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  • American Physiological Society  (10)
  • Biology  (10)
  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 1962
    In:  American Journal of Physiology-Legacy Content Vol. 202, No. 3 ( 1962-03-01), p. 429-436
    In: American Journal of Physiology-Legacy Content, American Physiological Society, Vol. 202, No. 3 ( 1962-03-01), p. 429-436
    Abstract: The gastric H + secretory responses to i.v. HCl, NaHCO 3 , and acetazolamide were studied in Heidenhain-pouch dogs that had been stimulated to secrete by feeding. Acetazolamide in low doses (5 mg/kg) gave a 65% reduction in H + output for 2–4 hr, after which H + secretion increased above normal, coincident with renal HCO 3 – loss and metabolic acidosis. Higher doses produced a greater systemic acidosis and resulted in less initial reduction of H + and greater augmentation. Doses of 75–100 mg/kg, given 17 hr before feeding to produce a systemic acidosis, resulted in increased secretion, even though sufficient drug remained in the plasma to inhibit tissue carbonic anhydrase. Metabolic acidosis (i.v. HCl) initially suppressed but later augmented gastric H + . Acetazolamide had no suppressive effect in the presence of either an HCl- or acetazolamide-induced acidosis. Metabolic alkalosis (i.v. NaHCO 3 ) reduced gastric H + in regular feeding experiments and in dogs made acidotic by acetazolamide.
    Type of Medium: Online Resource
    ISSN: 0002-9513
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    Language: English
    Publisher: American Physiological Society
    Publication Date: 1962
    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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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 2000
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 278, No. 1 ( 2000-01-01), p. H100-H105
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 278, No. 1 ( 2000-01-01), p. H100-H105
    Abstract: Pulmonary hypertension results in an increased afterload for the right ventricle (RV). To determine the effects of this increased afterload on RV contractile performance, we examined RV performance before and during 4 h of partial balloon occlusion of the pulmonary artery and again after releasing the occlusion in nine newborn lambs. RV contractile performance was quantified by indexes derived from systolic RV pressure-volume relations obtained by a combined pressure-conductance catheter during inflow reduction. An almost twofold increase of end-systolic RV pressure (from 22 to 38 mmHg) was maintained during 4 h. Cardiac output (CO) (0.74 ± 0.08 l/min) and stroke volume (4.3 ± 0.4 ml) were maintained, whereas end-diastolic volume (7.9 ± 1.3 ml) did not change significantly during this period. RV systolic function improved substantially; the end-systolic pressure-volume relation shifted leftward indicated by a significantly decreased volume intercept (up to 70%), together with a slightly increased slope. In this newborn lamb model, maintenance of CO during increased RV afterload is not obtained by an increased end-diastolic volume (Frank-Starling mechanism). Instead, the RV maintains its output by improving contractile performance through homeometric autoregulation.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1477308-9
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  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 280, No. 1 ( 2001-01-01), p. H392-H400
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 280, No. 1 ( 2001-01-01), p. H392-H400
    Abstract: Respiratory distress syndrome (RDS) causes pulmonary hypertension. It is often suggested that this increased afterload for the right ventricle (RV) might lead to cardiac dysfunction. To examine this, we studied biventricular function in an experimental model. RDS was induced by lung lavages in seven newborn lambs. Five additional lambs served as controls. Cardiac function was quantified by indexes derived from end-systolic pressure-volume relations obtained by pressure-conductance catheters. After lung lavages, a twofold increase of mean pulmonary arterial pressure (from 15 to 34 mmHg) was obtained and lasted for the full 4-h study period. Stroke volume was maintained (5.2 ± 0.6 ml at baseline and 6.1 ± 1.4 ml at 4 h of RDS), while RV end-diastolic volume showed only a slight increase (from 6.5 ± 2.3 ml at baseline to 7.7 ± 1.3 ml at 4 h RDS). RV systolic function improved significantly, as indicated by a leftward shift and increased slope of the end-systolic pressure-volume relation. Left ventricular systolic function showed no changes. In control animals, pulmonary arterial pressure did not increase and right and left ventricular systolic function remained unaffected. In the face of increased RV afterload, the newborn heart is able to maintain cardiac output, primarily by improving systolic RV function through homeometric autoregulation.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
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  • 4
    Online Resource
    Online Resource
    American Physiological Society ; 2013
    In:  Journal of Applied Physiology Vol. 114, No. 3 ( 2013-02-01), p. 411-420
    In: Journal of Applied Physiology, American Physiological Society, Vol. 114, No. 3 ( 2013-02-01), p. 411-420
