bluuebunny/crossref_metadata_2025 huggingface dataset:
Importance of airway blood flow on particle clearance from the lung
Authors: Wagner Elizabeth M. , Foster W. Michael
Published: December 2017

Wagner, Elizabeth M., and W. Michael Foster. Importance of airway blood flow on particle clearance from the lung. J. Appl. Physiol. 81(5): 1878–1883, 1996.—The role of the airway circulation in supporting mucociliary function has been essentially unstudied. We evaluated the airway clearance of inert, insoluble particles in anesthetized ventilated sheep ( n = 8), in which bronchial perfusion was controlled, to determine whether airway mucosal blood flow is essential for maintaining surface transport of particles through airways. The bronchial branch of the bronchoesophageal artery was cannulated and perfused with autologous blood at control flow (0.6 ml ⋅ min−1⋅ kg−1) or perfusion was stopped. With the sheep in a supine position and after a steady-state133Xe ventilation scan for designation of lung zones of interest, an inert99mTc-labeled sulfur colloid aerosol (2.1-μm diameter) was deposited in the lung. The clearance kinetics of the radiolabeled particles were determined from the activity-time data obtained for right and left lung zones. At 60 min postdeposition of aerosol, average airway particle retention for control bronchial blood flow conditions was 57 ± 7 (SE)% for the right and 53 ± 8% for the left lung zones. Clearance of particles was significantly impaired when bronchial blood flow was stopped, e.g., right and left lung zones averaged 77 ± 6 and 76 ± 7% at 60 min, respectively ( P < 0.05). These data demonstrate a significant influence of the bronchial circulation on mucociliary transport of insoluble particles. Potential mechanisms that may account for these results include the importance of the bronchial circulation for nutrient flow, maintenance of airway wall temperature and humidity, and release of mediators and sequelae associated with tissue ischemia.
CytochromecmRNA in skeletal muscles of immobilized limbs
Authors: Booth Frank W. , Lou Wei , Hamilton Marc T. , Yan Zhen
Published: December 2017

Booth, Frank W., Wei Lou, Marc T. Hamilton, and Zhen Yan.Cytochrome c mRNA in skeletal muscles of immobilized limbs. J. Appl. Physiol. 81(5): 1941–1945, 1996.—Even though immobilization of a slow skeletal muscle in a lengthened position prevents muscle atrophy, it is unknown whether this treatment would prevent a decrease in mitochondrial quantity. We found that, regardless of muscle length in immobilized limbs, the mRNA of a marker for mitochondrial quantity, cytochrome c, decreased. Cytochrome c mRNA per milligram of muscle was 62 and 72% less 1 wk after fixation of the soleus muscle in shortened and lengthened positions, respectively, than age-matched controls. Cytochrome cmRNA per milligram wet weight was 36 and 32% less in the tibialis anterior muscle fixed for 1 wk in the shortened and lengthened positions, respectively, compared with age-matched controls. Recently, in the 3′-untranslated region of cytochrome c mRNA a novel RNA-protein interaction that decreases in chronically stimulated rat skeletal muscle was identified.[Z. Yan, S. Salmons, Y. L. Dang, M. T. Hamilton, and F. W. Booth. Am. J. Physiol. 271 ( Cell Physiol. 40): C1157– C1166, 1996]. The RNA-protein interaction in the 3′-untranslated region of cytochrome c mRNA in soleus and tibialis anterior muscles was unaffected by fixation in either shortened or lengthened position. We conclude that, whereas lengthening muscle during limb fixation abates the loss of total muscle protein, the percentage decrease in cytochrome c mRNA is proportionally greater than total protein. This suggests that the design of countermeasures to muscle atrophy should include different exercises to maintain total protein and mitochondria.
Assessment of regional deposition of inhaled particles in human lungs by serial bolus delivery method
Authors: Kim Chong S. , Hu S. C. , Dewitt P. , Gerrity T. R.
Published: December 2017

Kim, Chong S., S. C. Hu, P. DeWitt, and T. R. Gerrity.Assessment of regional deposition of inhaled particles in human lungs by serial bolus delivery method. J. Appl. Physiol. 81(5): 2203–2213, 1996.—Detailed regional deposition of inhaled particles was investigated in young adults ( n = 11) by use of a serial bolus aerosol delivery technique. A small bolus (45 ml half-width) of monodisperse aerosols [1-, 3-, and 5-μm particle diameter ( Dp)] was delivered sequentially to a specific volumetric depth of the lung (100–500 ml in 50-ml increments), while the subject inhaled clean air via a laser aerosol photometer (25-ml dead volume) with a constant flow rate (Q˙ = 150, 250, and 500 ml/s) and exhaled with the same Q˙ without a pause to the residual volume. Deposition efficiency (LDE) and deposition fraction in 10 local volumetric regions and total deposition fraction of the lung were obtained. LDE increased monotonically with increasing lung depth for all three Dp. LDE was greater with smaller Q˙ values in all lung regions. Deposition was distributed fairly evenly throughout the lung regions with a tendency for an enhancement in the distal lung regions for Dp= 1 μm. Deposition distribution was highly uneven for Dp= 3 and 5 μm, and the region of the peak deposition shifted toward the proximal regions with increasing Dp. Surface dose was 1–5 times greater in the small airway regions and 2–17 times greater in the large airway regions than in the alveolar regions. The results suggest that local or regional enhancement of deposition occurs in healthy subjects and that the local enhancement can be an important factor in health risk assessment of inhaled particles.
Effects of DAP on diaphragm force and fatigue, including fatigue due to neurotransmission failure
Authors: Van Lunteren Erik , Moyer Michelle
Published: December 2017

