Transport ◽  
Short Circuit ◽  
Apical Cell ◽  
Apical Cell Membrane ◽  
Platichthys Stellatus ◽  
Current Voltage ◽  
Active Ion Transport ◽  
Voltage Clamping ◽  
Net Fluxes ◽  
Insight Into

The effects of voltage clamping on the flux ratios and unidirectional and net fluxes of Na and Cl were used to gain insight into the mechanisms of active and passive ion transport across urinary bladders isolated from seawater-(SW) and freshwater-acclimated (FW) flounder, Platichthys stellatus. Although the transepithelial conductance (Gt = 2.77 mS X cm-2) of FW bladders was much greater than that of SW bladders (Gt = 0.40 mS X cm-2), the current-voltage relationships of both SW and FW bladders were markedly nonlinear. Under short-circuit conditions there was a large difference in the serosal-to-mucosal Na flux (JNasm) between SW (0.10 mueq X cm-2 X h-1) and FW (1.71 mueq X cm-2 X h-1) bladders, but their mannitol permeabilities were identical. The results indicate that 1) the paracellular pathway of both SW and FW bladders is Cl selective and Cl movements through the shunt account for a maximum of 90% of Gt in SW bladders and 19% in FW bladders; 2) the larger Gt of FW bladders is due to greater conductance of the apical cell membrane; 3) the majority of the passive ion movement across these epithelia proceeds through nonconductive, presumably transcellular, pathways; and 4) active transport of Na and Cl occurs by neutral coupling to each other and to other unidentified ions.

Time-constant histograms from the forced expired volume signal

1981 ◽  
Vol 51 (6) ◽  
pp. 1581-1593 ◽  
Author(s):  
R. L. Pimmel ◽  
T. K. Miller ◽  
J. M. Fouke ◽  
J. G. Eyles
Keyword(s):  
Time Constant ◽  
Vital Capacity ◽  
Compartment Model ◽  
Normal Subjects ◽  
Fast Time ◽  
Slow Time ◽  
Criterion Function ◽  
Time Constants ◽  
Nonnegativity Constraints ◽  
Slow Time Constant

The forced expired volume signal was analyzed using a parallel compartment model in which each compartment emptied exponentially. With this model the forced expired volume signal was represented by a histogram showing the fraction of the vital capacity as a functional of compartmental time constants. We developed an algorithm to compute this histogram from the volume signal. The algorithm used the least-squares criterion function with both smoothness and nonnegativity constraints. In a stimulation study reasonable histograms were obtained even in the presence of realistic random error. Three dependent forced expired volume signals from 16 subjects were analyzed, and the histograms were reproducible. Most histograms were bimodal with fast time constants of 0.12–0.55 s and slow time constants of 1.3–2.7 s. In all normal subjects and patients with restrictive disease more than 75% of the vital capacity was in the fast time-constant mode. Subjects with obstructive disease had more than 40% of the vital capacity in the slow time-constant mode.

Insulin resistance, hypertension and cellular ion transport systems

1992 ◽  
Vol 29 (3-4) ◽  
pp. 196-200 ◽  
Author(s):  
Anna Solini ◽  
Ralph A. DeFronzo
Keyword(s):  
Insulin Resistance ◽  
Ion Transport ◽  
Transport Systems
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