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  • American Physiological Society  (9)
  • Biology  (9)
  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 2009
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 297, No. 4 ( 2009-10), p. H1243-H1253
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 297, No. 4 ( 2009-10), p. H1243-H1253
    Abstract: Carbon monoxide (CO) has anti-inflammatory properties. We previously reported that acute treatments with inhaled CO inhibit vascular inflammation and hypoxia-induced vasoocclusion in sickle cell disease mouse models. Therefore, we hypothesized that chronic CO inhalation would decrease vascular inflammation and organ pathology in a sickle cell disease mouse model. The treatment of sickle cell disease mice with 25 or 250 parts/million inhaled CO for 1 h/day, 3 days/wk for 8–10 wk significantly decreased the total mean white blood cell, neutrophil, and lymphocyte counts in peripheral blood. Eight weeks of 250 parts/million CO treatments reduced staining for myeloid and lymphoid markers in the bone marrow of sickle mice. Bone marrow from treated sickle mice exhibited a significant decrease in colony-forming unit granulocyte-macrophage during colony-forming cell assays. Anti-inflammatory signaling pathways phospho-Akt and phospho-p38 MAPK were markedly increased in CO-treated sickle livers. Importantly, CO-treated sickle mice had a significant reduction in liver parenchymal necrosis, reflecting the anti-inflammatory benefits of CO. We conclude that inhaled CO may be a beneficial anti-inflammatory therapy for sickle cell disease.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 1995
    In:  Journal of Applied Physiology Vol. 78, No. 3 ( 1995-03-01), p. 1121-1131
    In: Journal of Applied Physiology, American Physiological Society, Vol. 78, No. 3 ( 1995-03-01), p. 1121-1131
    Abstract: The role of leukotriene B4 (LTB4) in the pathogenesis of acute lung injury was examined in endotoxemic pigs. In a preliminary study, the activity and specificity of an LTB4-receptor antagonist, LY-306669, were evaluated. In vitro, LY-306669 completely blocked the functional upregulation of phagocyte opsonin receptors induced by LTB4 but had a much smaller effect on opsonin receptor upregulation induced by platelet-activating factor. In pigs treatment with LY-306669 prevented leukopenia induced by injection of authentic LTB4 but had no effect on the hematologic or hemodynamic effects of PAF or U-48816, a thromboxane-A2 mimetic. In a second study, pigs received an intravenous priming dose of lipopolysaccharide (LPS) at time (t) = -18 h and were randomized to receive 1) no further treatment (n = 5), 2) LPS (250 micrograms/kg over 1 h beginning at t = 0 h) and LY-306669 (10 mg/kg bolus and 3 mg.kg-1.h-1 infusion beginning at t = -15 min) (n = 7), or 3) LPS and vehicle (n = 6). Treatment with LY-306669 significantly ameliorated LPS-induced hypoxemia, pulmonary edema, and alveolitis. These data suggest that LTB4 is an important mediator of pulmonary dysfunction and transendothelial migration of neutrophils in LPS-induced acute lung injury.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
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    Language: English
    Publisher: American Physiological Society
    Publication Date: 1995
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 3
    In: Journal of Applied Physiology, American Physiological Society, Vol. 114, No. 4 ( 2013-02-15), p. 461-471
    Abstract: This study was undertaken to investigate physiological adaptation with two endurance-training periods differing in intensity distribution. In a randomized crossover fashion, separated by 4 wk of detraining, 12 male cyclists completed two 6-wk training periods: 1) a polarized model [6.4 (±1.4 SD) h/wk; 80%, 0%, and 20% of training time in low-, moderate-, and high-intensity zones, respectively]; and 2) a threshold model [7.5 (±2.0 SD) h/wk; 57%, 43%, and 0% training-intensity distribution] . Before and after each training period, following 2 days of diet and exercise control, fasted skeletal muscle biopsies were obtained for mitochondrial enzyme activity and monocarboxylate transporter (MCT) 1 and 4 expression, and morning first-void urine samples were collected for NMR spectroscopy-based metabolomics analysis. Endurance performance (40-km time trial), incremental exercise, peak power output (PPO), and high-intensity exercise capacity (95% maximal work rate to exhaustion) were also assessed. Endurance performance, PPOs, lactate threshold (LT), MCT4, and high-intensity exercise capacity all increased over both training periods. Improvements were greater following polarized rather than threshold for PPO [mean (±SE) change of 8 (±2)% vs. 3 (±1)%, P 〈 0.05], LT [9 (±3)% vs. 2 (±4)%, P 〈 0.05], and high-intensity exercise capacity [85 (±14)% vs. 37 (±14)%, P 〈 0.05]. No changes in mitochondrial enzyme activities or MCT1 were observed following training. A significant multilevel, partial least squares-discriminant analysis model was obtained for the threshold model but not the polarized model in the metabolomics analysis. A polarized training distribution results in greater systemic adaptation over 6 wk in already well-trained cyclists. Markers of muscle metabolic adaptation are largely unchanged, but metabolomics markers suggest different cellular metabolic stress that requires further investigation.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