Van Lunteren, Erik, and Michelle Moyer. Effects of DAP on diaphragm force and fatigue, including fatigue due to neurotransmission failure. J. Appl. Physiol. 81(5): 2214–2220, 1996.—Among the aminopyridines, 3,4-diaminopyridine (DAP) is a more effective K+ channel blocker than is 4-aminopyridine (4-AP), and, furthermore, DAP enhances neuromuscular transmission. Because 4-AP improves muscle contractility, we hypothesized that DAP would also increase force and, in addition, ameliorate fatigue and improve the neurotransmission failure component of fatigue. Rat diaphragm strips were studied in vitro (37°C). In field-stimulated muscle, 0.3 mM DAP significantly increased diaphragm twitch force, prolonged contraction time, and shifted the force-frequency relationship to the left without altering peak tetanic force, resulting in increased force at stimulation frequencies ≤50 Hz. During 20-Hz intermittent stimulation, DAP increased diaphragm peak force compared with control during a 150-s fatigue run and, furthermore, significantly improved maintenance of intratrain force. The relative contribution of neurotransmission failure to fatigue was estimated by comparing the force generated by phrenic nerve-stimulated muscles with that generated by curare-treated field-stimulated muscles. DAP significantly increased force in nerve-stimulated muscles and, in addition, reduced the neurotransmission failure contribution to diaphragm fatigue. Thus DAP increases muscle force at low-to-intermediate stimulation frequencies, improves overall force and intratrain fatigue during 20-Hz intermittent stimulation, and reduces neurotransmission failure.
Breath-to-breath relationships between respiratory cycle variables in humans at fixed end-tidal Pco2and Po2
Authors: Busso Thierry , Liang Pei-Ji , Robbins Peter A.
Published: December 2017

Busso, Thierry, Pei-Ji Liang, and Peter A. Robbins.Breath-to-breath relationships between respiratory cycle variables in humans at fixed end-tidal Pco2and Po2. J. Appl. Physiol. 81(5): 2287–2296, 1996.—This study examined the statistical properties of breath-to-breath variations in the inspiratory and expiratory volumes and times during rest and light exercise. Sixty data sets were analyzed. Initial data and residuals after fitting time-series models were examined for 1) sustained periodicities with use of spectral analysis, 2) temporal changes in signal power with use of evolutionary spectral analysis, and 3) auto- and cross correlations with use of a portmanteau test. The major findings were as follows: 1) no sustained periodic components were detected; 2) temporal changes in signal power were normally present, but these did not affect significantly the results from time-series modeling; 3) for all variables, a simple autoregressive moving average (ARMA) AR1MA1model generally described the autocorrelation; 4) considerable cross correlation remained between residuals from the AR1MA1model; 5) relationships between variables could be described by using a multivariate time-series model; 6) residual fluctuations in end-tidal Pco2had little influence; and 7) responses were broadly similar between rest and exercise, although some quantitative differences were found. The multivariate model provides a description of the structure of the interrelationships between cycle variables in a quantitative and a qualitative form.
Infrared spectroscopy of dystrophicmdx mouse muscle tissue distinguishes among treatment groups
Authors: Shaw R. A. , Mantsch H. H. , Anderson J. E.
Published: December 2017

Shaw, R. A., H. H. Mantsch, and J. E. Anderson.Infrared spectroscopy of dystrophic mdx mouse muscle tissue distinguishes among treatment groups. J. Appl. Physiol. 81(5): 2328–2335, 1996.—Four groups of mdx mice (deflazacort, high dose of 1.5 mg/kg and low dose of 0.75 mg/kg; prednisone, 1.0 mg/kg; and a placebo) were examined in a double-blind protocol. The experiments tested the hypothesis that infrared spectroscopy can distinguish among gastrocnemius muscle tissues derived from dystrophic animals ( n = 22) from different treatment groups and from control muscle tissue ( n = 23). Results showed that muscle, inflamed muscle, and tendon can be distinguished on the basis of their infrared absorption patterns. Distinctions among the spectra of the four treatment groups were sought with automated pattern-recognition methods. These classification methods, based either on spectral regions (900–1,500 cm−1) or on principal-component analysis, were in close agreement, assigning 15 or 16, respectively, of 22 mdx spectra to the correct treatment group. Both trials cleanly separated the high-dose deflazacort from the placebo group of muscles, whereas the prednisone and low-dose deflazacort groups were persistently confused in these classifications. Changes in the histology of muscle inflammation paralleled the spectral-classification results. Thus the proposed method, combining infrared spectroscopy with pattern-recognition algorithms, can distinguish treatment effects on muscle tissue. Specific spectral features characteristic of tissue type, disease progression, and treatment effects are not yet elucidated.
Friction in airway smooth muscle: mechanism, latch, and implications in asthma
Authors: Fredberg J. J. , Jones K. A. , Nathan M. , Raboudi S. , Prakash Y. S. , Shore S. A. , Butler J. P. , Sieck G. C.
Published: December 2017

Fredberg, J. J., K. A. Jones, M. Nathan, S. Raboudi, Y. S. Prakash, S. A. Shore, J. P. Butler, and G. C. Sieck. Friction in airway smooth muscle: mechanism, latch, and implications in asthma. J. Appl. Physiol. 81(6): 2703–2712, 1996.—In muscle, active force and stiffness reflect numbers of actin-myosin interactions and shortening velocity reflects their turnover rates, but the molecular basis of mechanical friction is somewhat less clear. To better characterize molecular mechanisms that govern mechanical friction, we measured the rate of mechanical energy dissipation and the rate of actomyosin ATP utilization simultaneously in activated canine airway smooth muscle subjected to small periodic stretches as occur in breathing. The amplitude of the frictional stress is proportional to ηE, where E is the tissue stiffness defined by the slope of the resulting force vs. displacement loop and η is the hysteresivity defined by the fatness of that loop. From contractile stimulus onset, the time course of frictional stress amplitude followed a biphasic pattern that tracked that of the rate of actomyosin ATP consumption. The time course of hysteresivity, however, followed a different biphasic pattern that tracked that of shortening velocity. Taken together with an analysis of mechanical energy storage and dissipation in the cross-bridge cycle, these results indicate, first, that like shortening velocity and the rate of actomyosin ATP utilization, mechanical friction in airway smooth muscle is also governed by the rate of cross-bridge cycling; second, that changes in cycling rate associated with conversion of rapidly cycling cross bridges to slowly cycling latch bridges can be assessed from changes of hysteresivity of the force vs. displacement loop; and third, that steady-state force maintenance (latch) is a low-friction contractile state. This last finding may account for the unique inability of asthmatic patients to reverse spontaneous airways obstruction with a deep inspiration.
Effects of carotid body hypocapnia during ventilatory acclimatization to hypoxia
Authors: Dwinell M. R. , Janssen P. L. , Pizarro J. , Bisgard G. E.
Published: December 2017

