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  • American Physiological Society  (13)
  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 1989
    In:  American Journal of Physiology-Renal Physiology Vol. 257, No. 2 ( 1989-08-01), p. F218-F224
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 257, No. 2 ( 1989-08-01), p. F218-F224
    Abstract: The papillary surface epithelium (PSE) covers the mammalian renal papilla. It has been proposed that water or solute fluxes across the PSE might result in changes in urine or medullary interstitial fluid composition. To study osmotic water and chloride permeabilities, the PSE was dissected from underlying medullary tissue and mounted in a small Ussing chamber. Osmotic water permeability was low (14.2 +/- 3.0 microns/s) and was unaffected by 100 nM vasopressin added to the basolateral surface. In contrast, the PSE showed a substantial chloride permeability of 3.1 +/- 0.4 x 10(-5) cm/s that decreased reversibly to 2.2 +/- 0.3 x 10(-5) cm/s (P less than 0.01) with vasopressin. Vasopressin also reversibly increased the transepithelial resistance of the PSE from 87 +/- 9 to 106 +/- 13 omega.cm2 (P less than 0.02). Apical bumetanide (10(-6) M) had no significant effect on PSE chloride permeability. The apparent Na-Cl permeability ratio (0.75 +/- 0.01) calculated from dilution potential measurements was not affected significantly by vasopressin or apical bumetanide. We conclude that it is unlikely that physiologically significant osmotic water fluxes occur across the papillary surface epithelium. However, the NaCl permeability is sufficiently high that physiologically significant transepithelial NaCl fluxes could occur under conditions associated with reflux of urine backward from the papillary tip.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1989
    detail.hit.zdb_id: 1477287-5
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 1997
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 272, No. 3 ( 1997-03-01), p. H1382-H1390
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 272, No. 3 ( 1997-03-01), p. H1382-H1390
    Abstract: Exercise training improves functional class in patients with chronic heart failure (CHF) via effects on the periphery with no previously documented effect on intrinsic left ventricular (LV) properties. However, because methods used to evaluate in vivo LV function are limited, it is possible that some effects of exercise training on the failing heart have thus far eluded detection. Twelve dogs were instrumented for cardiac pacing and hemodynamic recordings. Hearts were paced rapidly for 4 wk. Six of the dogs received daily treadmill exercise (CHF(EX), 4.4 km/h, 2 h/day) concurrent with rapid pacing, while the other dogs remained sedentary (CHFs). Hemodynamic measurements taken in vivo at the end of 4 wk revealed relative preservation of maximum rate of pressure rise (2,540 +/- 440 vs. 1,720 +/- 300 mmHg/s, P 〈 0.05) and LV end-diastolic pressure (9 +/- 5 vs. 19 +/- 4 mmHg, P 〈 0.05) in CHF(EX) compared with CHFs. The hearts were then isolated and cross perfused for in vitro measurement of isovolumic pressure-volume relations; these results were compared with those of six normal dogs (N). Systolic function was similarly depressed in both groups of pacing animals [end-systolic elastance (Ees) values of 1.66 +/- 0.47 in CHFs, 1.77 +/- 0.38 in CHF(EX), and 3.05 +/- 0.81 mmHg/ml in N, with no changes in volume axis interceptors of the end-systolic pressure-volume relationship]. The diastolic myocardial stiffness constant, k, was elevated in CHFs and was normalized by exercise training (32 +/- 3 in CHFs, 21 +/- 3 in CHF(EX), 20 +/- 4 in N). Thus daily exercise training preserved in vivo hemodynamics during 4 wk of rapid cardiac pacing and was accompanied by a significant change in diastolic myocardial stiffness in vitro. These findings suggest that changes in heart function may contribute to the overall beneficial hemodynamic effects of exercise training in CHF by a significant effect on diastolic properties.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1997
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 1990
    In:  American Journal of Physiology-Renal Physiology Vol. 258, No. 4 ( 1990-04-01), p. F893-F899
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 258, No. 4 ( 1990-04-01), p. F893-F899
    Abstract: The rabbit papillary surface epithelium (PSE) is a simple cuboidal epithelium that covers the outer surface of the renal papilla and has an apical surface that faces the urinary space. We studied acid-base transport in this epithelium by dissecting it from the papilla, mounting it in a modified Ussing chamber, and following pH changes in the apical bathing solution. The experiments demonstrated that the PSE is capable of acidifying the apical solution at a substantial rate. The acidification rate was similar with 100% nitrogen and 100% oxygen (with and without 10 microM antimycin A), ruling out a dependence on oxidative metabolism. Addition of 1 mM iodoacetate decreased apical acidification by 55%, suggesting a dependence on glycolysis. The net rate of lactate secretion was only 17% of the total acid secretion rate, indicating that apical acidification was not directly caused by secretion of lactic acid alone. Removal of sodium or potassium from the apical solutions or the addition of 1 mM N-ethylmaleimide failed to eliminate the apical acidification. Although the rate of PSE apical acidification is comparable to that of the rabbit outer medullary collecting duct (on a unit surface area basis), its contribution to urinary net acid excretion is likely to be small, owing to the small relative surface area of the PSE. However, by altering the pH of urine locally within the pelvic recesses, the PSE has the potential of modifying the formation of renal stones within the pelvic recesses.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1990