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    Language: English
    Publisher: American Physiological Society
    Publication Date: 2013
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 4
    In: Journal of Applied Physiology, American Physiological Society, Vol. 122, No. 5 ( 2017-05-01), p. 1088-1094
    Abstract: Calcification of the tunica media of the axial pulmonary arteries (PA) has been reported in a large proportion of racehorses. In humans, medial calcification is a significant cause of arterial stiffening and is implicated in the pathogenesis of cardiac, cerebral, and renal microvascular diseases. Pulse wave velocity (PWV) provides a measure of arterial stiffness. This study aimed to develop a technique to determine PA-PWV in horses and, secondarily, to investigate a potential association between PA-PWV and arterial fibro-calcification. A dual-pressure sensor catheter (PSC) was placed in the main PA of 10 sedated horses. The pressure waves were used to determine PWV along the PA, using the statistical phase offset method. Histological analysis of the PA was performed to investigate the presence of fibro-calcified lesions. The mean (±SD) PWV was 2.3 ± 0.7 m/s in the proximal PA trunk and 1.1 ± 0.1 m/s further distal (15 cm) in a main PA branch. The mean (±SD) of mean arterial pressures in the proximal PA trunk was 30.1 ± 5.2 mmHg, and 22.0 ± 6.0 mmHg further distal (15 cm) within the main PA branch. The mean (±SD) pulse pressure in the proximal PA trunk was 15.0 ± 4.7 mmHg, and 13.5 ± 3.3 mmHg further distal (15 cm) within the main PA branch. Moderate to severe lesions of the tunica media of the PAs were observed in seven horses, but a correlation with PWV could not be established yet. Pulmonary artery PWV may be determined in standing horses. The technique described may allow further investigation of the effect of calcification of large PAs in the pathogenesis of equine pulmonary circulatory disorders. NEW & NOTEWORTHY Pulmonary artery pulse wave velocity was determined safely in standing sedated horses. The technique described may allow further investigation of the effect of calcification of large pulmonary arteries in the pathogenesis of pulmonary circulatory disorders in horses.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2017
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 5
    In: Journal of Applied Physiology, American Physiological Society, Vol. 112, No. 8 ( 2012-04-15), p. 1403-1409
    Abstract: Coronary collaterals preserve left ventricular (LV) function during coronary occlusion by reducing myocardial ischemia and may directly influence LV compliance. We aimed to re-evaluate the relationship between coronary collaterals, measured quantitatively with a pressure wire, and simultaneously recorded LV contractility from conductance catheter data during percutaneous coronary intervention (PCI) in humans. Twenty-five patients with normal LV function awaiting PCI were recruited. Pressure-derived collateral flow index (CFI p ): CFI p = (P w − P v )/(P a − P v ) was calculated from pressure distal to coronary balloon occlusion (P w ), central venous pressure (P v ), and aortic pressure (P a ). CFI p was compared with the changes in simultaneously recorded LV end-diastolic pressure (ΔLVEDP), end-diastolic volume, maximum rate of rise in pressure (ΔLVdP/dt max ; systolic function), and time constant of isovolumic relaxation (ΔLV τ; diastolic function), measured by a LV cavity conductance catheter. Measurements were recorded at baseline and following a 1-min coronary occlusion and were duplicated after a 30-min recovery period. There was significant LV diastolic dysfunction following coronary occlusion (ΔLVEDP: +24.5%, P 〈 0.0001; and ΔLV τ: +20.0%, P 〈 0.0001), which inversely correlated with CFI p (ΔLVEDP vs. CFI p : r = −0.54, P 〈 0.0001; ΔLV τ vs. CFI p : r = −0.46, P = 0.0009). Subjects with fewer collaterals had lower LVEDP at baseline (r = 0.33, P = 0.02). CFI p was inversely related to the coronary stenosis pressure gradient at rest (r = −0.31, P = 0.03). Collaterals exert a direct hemodynamic effect on the ventricle and attenuate ischemic LV diastolic dysfunction during coronary occlusion. Vessels with lesions of greater hemodynamic significance have better collateral supply.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2012
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 6
    Online Resource
    Online Resource
    American Physiological Society ; 1918
    In:  American Journal of Physiology-Legacy Content Vol. 47, No. 1 ( 1918-09-01), p. 143-155
    In: American Journal of Physiology-Legacy Content, American Physiological Society, Vol. 47, No. 1 ( 1918-09-01), p. 143-155
    Type of Medium: Online Resource
    ISSN: 0002-9513
    RVK:
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    Language: English
    Publisher: American Physiological Society
    Publication Date: 1918
    detail.hit.zdb_id: 1477334-X
    detail.hit.zdb_id: 2065807-2
    detail.hit.zdb_id: 1477287-5
    detail.hit.zdb_id: 1477308-9
    detail.hit.zdb_id: 1477297-8
    detail.hit.zdb_id: 1477331-4
    detail.hit.zdb_id: 1477300-4
    detail.hit.zdb_id: 1477329-6
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    American Physiological Society ; 1918
    In:  American Journal of Physiology-Legacy Content Vol. 47, No. 1 ( 1918-09-01), p. 137-142
    In: American Journal of Physiology-Legacy Content, American Physiological Society, Vol. 47, No. 1 ( 1918-09-01), p. 137-142