Dwinell, M. R., P. L. Janssen, J. Pizarro, and G. E. Bisgard. Effects of carotid body hypocapnia during ventilatory acclimatization to hypoxia. J. Appl. Physiol. 82(1): 118–124, 1997.—Hypoxic ventilatory sensitivity is increased during ventilatory acclimatization to hypoxia (VAH) in awake goats, resulting in a time-dependent increase in expired ventilation (V˙e). The objectives of this study were to determine whether the increased carotid body (CB) hypoxic sensitivity is dependent on the level of CB CO2 and whether the CB CO2 gain is changed during VAH. Studies were carried out in adult goats with CB blood gases controlled by an extracorporeal circuit while systemic (central nervous system) blood gases were regulated independently by the level of inhaled gases. Acute V˙e responses to CB hypoxia (CB [Formula: see text] 40 Torr) and CB hypercapnia (CB [Formula: see text] 50 and 60 Torr) were measured while systemic normoxia and isocapnia were maintained. CB[Formula: see text] was then lowered to 40 Torr for 4 h while the systemic blood gases were kept normoxic and normocapnic. During the 4-h CB hypoxia, V˙e increased in a time-dependent manner. Thirty minutes after return to normoxia, the ventilatory response to CB hypoxia was significantly increased compared with the initial response. The slope of the CB CO2 response was also elevated after VAH. An additional group of goats ( n = 7) was studied with a similar protocol, except that CB [Formula: see text]was lowered throughout the 4-h hypoxic exposure to prevent reflex hyperventilation. CB [Formula: see text] was progressively lowered throughout the 4-h CB hypoxic period to maintainV˙e at the control level. After the 4-h CB hypoxic exposure, the ventilatory response to hypoxia was also significantly elevated. However, the slope of the CB CO2 response was not elevated after the 4-h hypoxic exposure. These results suggest that CB sensitivity to both O2 and CO2 is increased after 4 h of CB hypoxia with systemic isocapnia. The increase in CB hypoxic sensitivity is not dependent on the level of CB CO2 maintained during the 4-h hypoxic period.
Effect of an 18-wk weight-training program on energy expenditure and physical activity
Authors: Van Etten Ludo M. L. A. , Westerterp Klaas R. , Verstappen Frans T. J. , Boon Bart J. B. , Saris Wim H. M.
Published: December 2017

Van Etten, Ludo M. L. A., Klaas R. Westerterp, Frans T. J. Verstappen, Bart J. B. Boon, and Wim H. M. Saris. Effect of an 18-wk weight-training program on energy expenditure and physical activity. J. Appl. Physiol. 82(1): 298–304, 1997.—The purpose of this study was to examine the effect of an 18-wk weight-training program on average daily metabolic rate (ADMR). Before the intervention and in weeks 8 and 18(T0, T8, and T18, respectively) data on body composition, sleeping metabolic rate (SMR), food intake, energy cost of the weight-training program (EEex), and nontraining physical activity (accelerometer) were collected in the exercise group (EXER, n = 18 males). ADMR was determined in a subgroup (EX12, n = 12) by using doubly labeled water. At T0 and T18, data (except ADMR) were also collected in a control group (Con, n = 8). Body mass did not change in EXER or Con. Fat-free mass increased only in EXER with 2.1 ± 1.2 kg, whereas fat mass decreased in EXER as well as Con (2.0 ± 1.8 and 1.4 ± 1.0 kg, respectively). Initial ADMR (12.4 ± 1.2 MJ/day) increased at T8 (13.5 ± 1.3 MJ/day, P < 0.001) with no further increase at T18 (13.5 ± 1.9 MJ/day). SMR did not change in EXER (4.8 ± 0.5, 4.9 ± 0.5, 4.8 ± 0.5 kJ/min) or Con (4.7 ± 0.4, 4.8 ± 0.4 kJ/min). Energy intake did not change in EXER (10.1 ± 1.8, 9.7 ± 1.8, 9.2 ± 1.9 MJ/day) or Con (10.2 ± 2.6, 9.4 ± 1.8, 10.1 ± 1.5 MJ/day) and was systematically underreported in EX12 (−21 ± 14, −28 ± 18, −34 ± 14%, P < 0.001). EEex (0.47 ± 0.20, 0.50 ± 0.18 MJ/day) could only explain 40% of the increase in ADMR. Nontraining physical activity did not change in both groups. In conclusion, although of modest energy cost, weight-training induces a significant increase in ADMR.
Effects of caffeine on carotid sinus nerve chemosensory discharge in kittens and cats
Authors: Bairam A. , De Grandpré P. , Dauphin C. , Marchal F.
Published: December 2017