    detail.hit.zdb_id: 1477287-5
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  • 4
    Online Resource
    Online Resource
    American Physiological Society ; 2010
    In:  Journal of Neurophysiology Vol. 104, No. 6 ( 2010-12), p. 3691-3704
    In: Journal of Neurophysiology, American Physiological Society, Vol. 104, No. 6 ( 2010-12), p. 3691-3704
    Abstract: Fluorescent calcium indicators are becoming increasingly popular as a means for observing the spiking activity of large neuronal populations. Unfortunately, extracting the spike train of each neuron from a raw fluorescence movie is a nontrivial problem. This work presents a fast nonnegative deconvolution filter to infer the approximately most likely spike train of each neuron, given the fluorescence observations. This algorithm outperforms optimal linear deconvolution (Wiener filtering) on both simulated and biological data. The performance gains come from restricting the inferred spike trains to be positive (using an interior-point method), unlike the Wiener filter. The algorithm runs in linear time, and is fast enough that even when simultaneously imaging 〉 100 neurons, inference can be performed on the set of all observed traces faster than real time. Performing optimal spatial filtering on the images further refines the inferred spike train estimates. Importantly, all the parameters required to perform the inference can be estimated using only the fluorescence data, obviating the need to perform joint electrophysiological and imaging calibration experiments.
    Type of Medium: Online Resource
    ISSN: 0022-3077 , 1522-1598
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 80161-6
    detail.hit.zdb_id: 1467889-5
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  • 5
    Online Resource
    Online Resource
    American Physiological Society ; 2011
    In:  Journal of Neurophysiology Vol. 106, No. 2 ( 2011-08), p. 1038-1053
    In: Journal of Neurophysiology, American Physiological Society, Vol. 106, No. 2 ( 2011-08), p. 1038-1053
    Abstract: Recent advances in experimental stimulation methods have raised the following important computational question: how can we choose a stimulus that will drive a neuron to output a target spike train with optimal precision, given physiological constraints? Here we adopt an approach based on models that describe how a stimulating agent (such as an injected electrical current or a laser light interacting with caged neurotransmitters or photosensitive ion channels) affects the spiking activity of neurons. Based on these models, we solve the reverse problem of finding the best time-dependent modulation of the input, subject to hardware limitations as well as physiologically inspired safety measures, that causes the neuron to emit a spike train that with highest probability will be close to a target spike train. We adopt fast convex constrained optimization methods to solve this problem. Our methods can potentially be implemented in real time and may also be generalized to the case of many cells, suitable for neural prosthesis applications. With the use of biologically sensible parameters and constraints, our method finds stimulation patterns that generate very precise spike trains in simulated experiments. We also tested the intracellular current injection method on pyramidal cells in mouse cortical slices, quantifying the dependence of spiking reliability and timing precision on constraints imposed on the applied currents.
    Type of Medium: Online Resource
    ISSN: 0022-3077 , 1522-1598
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2011
    detail.hit.zdb_id: 80161-6
    detail.hit.zdb_id: 1467889-5
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  • 6
    Online Resource
    Online Resource
    American Physiological Society ; 1997
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 272, No. 1 ( 1997-01-01), p. H186-H194
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 272, No. 1 ( 1997-01-01), p. H186-H194
    Abstract: Myocardial mechanics and energetics were investigated in an animal model of moderate chronic heart failure (CHF) created by repeated coronary microembolizations in six dogs. The final fractional area change was 34 +/- 4%. Hearts of these animals were isolated and cross-perfused, and balloons were placed in the left ventricle (LV). Chamber contractile state was markedly depressed in embolized hearts as assessed by the slope (Ees 2.74 +/- 0.49 vs. 4.00 +/- 1.18 mmHg/ml, P 〈 0.01) and volume axis intercept (V: 8.7 +/- 5.9 vs. 1.0 +/- 3.2 ml, P 〈 0.01) of end-systolic pressure-volume relation compared with a group of six normal dogs. The end-diastolic pressure-volume relation of embolized hearts was shifted to the right, indicating a dilation of the LV. However, systolic and diastolic stress strain relationships were similar in the two groups, suggesting that the average myocardial properties of the embolized hearts are similar to those of normal hearts. The relationship between oxygen consumption and pressure-volume area in embolized hearts had smaller intercept (2.98 +/- 0.44 vs 3.92 +/- 0.39 x 10(-2) ml O2.beat-1.100 g LV-1, P 〈 0.01) compared with the control group, with no change in the slope. These results contrast with previous findings in pacing CHF and serve as an important characterization of ventricular properties in this model of CHF from different etiology.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1997
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    American Physiological Society ; 1992