    Type of Medium: Online Resource
    ISSN: 0002-9513
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1918
    detail.hit.zdb_id: 1477334-X
    detail.hit.zdb_id: 2065807-2
    detail.hit.zdb_id: 1477287-5
    detail.hit.zdb_id: 1477308-9
    detail.hit.zdb_id: 1477297-8
    detail.hit.zdb_id: 1477331-4
    detail.hit.zdb_id: 1477300-4
    detail.hit.zdb_id: 1477329-6
    SSG: 12
    Location Call Number Limitation Availability
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  • 8
    In: Journal of Applied Physiology, American Physiological Society, Vol. 134, No. 3 ( 2023-03-01), p. 622-637
    Abstract: Failure to recover following severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) may have a profound impact on individuals who participate in high-intensity/volume exercise as part of their occupation/recreation. The aim of this study was to describe the longitudinal cardiopulmonary exercise function, fatigue, and mental health status of military-trained individuals (up to 12-mo postinfection) who feel recovered, and those with persistent symptoms from two acute disease severity groups (hospitalized and community-managed), compared with an age-, sex-, and job role-matched control. Eighty-eight participants underwent cardiopulmonary functional tests at baseline (5 mo following acute illness) and 12 mo; 25 hospitalized with persistent symptoms (hospitalized-symptomatic), 6 hospitalized and recovered (hospitalized-recovered); 28 community-managed with persistent symptoms (community-symptomatic); 12 community-managed, now recovered (community-recovered), and 17 controls. Cardiopulmonary exercise function and mental health status were comparable between the 5 and 12-mo follow-up. At 12 mo, symptoms of fatigue (48% and 46%) and shortness of breath (SoB; 52% and 43%) remain high in hospitalized-symptomatic and community-symptomatic groups, respectively. At 12 mo, COVID-19-exposed participants had a reduced capacity for work at anaerobic threshold and at peak exercise levels of deconditioning persist, with many individuals struggling to return to strenuous activity. The prevalence considered “fully fit” at 12 mo was lowest in symptomatic groups (hospitalized-symptomatic, 4%; hospitalized-recovered, 50%; community-symptomatic, 18%; community-recovered, 82%; control, 82%) and 49% of COVID-19-exposed participants remained medically nondeployable within the British Armed Forces. For hospitalized and symptomatic individuals, cardiopulmonary exercise profiles are consistent with impaired metabolic efficiency and deconditioning at 12 mo postacute illness. The long-term deployability status of COVID-19-exposed military personnel is uncertain. NEW & NOTEWORTHY Subjective exercise limiting symptoms such as fatigue and shortness of breath reduce but remain prevalent in symptomatic groups. At 12 mo, COVID-19-exposed individuals still have a reduced capacity for work at the anaerobic threshold (which best predicts sustainable intensity), despite oxygen uptake comparable to controls. The prevalence of COVID-19-exposed individuals considered “medically non-deployable” remains high at 47%.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2023
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 9
    Online Resource
    Online Resource
    American Physiological Society ; 2016
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 310, No. 1 ( 2016-01-01), p. H80-H91
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 310, No. 1 ( 2016-01-01), p. H80-H91
    Abstract: Dilated cardiomyopathy (DCM) is a major type of heart failure resulting from loss of systolic function. Naturally occurring canine DCM is a widely accepted experimental paradigm for studying human DCM. 2-Deoxyadenosine triphosphate (dATP) can be used by myosin and is a superior energy substrate over ATP for cross-bridge formation and increased systolic function. The objective of this study was to evaluate the beneficial effect of dATP on contractile function of cardiac myofibrils from dogs with naturally occurring DCM. We measured actomyosin NTPase activity and contraction/relaxation properties of isolated myofibrils from nonfailing (NF) and DCM canine hearts. NTPase assays indicated replacement of ATP with dATP significantly increased myofilament activity in both NF and DCM samples. dATP significantly improved maximal tension of DCM myofibrils to the NF sample level. dATP also restored Ca 2+ sensitivity of tension that was reduced in DCM samples. Similarly, dATP increased the kinetics of contractile activation (k ACT ), with no impact on the rate of cross-bridge tension redevelopment (k TR ). Thus, the activation kinetics (k ACT /k TR ) that were reduced in DCM samples were restored for dATP to NF sample levels. dATP had little effect on relaxation. The rate of early slow-phase relaxation was slightly reduced with dATP, but its duration was not, nor was the fast-phase relaxation or times to 50 and 90% relaxation. Our findings suggest that myosin utilization of dATP improves cardiac myofibril contractile properties of naturally occurring DCM canine samples, restoring them to NF levels, without compromising relaxation. This suggests elevation of cardiac dATP is a promising approach for the treatment of DCM.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2016
    detail.hit.zdb_id: 1477308-9
    SSG: 12
    Location Call Number Limitation Availability
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