Bairam, A., P. De Grandpré, C. Dauphin, and F. Marchal. Effects of caffeine on carotid sinus nerve chemosensory discharge in kittens and cats. J. Appl. Physiol. 82(2): 413–418, 1997.—Caffeine (C) decreases apneic episodes in premature infants and is thought to stimulate breathing mainly by a central mechanism. While the methylxanthines theophylline and aminophylline are known to alter the carotid chemoreceptor activity, there are little data on C. The aim of the study was to examine the effects of C on the carotid sinus nerve discharge (CSND) in developing animals. Nine kittens 17–21 days old and six adult cats that were anesthetized and artificially ventilated were studied. They received four consecutive doses of C, each of 10 mg/kg, administered at intervals of 20 min either as intravenous bolus injection (6 kittens, 3 cats) or continuous infusion (3 kittens, 3 cats). Bolus injections of C invariably induced a prompt but transient increase in the CSND from 4.1 ± 0.6 to 8.1 ± 1.0 (SE) impulses/s in kittens ( P = 0.01) and from 3.9 ± 0.1 to 7.9 to 1.0 impulses/s in cats (after the first injection). This response was associated with a significant decrease in arterial blood pressure. Continuous infusion of C did not induce any early change in either CSND or blood pressure in kittens or cats. Fifteen minutes after C injection or infusion was begun, CSND values in air, 8% O2-balance N2, or 100% O2 were not significantly different from control. Haloperidol administered at the end of the experiment in four cats and four kittens significantly increased CSND and did not suppress the early response to C injection. It is concluded that caffeine administered by bolus in the kitten induces a transient stimulation of the CSND that is associated with a decrease in the arterial blood pressure and is independent of the dopaminergic mechanisms in the carotid body. The lack of sustained effect implies the main mechanism to the ventilatory stimulation by C must be central.
Respective oxidation of13C-labeled lactate and glucose ingested simultaneously during exercise
Authors: Péronnet F. , Burelle Y. , Massicotte D. , Lavoie C. , Hillaire-Marcel C.
Published: December 2017

Péronnet, F., Y. Burelle, D. Massicotte, C. Lavoie, and C. Hillaire-Marcel. Respective oxidation of13C-labeled lactate and glucose ingested simultaneously during exercise. J. Appl. Physiol. 82(2): 440–446, 1997.—The purpose of this experiment was to measure, by using13C labeling, the oxidation rate of exogenous lactate (25 g, as Na+, K+, Ca2+, and Mg2+ salts) and glucose (75 g) ingested simultaneously (in 1,000 ml of water) during prolonged exercise (120 min, 65 ± 3% maximum oxygen uptake in 6 male subjects). The percentage of exogenous glucose and lactate oxidized were similar (48 ± 3 vs. 45 ± 5%, respectively). However, because of the small amount of oral lactate that could be tolerated without gastrointestinal discomfort, the amount of exogenous lactate oxidized was much smaller than that of exogenous glucose (11.1 ± 0.5 vs. 36.3 ± 1.3 g, respectively) and contributed to only 2.6 ± 0.4% of the energy yield (vs. 8.4 ± 1.9% for exogenous glucose). The cumulative amount of exogenous glucose and lactate oxidized was similar to that observed when 100 g of [13C]glucose were ingested (47.3 ± 1.8 vs. 50.9 ± 1.2 g, respectively). When [13C]glucose was ingested, changes in the plasma glucose13C/12C ratio indicated that between 39 and 61% of plasma glucose derived from exogenous glucose. On the other hand, the plasma glucose13C/12C ratio remained unchanged when [13C]lactate was ingested, suggesting no prior conversion into glucose before oxidation.
Ventilatory effects of specific carotid body hypocapnia and hypoxia in awake dogs
Authors: Smith Curtis A. , Harms Craig A. , Henderson Kathleen S. , Dempsey Jerome A.
Published: December 2017

Smith, Curtis A., Craig A. Harms, Kathleen S. Henderson, and Jerome A. Dempsey. Ventilatory effects of specific carotid body hypocapnia and hypoxia in awake dogs. J. Appl. Physiol. 82(3): 791–798, 1997.—Specific carotid body (CB) hypocapnia in the −10-Torr (less than eupneic) range reduced ventilation in the awake and sleeping dog to the same degree as did CB hyperoxia [CB [Formula: see text]([Formula: see text]); >500 Torr; C. A. Smith, K. W. Saupe, K. S. Henderson, and J. A. Dempsey. J. Appl. Physiol. 79: 689–699, 1995], suggesting a powerful inhibitory effect of hypocapnia at the carotid chemosensor over a range of[Formula: see text] encountered commonly in physiological hyperpneas. The primary purpose of this study was to assess the ventilatory effect of CB hypocapnia on the ventilatory response to concomitant CB hypoxia. The secondary purpose was to assess the relative gains of the CB and central chemoreceptors to hypocapnia. In eight awake female dogs the vascularly isolated CB was perfused with hypoxic blood (mild,[Formula: see text]≅ 50 Torr or severe,[Formula: see text]≅ 36 Torr) in a background of normocapnia or hypocapnia (10 Torr less than eupneic arterial [Formula: see text]) in the perfusate. The systemic (and brain) circulation was normoxic throughout, and arterial Pco 2 was not controlled (poikilocapnia). With CB hypocapnia, the peak ventilation (range 19–27 s) in response to hypoxic CB perfusion increased 48% (mild) and 77% (severe) due to increased tidal volume. When CB hypocapnia was present, these increases in ventilation were reduced to 21 and 27%, respectively. With systemic hypocapnia, with the isolated CB maintained normocapnic and hypoxic for >70 s, the steady-state poikilocapnic ventilatory response (i.e., to systemic hypocapnia alone) decreased 15% (mild CB hypoxia) and 27% (severe CB hypoxia) from the peak response, respectively. We conclude that carotid body hypocapnia can be a major source of inhibitory feedback to respiratory motor output during the hyperventilatory response to hypoxic carotid body stimulation.
XO increases neutrophil adherence to endothelial cells by a dual ICAM-1 and P-selectin-mediated mechanism
Authors: Terada Lance S. , Hybertson Brooks M. , Connelly Kevin G. , Weill David , Piermattei Dale , Repine John E.
Published: December 2017