    In:  American Journal of Physiology-Renal Physiology Vol. 262, No. 6 ( 1992-06-01), p. F999-F1006
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 262, No. 6 ( 1992-06-01), p. F999-F1006
    Abstract: To study mechanisms involved in renal glutamate dehydrogenase (GDH) regulation in response to systemic acid loading, we have measured blood pH, ammonium excretion, renal GDH mRNA levels, and GDH activity in rats. Acid intake (0.28 M NH4Cl in drinking water for 3 days) increased GDH mRNA levels in the renal cortex, but had no effect in the outer stripe of the outer medulla, inner stripe of the outer medulla, or the inner medulla. Rats were subjected to a step change in acid intake by alkali loading for 3 days (7.2 meq NaHCO3 per day in food slurry) and shifting to acid loading for up to 7 days (7.2 meq NH4Cl in food slurry). Ammonium excretion rose rapidly, increasing by 14-fold in the first 24-h period and 38-fold in the second 24-h period. Cortical GDH mRNA levels were increased relative to alkali-loaded values by 3.7-fold in 24 h, 4.3-fold in 4 days, but only 2.2-fold in 7 days. GDH activity was unchanged after 24 h of acid intake, but was significantly increased after 48 h. We concluded the following: 1) GDH mRNA is present in all regions of the kidney, but levels increase in response to acid loading only in the renal cortex; 2) GDH mRNA levels increase within 1 day after the initiation of acid loading, but the associated increase in functional enzyme activity takes 2 or more days; and 3) the large increases in ammonium excretion that occur in the first day after initiation of acid loading are not dependent on increased GDH activity.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1992
    detail.hit.zdb_id: 1477287-5
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  • 8
    Online Resource
    Online Resource
    American Physiological Society ; 1984
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 246, No. 6 ( 1984-06-01), p. E535-E543
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 246, No. 6 ( 1984-06-01), p. E535-E543
    Abstract: Three weeks of dietary iron deficiency in weanling rats resulted in anemia (Hb, 3.9 vs. 14.2 g/dl in controls) and decreased oxidative capacities of skeletal muscle (as much as 90% below control values). Whole-animal maximal O2 consumption (VO2max), measured in a brief treadmill run of progressively increasing work load, was approximately 50% lower for iron-deficient rats than for controls, and maximal endurance capacity (time to exhaustion in a separate treadmill run at a constant, sub-Vo2max work load) was 90% lower for iron-deficient rats than for controls. Exchange transfusion, with packed erythrocytes or plasma, was used to adjust Hb to an intermediate concentration of approximately 9.5 g/dl in both iron-deficient and and control rats. This procedure corrected the Vo2max of iron-deficient rats to within 15% of control values, whereas endurance capacity showed no improvement. Our experimental dissociation of Vo2max and endurance capacity provides further evidence that Vo2max is not the sole determinant of endurance. We propose that defects in Vo2max during iron deficiency result primarily from diminished O2 delivery, whereas decreased endurance capacity reflects impaired muscle mitochondrial function.
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1984
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    American Physiological Society ; 1989
    In:  Physiological Reviews Vol. 69, No. 1 ( 1989-01), p. 179-249
    In: Physiological Reviews, American Physiological Society, Vol. 69, No. 1 ( 1989-01), p. 179-249
    Type of Medium: Online Resource
    ISSN: 0031-9333 , 1522-1210
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1989
    detail.hit.zdb_id: 1471693-8
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    American Physiological Society ; 1986
    In:  American Journal of Physiology-Cell Physiology Vol. 251, No. 3 ( 1986-09-01), p. C435-C442
    In: American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 251, No. 3 ( 1986-09-01), p. C435-C442
    Abstract: It seems fairly well established that in the early phase of smooth muscle contraction cross bridges cycle at a relatively rapid rate. Later on these are replaced by very slowly cycling cross bridges or "latch bridges," operating with high economy. We describe a method to identify the time at which the transition occurs. By abruptly applying a light afterload at varying time intervals after stimulation of a canine tracheal smooth muscle, a point in time could be identified when cross-bridge cycling slowed. This was called the transition time. Because this transition was load dependent, the study was repeated with the preload abruptly reduced to zero. This permitted analysis of data in terms of cross-bridge activity. Maximum zero load velocity (Vo) of the contractile machinery was plotted against time and yielded a biphasic curve. The descending limb of the curve was fitted by a curve of the form Vo(t) = alpha e-K1t + beta e-K2t; K1 was almost three times greater than K2. We speculate that the faster rate constant represented activity of the early rapidly cycling cross bridges, and the slower constant reflected cycling rates in the latch state. These results are consistent with the latch bridge hypothesis put forward by Dillon et al. and enable us to provide a first approximation of the relative velocities of the two types of cross bridges.
    Type of Medium: Online Resource
    ISSN: 0363-6143 , 1522-1563
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1986
    detail.hit.zdb_id: 1477334-X
    SSG: 12
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