    Abstract: In sport, high training load required to reach peak performance pushes human adaptation to their limits. In that process, athletes may experience general fatigue, impaired performance, and may be identified as overreached (OR). When this state lasts for several months, an overtraining syndrome is diagnosed (OT). Until now, no variable per se can detect OR, a requirement to prevent the transition from OR to OT. It encouraged us to further investigate OR using a multivariate approach, including physiological, biomechanical, cognitive, and perceptive monitoring. Twenty-four highly trained triathletes were separated into an overload group and a normo-trained group (NT) during 3 wk of training. Given the decrement of their running performance, 11 triathletes were diagnosed as OR after this period. A discriminant analysis showed that the changes of eight parameters measured during a maximal incremental test could explain 98.2% of the OR state (lactatemia, heart rate, biomechanical parameters and effort perception). Variations in heart rate and lactatemia were the two most discriminating factors. When the multifactorial analysis was restricted to these variables, the classification score reached 89.5%. Catecholamines and creatine kinase concentrations at rest did not change significantly in both groups. Running pattern was preserved and cognitive performance decrement was observed only at exhaustion in OR subjects. This study showed that monitoring various variables is required to prevent the transition between NT and OR. It emphasized that an OR index, which combines heart rate and blood lactate concentration changes after a strenuous training period, could be helpful to routinely detect OR.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
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    Language: English
    Publisher: American Physiological Society
    Publication Date: 2013
    detail.hit.zdb_id: 1404365-8
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  • 5
    Online Resource
    Online Resource
    American Physiological Society ; 2000
    In:  Journal of Applied Physiology Vol. 89, No. 5 ( 2000-11-01), p. 2092-2098
    In: Journal of Applied Physiology, American Physiological Society, Vol. 89, No. 5 ( 2000-11-01), p. 2092-2098
    Abstract: Cultured airway smooth muscle cells subjected to cyclic deformational strain have increased cell content of myosin light chain kinase (MLCK) and myosin and increased formation of actin filaments. To determine how these changes may increase cell contractility, we measured isometric force production with changes in cytosolic calcium in individual permeabilized cells. The pCa for 50% maximal force production was 6.6 ± 0.4 in the strain cells compared with 5.9 ± 0.3 in control cells, signifying increased calcium sensitivity in strain cells. Maximal force production was also greater in strain cells (8.6 ± 2.9 vs. 5.7 ± 3.1 μN). The increased maximal force production in strain cells persisted after irreversible thiophosphorylation of myosin light chain, signifying that increased force could not be explained by differences in myosin light chain phosphorylation. Cells strained for brief periods sufficient to increase cytoskeletal organization but insufficient to increase contractile protein content also produced more force, suggesting that strain-induced cytoskeletal reorganization also increases force production.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
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    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1404365-8
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  • 6
    In: Journal of Applied Physiology, American Physiological Society, Vol. 104, No. 2 ( 2008-02), p. 446-450
    Abstract: Dexamethasone is clinically applied in preterm infants to treat or prevent chronic lung disease. However, concern has emerged about adverse side effects. The cardiovascular short-term side effects of neonatal dexamethasone treatment are well documented, but long-term consequences are unknown. Previous studies showed suppressed mitosis during dexamethasone treatment, leading to reduced ventricular weight, depressed systolic function, and compensatory dilatation in prepubertal rats. In addition, recent data indicated a reduced life expectancy. Therefore, we investigated the long-term effects of neonatal dexamethasone treatment on cardiovascular function. Neonatal rats were treated with dexamethasone or received saline. Cardiac function was determined in 8-, 50-, and 80-wk-old animals, representing young adult, middle-aged, and elderly stages. A pressure-conductance catheter was introduced into the left ventricle to measure pressure-volume loops. Subsequently, the hearts were collected for histological examination. Our results showed reduced ventricular and body weights in dexamethasone-treated rats at 8 and 80 wk, but not at 50 wk. Cardiac output and diastolic function were unchanged, but systolic function was depressed at 50 and 80 wk, evidenced by reduced ejection fractions and rightward shifts of the end-systolic pressure-volume relationships. We concluded that previously demonstrated early adverse effects of neonatal dexamethasone treatment are transient but that reduced ventricular weight and systolic dysfunction become manifest again in elderly rats. Presumably, cellular hypertrophy initially compensates for the dexamethasone treatment-induced lower number of cardiomyocytes, but this mechanism falls short at a later stage, leading to systolic dysfunction. If applicable to humans, cardiac screening of a relatively large patient group to enable secondary prevention may be indicated.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
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    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 1404365-8
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  • 7
    Online Resource
    Online Resource
    American Physiological Society ; 2006
    In:  Journal of Applied Physiology Vol. 100, No. 4 ( 2006-04), p. 1124-1133
    In: Journal of Applied Physiology, American Physiological Society, Vol. 100, No. 4 ( 2006-04), p. 1124-1133