Terada, Lance S., Brooks M. Hybertson, Kevin G. Connelly, David Weill, Dale Piermattei, and John E. Repine. XO increases neutrophil adherence to endothelial cells by a dual ICAM-1 and P-selectin-mediated mechanism. J. Appl. Physiol. 82(3): 866–873, 1997.—Circulating xanthine oxidase (XO) can modify adhesive interactions between neutrophils and the vascular endothelium, although the mechanisms underlying this effect are not clear. We found that treatment with XO of bovine pulmonary artery endothelial cells (EC), but not neutrophils or plasma, increased adherence, suggesting that XO had its primary effect on EC. The mechanism by which XO increased neutrophil adherence to EC involved binding of XO to EC and production of H2O2. XO also increased platelet-activating factor production by EC by a H2O2-dependent mechanism. Similarly, the platelet-activating factor-receptor antagonist WEB-2086 completely blocked XO-mediated neutrophil EC adherence. In addition, neutrophil adherence was dependent on the β2-integrin Mac-1 (CD11b/CD18) but not on leukocyte functional antigen-1 (CD11a/CD18). Treatment of EC with XO for 30 min did not alter intercellular adhesion molecule-1 surface expression but increased expression of P-selectin and release of von Willibrand factor. Antibodies against P-selectin (CD62) did not affect XO-mediated neutrophil adherence under static conditions but decreased both rolling and firm adhesive interactions under conditions of shear. We conclude that extracellular XO associates with the endothelium and promotes neutrophil-endothelial cell interactions through dual intercellular adhesion molecule-1 and P-selectin ligation, by a mechanism that involves platelet-activating factor and H2O2as intermediates.
Endogenous nitric oxide decreases xanthine oxidase-mediated neutrophil adherence: role of P-selectin
Authors: Terada Lance S. , Repine John E. , Piermattei Dale , Hybertson Brooks M.
Published: December 2017

Terada, Lance S., John E. Repine, Dale Piermattei, and Brooks M. Hybertson. Endogenous nitric oxide decreases xanthine oxidase-mediated neutrophil adherence: role of P-selectin. J. Appl. Physiol. 82(3): 913–917, 1997.—The oxygen radical-producing enzyme xanthine oxidase (XO) can promote neutrophil adherence to endothelium. Recognizing that a balance often exists in inflammatory processes, we sought to determine whether XO initiates antiadherent pathways. We found that bovine pulmonary arterial endothelial cells (EC) exposed to XO released increased amounts of nitrite into the media, reflecting an increased production of nitric oxide (NO). When EC were subjected to shear stress, treatment with XO and/or the NO synthase inhibitor Nω-nitro-l-arginine (l-NNA) increased neutrophil rolling behavior and firm neutrophil adherence to EC in an additive fashion. Both rolling and adherent interactions were abolished by monoclonal antibodies directed against P-selectin. In addition, treatment of EC with XO and/orl-NNA increased both surface expression of P-selectin and release of von Willebrand factor into media. Finally, treatment of EC with the NO donor sodium nitroprusside decreased XO-mediated neutrophil rolling and adherence. We conclude that XO stimulates EC to produce NO and that NO decreases the P-selectin-dependent neutrophil adhesion initiated by XO. Such increases in endogenous NO may constitute an important negative-feedback response to the acute proadhesive effects of XO.
Computer determination of perfusion patterns in pulmonary capillary networks
Authors: Hanger Christopher C. , Presson Robert G. , Okada Osamu , Janke Steven J. , Watkins John J. , Wagner Wiltz W. , Capen Ronald L.
Published: December 2017

Hanger, Christopher C., Robert G. Presson, Jr., Osamu Okada, Steven J. Janke, John J. Watkins, Wiltz W. Wagner, Jr., and Ronald L. Capen. Computer determination of perfusion patterns in pulmonary capillary networks. J. Appl. Physiol.82(4): 1283–1289, 1997.—Individual pulmonary capillaries are not steadily perfused. By using in vivo microscopy, it can readily be demonstrated that perfusion continually switches between capillary segments and between portions of the network within a single alveolar wall. These changes in capillary perfusion occur even when upstream pressure and flow are constant. Flow switching between capillary segments in the absence of hemodynamic changes in large upstream vessels suggests that capillary perfusion patterns could be random. To calculate the probability that perfusion patterns could occur by chance, it is necessary to know the total number of possible perfusion patterns in a given capillary network. We developed a computer program that can determine every possible perfusion pattern for any given capillary network, and from that information we can calculate whether perfusion of individual segments in the network is random. With the results of the computer program, we have obtained statistical evidence that some capillary segments in a network are nonrandomly perfused.
Effects of supplemental oxygen on forearm vasodilation in humans
Authors: Crawford Paul , Good Peter A. , Gutierrez Eric , Feinberg Joshua H. , Boehmer John P. , Silber David H. , Sinoway Lawrence I.
Published: December 2017

Crawford, Paul, Peter A. Good, Eric Gutierrez, Joshua H. Feinberg, John P. Boehmer, David H. Silber, and Lawrence I. Sinoway.Effects of supplemental oxygen on forearm vasodilation in humans. J. Appl. Physiol. 82(5): 1601–1606, 1997.—Supplemental O2reduces cardiac output and raises systemic vascular resistance in congestive heart failure. In this study, 100% O2was given to normal subjects and peak forearm flow was measured. In experiment 1, 100% O2reduced blood flow and increased resistance after 10 min of forearm ischemia (flow 56.7 ± 7.9 vs. 47.8 ± 6.7 ml ⋅ min−1⋅ 100 ml−1; P < 0.02; vascular resistance 1.7 ± 0.2 vs. 2.4 ± 0.4 mmHg ⋅ min ⋅ 100 ml ⋅ ml−1; P < 0.03). In experiment 2, lower body negative pressure (LBNP; −30 mmHg) and venous congestion (VC) simulated the high sympathetic tone and edema of congestive heart failure. Postischemic forearm flow and resistance were measured under four conditions: room air breathing (RA); LBNP+RA; RA+LBNP+VC; and 100% O2+LBNP+VC. LBNP and VC did not lower peak flow. However, O2raised minimal resistance (2.3 ± 0.4 RA; 2.8 ± 0.5 O2+LBNP+VC, P < 0.04). When O2alone ( experiment 1) was compared with O2+LBNP+VC ( experiment 2), no effect of LBNP+VC on peak flow or minimum resistance was noted, although the return rate of flow and resistance toward baseline was increased. O2reduces peak forearm flow even in the presence of LBNP and VC.
Intracerebroventricular propranolol prevented vascular resistance increases on arousal from sleep apnea
Authors: Zinkovska Sophia , Kirby Debra A.
Published: December 2017

Zinkovska, Sophia, and Debra A. Kirby.Intracerebroventricular propranolol prevented vascular resistance increases on arousal from sleep apnea. J. Appl. Physiol. 82(5): 1637–1643, 1997.—Despite the increased risk of sudden cardiac death associated with sleep apnea, little is known about mechanisms controlling cardiovascular responses to sleep apnea and arousal. Chronically instrumented pigs were used to investigate the effects of airway obstruction (AO) during rapid-eye-movement (REM) and non-REM (NREM) sleep and arousal on mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR). A stainless steel cannula was implanted in the lateral cerebral ventricle. During REM sleep, HR was 133 ± 10 beats/min, MAP was 65 ± 3 mmHg, CO was 1,435 ± 69 ml/min, and TPR was 0.046 ± 0.004 mmHg ⋅ ml−1 ⋅ min. During AO, CO decreased by 90 ± 17 ml/min ( P < 0.05). On arousal from AO, MAP increased by 15 ± 3 mmHg, HR increased by 10 ± 3 beats/min, and TPR increased by 0.008 ± 0.001 mmHg ⋅ ml−1 ⋅ min (all P < 0.05). Changes during NREM were similar but were more modest during AO. After the intracerebroventricular administration of propranolol (50 μg/kg; a β-adrenoreceptor blocking agent), decreases in CO during AO and increases in HR during arousal were intact, but increases in MAP and TPR were no longer significant. These data suggest that vascular responses to AO during sleep may be regulated in part by β-adrenergic receptors in the central nervous system.
Changes in leg vein filling and emptying characteristics and leg volumes during long-term head-down bed rest
Authors: Louisy Francis , Schroiff Philippe , Güell Antonio
Published: December 2017

Louisy, Francis, Philippe Schroiff, and Antonio Güell.Changes in leg vein filling and emptying characteristics and leg volumes during long-term head-down bed rest. J. Appl. Physiol. 82(6): 1726–1733, 1997.—Leg venous hemodynamics [venous distensibility index (VDI), arterial flow index (AFI), half-emptying time (T1/2)], and leg volumes (LV) were assessed by mercury strain-gauge plethysmography with venous occlusion and volometry, respectively, in seven men before, during, and after 42 days of 6° head-down bed rest. Results showed a high increase in VDI up to day 26 of bed rest (+50% vs. control at day 26, P < 0.05), which tended to subside thereafter (+20% increase vs. control value at day 41, P < 0.05). VDI changes were associated with parallel changes in T1/2 (+54% vs. control at day 26 of bed rest, P < 0.05, and +25% vs. control at day 41, P < 0.05) and with a decrease in AFI (−49% at day 41 vs. control, P < 0.05). LV continuously decreased throughout bed rest (−13% vs. control at day 41, P < 0.05) but was correlated with VDI only during the first month of bed rest. These results show that during long-term 6° head-down bed rest alterations of leg venous compliance are associated with impairment of venous emptying capacities and arterial flow. Changes in skeletal muscle mass and fluid shifts may account for venous changes during the first month of bed rest but, subsequently, other physiological factors, to be determined, may also be involved in leg venous hemodynamic alterations.
CO2transport in normovolemic anemia: complete compensation and stability of blood CO2tensions
Authors: Deem Steven , Alberts Michael K. , Bishop Michael J. , Bidani Akhil , Swenson Erik R.
Published: December 2017

Deem, Steven A., Michael K. Alberts, Michael J. Bishop, Akhil Bidani, and Erik R. Swenson.CO2transport in normovolemic anemia: complete compensation and stability of blood CO2tensions. J. Appl. Physiol. 83(1): 240–246, 1997.—Isovolemic hemodilution does not appear to impair CO2elimination nor cause CO2retention despite the important role of red blood cells in blood CO2transport. We studied this phenomenon and its physiological basis in eight New Zealand White rabbits that were anesthetized, paralyzed, and mechanically ventilated at a fixed minute ventilation. Isovolemic anemia was induced by simultaneous blood withdrawal and infusion of 6% hetastarch in sequential stages; exchange transfusions ranged from 15–30 ml in volume. Variables measured after each hemodilution included hematocrit (Hct), arterial and venous blood gases, mixed expired[Formula: see text] and[Formula: see text], and blood pressure; also, O2consumption, CO2production, cardiac output (Q˙), and physiological dead space were calculated. Data were analyzed by comparison of changes in variables with changes in Hct and by using the model of capillary gas exchange described by Bidani ( J. Appl. Physiol. 70: 1686–1699, 1991). There was complete compensation for anemia with stability of venous and arterial [Formula: see text]between Hct values of 36 ± 3 and 12 ± 1%, which was predicted by the mathematical model. Over this range of hemodilution,Q˙ rose 50%, and the O2extraction ratio increased 61% without a decline in CO2production or a rise in alveolar ventilation. The dominant compensations maintaining CO2transport in normovolemic anemia include an increasedQ˙ and an augmented Haldane effect arising from the accompanying greater O2extraction.
Effect of inotropic interventions on contraction and Ca2+transients in the human heart
Authors: Brixius Klara , Pietsch Marcus , Hoischen Susanne , Müller-Ehmsen Jochen , Schwinger Robert H. G.
Published: December 2017