    Abstract: Leukocytosis following exercise is a well-described phenomenon of stress/inflammatory activation in healthy humans. We hypothesized that, despite this increase in circulating inflammatory cells, exercise would paradoxically induce expression of both pro- and anti-inflammatory cytokines and growth factors within these cells. To test this hypothesis, 11 healthy adult men, 18–30 yr old, performed a 30-min bout of heavy cycling exercise; blood sampling was at baseline, end-exercise, and 60 min into recovery. The percentage of leukocytes positive for intracellular cytokines and growth factors and mean fluorescence intensity was obtained by flow cytometry. Proinflammatory cytokines (IL-1α, IL-2, IFN-γ, and TNF-α), a pleiotropic cytokine (IL-6), and anti-inflammatory cytokines and growth factors [IL-4, IL-10, growth hormone (GH), and IGF-I] were examined. Median fluorescence intensity was not affected by exercise; however, we found a number of significant changes ( P 〈 0.05 by mixed linear model and modified t-test) in the numbers of circulating cells positive for particular mediators. The pattern of expression reflected both pro- and anti-inflammatory functions. In T-helper lymphocytes, TNF-α, but also IL-6, and IL-4 were significantly increased. In monocytes, both IFN-γ and IL-4 increased. B-lymphocytes positive for GH and IGF-I increased significantly. GH-positive granulocytes also significantly increased. Collectively, these observations indicate that exercise primes an array of pro- and anti-inflammatory and growth factor expression within circulating leukocytes, perhaps preparing the organism to effectively respond to a variety of stressors imposed by exercise.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
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    Language: English
    Publisher: American Physiological Society
    Publication Date: 2006
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 8
    Online Resource
    Online Resource
    American Physiological Society ; 1950
    In:  Journal of Applied Physiology Vol. 3, No. 5 ( 1950-11), p. 282-290
    In: Journal of Applied Physiology, American Physiological Society, Vol. 3, No. 5 ( 1950-11), p. 282-290
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
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    Language: English
    Publisher: American Physiological Society
    Publication Date: 1950
    detail.hit.zdb_id: 1404365-8
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  • 9
    In: Physiological Reviews, American Physiological Society, Vol. 103, No. 4 ( 2023-10-01), p. 2679-2757
    Abstract: Mechanisms underlying mechanical overload-induced skeletal muscle hypertrophy have been extensively researched since the landmark report by Morpurgo (1897) of “work-induced hypertrophy” in dogs that were treadmill trained. Much of the preclinical rodent and human resistance training research to date supports that involved mechanisms include enhanced mammalian/mechanistic target of rapamycin complex 1 (mTORC1) signaling, an expansion in translational capacity through ribosome biogenesis, increased satellite cell abundance and myonuclear accretion, and postexercise elevations in muscle protein synthesis rates. However, several lines of past and emerging evidence suggest that additional mechanisms that feed into or are independent of these processes are also involved. This review first provides a historical account of how mechanistic research into skeletal muscle hypertrophy has progressed. A comprehensive list of mechanisms associated with skeletal muscle hypertrophy is then outlined, and areas of disagreement involving these mechanisms are presented. Finally, future research directions involving many of the discussed mechanisms are proposed.
    Type of Medium: Online Resource
    ISSN: 0031-9333 , 1522-1210
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2023
    detail.hit.zdb_id: 1471693-8
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  • 10
    In: Journal of Applied Physiology, American Physiological Society, Vol. 98, No. 3 ( 2005-03), p. 1044-1049
    Abstract: Infant respiratory distress syndrome (RDS) involves inflammatory processes, causing an increased expression of inducible heme oxygenase with subsequent production of carbon monoxide (CO). We hypothesized that increased production of CO during RDS might be responsible for increased plasma levels of vasodilatory cGMP and, consequently, low blood pressure observed in infants with RDS. Fifty-two infants (no-RDS, n = 21; RDS, n = 31), consecutively admitted to the neonatal intensive care unit (NICU) between January and October 2003 were included. Hemoglobin-bound carbon monoxide (COHb), plasma cGMP, plasma nitric oxide (NOx), and bilirubin were determined at 0–12, 48–72, and at 168 h postnatally, with simultaneous registration of arterial blood pressure. Infants with RDS had higher levels of cGMP and COHb compared with no-RDS infants (RDS vs. no-RDS: cGMP ranging from 76 to 101 vs. 58 to 82 nmol/l; COHb ranging from 1.2 to 1.4 vs. 0.9 to 1.0%). Highest values were reached at 48–72 h [RDS vs. no-RDS mean (SD): cGMP 100 (39) vs. 82 (25) nmol/l ( P 〈 0.001); COHb 1.38 (0.46) vs. 0.91 (0.26)% ( P 〈 0.0001)]. Arterial blood pressure was lower and more blood pressure support was needed in RDS infants at that point of time [RDS vs. no-RDS mean (SD): mean arterial blood pressure 33 (6) vs. 42 (5) mmHg ( P 〈 0.05)]. NOx was not different between groups and did not vary with time. Multiple linear regression analysis showed a significant correlation between cGMP and COHb, suggesting a causal relationship. Mean arterial blood pressure appeared to be primarily correlated to cGMP levels ( P 〈 0.001). We conclude that a CO-mediated increase in cGMP causes systemic vasodilation with a consequent lower blood pressure and increased need for blood pressure support in preterm infants with RDS.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
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    Language: English
    Publisher: American Physiological Society
    Publication Date: 2005
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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