Brixius, Klara, Marcus Pietsch, Susanne Hoischen, Jochen Müller-Ehmsen, and Robert H. G. Schwinger. Effect of inotropic interventions on contraction and on Ca2+transients in the human heart. J. Appl. Physiol. 83(2): 652–660, 1997.—The present study investigated the influences of inotropic intervention on the intracellular Ca2+transient {intracellular Ca2+concentration ([Ca2+]i)} and contractile twitch. Isometric twitch and [Ca2+]i(fura 2 ratio method) were measured simultaneously (1 Hz, 37°C) after stimulation with Ca2+(0.9–3.2 mM), the cardiac glycoside ouabain (Oua; 0.1 μM), the β1- and β2-adrenoceptor-agonist isoprenaline (Iso; 1–10 nM), and the Ca2+sensitizer EMD-57033 (30 μM) by using isolated human nonfailing right auricular trabeculae ( n = 19). Inotropic interventions increased force of contraction and peak rate of tension rise (+ T) significantly. Only Iso stimulated peak rate of tension decay (− T) higher than + T ( P< 0.05), thereby reducing time of contraction ( Ttwitch). EMD-57033 increased + T more effectively than − T and prolonged Ttwitch( P < 0.05). Ca2+, Oua, and Iso, but not EMD-57033, increased systolic Ca2+. Diastolic Ca2+increased after stimulation with Oua or Ca2+, but not in the presence of EMD-57033. Iso shortened the Ca2+transient and did not influence diastolic Ca2+. In conclusion, positive inotropic agents differently affect force and [Ca2+]idepending on their mode of action. Inotropic interventions influence diastolic Ca2+and thus may be less advantageous in a situation with altered intracellular Ca2+homeostasis (e.g., heart failure due to dilated cardiomyopathy).
Role of vagal fibers in the hypoxia-induced increases in end-expiratory lung volume and diaphragmatic activity
Authors: Bonora M. , Vizek M.
Published: December 2017

Bonora, M., and M. Vizek. Role of vagal fibers in the hypoxia-induced increases in end-expiratory lung volume and diaphragmatic activity. J. Appl. Physiol. 83(3): 700–706, 1997.—The possible role of pulmonary C fibers in the hypoxia-induced concomitant increases in end-expiratory lung volume (EELV) and in the activity of the diaphragm at the end of expiration (De) were evaluated by measuring the effects of hypoxia (10% O2) on ventilation, EELV, and De in eight chloralose-urethan anesthetized rats. Recordings were made before and after blocking vagal C fibers and after bilateral vagotomy. C-fiber conduction was blocked by applying capsaicin perineurally to the cervical vagi. The efficiency of C-fiber blockade was tested with intravenous capsaicin and its selectivity by the Hering-Breuer reflex. Perineural capsaicin abolished the reflex apnea induced by intravenous capsaicin and transiently reduced Hering-Breuer reflex. Perineural capsaicin affected neither ventilation, De, and EELV in air nor the hypoxia-induced increases in these parameters. Vagotomy caused the typical changes of breathing pattern in air, but the ventilatory response to hypoxia was unchanged. Vagotomy performed during hypoxia resulted in large decreases in De and EELV. Hypoxia increased De and EELV in vagotomized rats but less than in intact rats. We conclude that the hypoxia-induced increases in EELV and diaphragmatic activity are probably not mediated by vagal C fibers and that vagal afferents are involved but not fully responsible for this phenomenon.
Aerosol dispersion in human lung: comparison between numerical simulations and experiments for bolus tests
Authors: Darquenne Chantal , Brand Peter , Heyder Joachim , Paiva Manuel
Published: December 2017

Darquenne, Chantal, Peter Brand, Joachim Heyder, and Manuel Paiva. Aerosol dispersion in human lung: comparison between numerical simulations and experiments for bolus tests. J. Appl. Physiol. 83(3): 966–974, 1997.—Bolus inhalations of 0.87-μm-diameter particles were administered to 10 healthy subjects, and data were compared with numerical simulations based on a one-dimensional model of aerosol transport and deposition in the human lung ( J. Appl. Physiol. 77: 2889–2898, 1994). Aerosol boluses were inhaled at a constant flow rate into various volumetric lung depths up to 1,500 ml. Parameters such as bolus half-width, mode shift, skewness, and deposition were used to characterize the bolus and to display convective mixing. The simulations described the experimental results reasonably well. The sensitivity of the simulations to different parameters was tested. Simulated half-width appeared to be insensitive to altered values of the deposition term, whereas it was greatly affected by modified values of the apparent diffusion in the alveolar zone of the lung. Finally, further simulations were compared in experiments with a fixed penetration volume and various flow rates. Comparison showed good agreement, which may be explained by the fact that half-width, mode shift, and skewness were little affected by the flow rate.
Skeletal troponin I as a marker of exercise-induced muscle damage
Authors: Sorichter Stephan , Mair Johannes , Koller Arnold , Gebert Walter , Rama Daniel , Calzolari Charles , Artner-Dworzak Erika , Puschendorf Bernd
Published: December 2017

Sorichter, Stephan, Johannes Mair, Arnold Koller, Walter Gebert, Daniel Rama, Charles Calzolari, Erika Artner-Dworzak, and Bernd Puschendorf. Skeletal troponin I as a marker of exercise-induced muscle damage. J. Appl. Physiol.83(4): 1076–1082, 1997.—The utility of skeletal troponin I (sTnI) as a plasma marker of skeletal muscle damage after exercise was compared against creatine kinase (CK), myoglobin (Mb), and myosin heavy chain (MHC) fragments. These markers were serially measured in normal physical education teacher trainees after four different exercise regimens: 20 min of level or downhill (16% decline) running (intensity: 70% maximal O2uptake), high-force eccentric contractions (70 repetitions), or high-force isokinetic concentric contractions of the quadriceps group (40 repetitions). Eccentrically biased exercise (downhill running and eccentric contractions) promoted greater increases in all parameters. The highest plasma concentration were found after downhill running {median peaks: 309 U/l CK concentration ([CK])}, 466 μg/l Mb concentration ([Mb]), 1,021 μU/l MHC concentration ([MHC]), and 27.3 μg/l sTnI concentration ([sTnI]). Level running produced a moderate response (median peaks: 178 U/l [CK], 98 μg/l [Mb], 501 μU/l [MHC], and 6.6 μg/l [sTnI]), whereas the concentric contraction protocol did not elicit significant changes in any of the markers assayed. sTnI increased and peaked in parallel to CK and stayed elevated (>2.2 μg/l) for at least 1–2 days after exercise. In contrast to MHC, sTnI is an initial, specific marker of exercise-induced muscle injury, which may be partly explained by their different intracellular compartmentation with essentially no (MHC <0.1%) or a small soluble pool (sTnI: median 3.4%).
Effects of bovine colostrum supplementation on serum IGF-I, IgG, hormone, and saliva IgA during training
Authors: Mero Antti , Miikkulainen Heidi , Riski Jarmo , Pakkanen Raimo , Aalto Jouni , Takala Timo
Published: December 2017

Mero, Antti, Heidi Miikkulainen, Jarmo Riski, Raimo Pakkanen, Jouni Aalto, and Timo Takala. Effects of bovine colostrum supplementation on serum IGF-I, IgG, hormone, and saliva IgA during training. J. Appl. Physiol.83(4): 1144–1151, 1997.—The purpose of this study was to examine the effects of bovine colostrum supplementation (Bioenervi) on serum insulin-like growth factor I (IGF-I), immunoglobulin G, hormone, and amino acid and saliva immunoglobulin A concentrations during a strength and speed training period. Nine male sprinters and jumpers underwent three randomized experimental training treatments of 8 days separated by 13 days. The only difference in the treatments was the drink of 125 ml consumed per day. Posttraining increases were noticed for serum IGF-I in the 25-ml Bioenervi treatment (125 ml contained 25 ml Bioenervi) and especially in the 125-ml Bioenervi treatment (125 ml contained 125 ml Bioenervi) compared with the placebo (normal milk whey) treatment ( P < 0.05). The change in IGF-I concentration during the 8-day periods correlated positively with the change in insulin concentration during the same periods with 25-ml Bioenervi treatment ( r = 0.68; P = 0.045) and with 125-ml Bioenervi treatment ( r = 0.69; P = 0.038). Serum immunoglobulin G, hormone, and amino acid and saliva immunoglobulin A responses were similar during the three treatments. It appears that a bovine colostrum supplement (Bioenervi) may increase serum IGF-I concentration in athletes during strength and speed training.
Cardiovascular changes during deep breath-hold dives in a pressure chamber
Authors: Ferrigno Massimo , Ferretti Guido , Ellis Avery , Warkander Dan , Costa Mario , Cerretelli Paolo , Lundgren Claes E. G.
Published: December 2017

Ferrigno, Massimo, Guido Ferretti, Avery Ellis, Dan Warkander, Mario Costa, Paolo Cerretelli, and Claes E. G. Lundgren. Cardiovascular changes during deep breath-hold dives in a pressure chamber. J. Appl. Physiol.83(4): 1282–1290, 1997.—Electrocardiogram, cardiac output, and blood lactate accumulation were recorded in three elite breath-hold divers diving to 40–55 m in a pressure chamber in thermoneutral (35°C) or cool (25°C) water. In two of the divers, invasive recordings of arterial blood pressure were also obtained during dives to 50 m in cool water. Bradycardia during the dives was more pronounced and developed more rapidly in the cool water, with heart rates dropping to 20–30 beats/min. Arrhythmias occurred, particularly during the dives in cool water, when they were often more frequent than sinus beats. Because of bradycardia, cardiac output decreased during the dives, especially in cool water (to <3 l/min in 2 of the divers). Arterial blood pressure increased dramatically, reaching values as high as 280/200 and 290/150 mmHg in the two divers, respectively. This hypertension was secondary to peripheral vasoconstriction, which also led to anaerobic metabolism, reflected in increased blood lactate concentration. The diving response of these divers resembles the one described for diving animals, although the presence of arrhythmias and large increases in blood pressure indicate a less perfect adaptation in humans.
Roles of hydration, sodium, and chloride in regulation of canine mucociliary transport system
Authors: Winters Scot L. , Yeates Donovan B.
Published: December 2017

Winters, Scot L., and Donovan B. Yeates. Roles of hydration, sodium, and chloride in regulation of canine mucociliary transport system. J. Appl. Physiol.83(4): 1360–1369, 1997.—To gain insight into the homeostatic mechanisms regulating airway ion/water fluxes and mucociliary transport, the canine tracheobronchial airway fluid was perturbed by deposition of hypo- and hyperosmotic aerosols for >1 h. Tracheal ciliary beat frequency (CBF) was measured by using heterodyne laser light scattering. Tracheal mucus velocity (TMV) and bronchial mucociliary clearance (BMC) were measured by using radioaerosols and nuclear imaging. Respiratory tract fluid output (RTFO) was collected by using a secretion-collecting endotracheal tube. In six dogs, CBF increased during water deposition in the airways to 180 ± 30 mg/min and RTFO increased from 2.2 ± 0.5 to 18.3 ± 1.6 mg/min, accounting for <10% of the fluid deposition. TMV and BMC were unchanged. CBF, TMV, and BMC were markedly increased by inhalation of aerosolized 3.4 M NaCl. Aerosolized 0.85 M NaCl, in contrast, decreased BMC. In this case, RTFO represented 24% of aerosol deposition. Aerosolized 0.85 M choline chloride and 0.85 M sodium gluconate enhanced BMC and TMV concurrent with a decrease in CBF. RTFO of sodium gluconate studies exceeded 50% of aerosol deposition. Thus the airways appear to have transepithelial compensatory mechanisms that reduce the impact of a moderate increases in NaCl and hydration load, but when these responses cannot adequately respond because of the delivery of impermeable ions or very high tonicity, removal of the challenges are affected by a stimulation of mucociliary transport.