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  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 1995
    In:  Journal of Applied Physiology Vol. 78, No. 1 ( 1995-01-01), p. 76-81
    In: Journal of Applied Physiology, American Physiological Society, Vol. 78, No. 1 ( 1995-01-01), p. 76-81
    Abstract: The purpose of this study was to determine the interactive effects of 10–12 wk of streptozotocin-induced diabetes (65 mg/kg) and moderate-intensity exercise training on total myocardial GLUT-4 and GLUT-1 proteins. Sprague-Dawley rats (n = 52) were randomly divided into sedentary control (SC), exercise-trained control (ETC), sedentary diabetic (SD), and exercise-trained control (ETD) groups. Diabetes (SD), and exercise-trained diabetic (ETD) groups. Diabetes resulted in a 70% reduction in myocardial GLUT-4 (28.3+/- 3.1 and 94.6 +/- 3.4% for SD and SC, respectively; P 〈 0.0001) and an 18.5% decrease in GLUT-1 (62.5 +/- 4.7 and 76.8 +/- 4.5% for SD and SC, respectively; P = 0.06). Exercise training increased citrate synthase activity in the medial and long heads of the triceps brachii in both groups (P 〈 0.001). Fasting blood glucose improved with training in diabetic animals (348 +/- 27 and 569 +/- 28 mg/dl for ETD and SD, respectively; P 〈 0.05). The diabetes-induced reduction in GLUT-4 was attenuated with exercise training (46.8 +/- 9.3% for ETD; P 〈 0.02 compared with SD). In contrast, training resulted in a further 25% decrease compared with SD in GLUT-1 in ETD (46.8 +/- 9.3%; P 〈 0.03 compared with SD). Exercise training had no effect on either GLUT-4 (87.2 +/- 4.0%) or GLUT-1 (75.4 +/- 5.1%) in ETC. GLUT-4 inversely correlated (r = -0.81; P 〈 or = 0.001) with fasting blood glucose. In conclusion, diabetes resulted in a 70% reduction in myocardial GLUT-4 and an 18% decrease in GLUT-1.(ABSTRACT TRUNCATED AT 250 WORDS)
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
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    Language: English
    Publisher: American Physiological Society
    Publication Date: 1995
    detail.hit.zdb_id: 1404365-8
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    SSG: 31
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  • 2
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 313, No. 6 ( 2017-12-01), p. H1168-H1179
    Abstract: Oxidative stress plays a fundamental role in abdominal aortic aneurysm (AAA) formation. Activated polymorphonuclear leukocytes (or neutrophils) are associated with AAA and express myeloperoxidase (MPO), which promotes inflammation, matrix degradation, and other pathological features of AAA, including enhanced oxidative stress through generation of reactive oxygen species. Both plasma and aortic MPO levels are elevated in patients with AAA, but the role of MPO in AAA pathogenesis has, heretofore, never been investigated. Here, we show that MPO gene deletion attenuates AAA formation in two animal models: ANG II infusion in apolipoprotein E-deficient mice and elastase perfusion in C57BL/6 mice. Oral administration of taurine [1% or 4% (wt/vol) in drinking water], an amino acid known to react rapidly with MPO-generated oxidants like hypochlorous acid, also prevented AAA formation in the ANG II and elastase models as well as the CaCl 2 application model of AAA formation while reducing aortic peroxidase activity and aortic protein-bound dityrosine levels, an oxidative cross link formed by MPO. Both MPO gene deletion and taurine supplementation blunted aortic macrophage accumulation, elastin fragmentation, and matrix metalloproteinase activation, key features of AAA pathogenesis. Moreover, MPO gene deletion and taurine administration significantly attenuated the induction of serum amyloid A, which promotes ANG II-induced AAAs. These data implicate MPO in AAA pathogenesis and suggest that studies exploring whether taurine can serve as a potential therapeutic for the prevention or treatment of AAA in patients merit consideration. NEW & NOTEWORTHY Neutrophils are abundant in abdominal aortic aneurysm (AAA), and myeloperoxidase (MPO), prominently expressed in neutrophils, is associated with AAA in humans. This study demonstrates that MPO gene deletion or supplementation with the natural product taurine, which can scavenge MPO-generated oxidants, can prevent AAA formation, suggesting an attractive potential therapeutic strategy for AAA.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2017
    detail.hit.zdb_id: 1477308-9
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  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 1991
    In:  Journal of Applied Physiology Vol. 70, No. 6 ( 1991-06-01), p. 2650-2655
    In: Journal of Applied Physiology, American Physiological Society, Vol. 70, No. 6 ( 1991-06-01), p. 2650-2655
    Abstract: Six male Quechua Indians (34.0 +/- 1.1 yr, 159.5 +/- 2.1 cm, 60.5 +/- 1.6 kg), life-long residents of La Raya, Peru (4,350-m altitude with an average barometric pressure of 460 Torr), were studied using noninvasive methods to determine the structural and functional changes in the cardiovascular system in response to a 6-wk deacclimation period at sea level. Cardiac output, stroke volume, and left ventricular ejection fractions were determined using radionuclide angiographic techniques at rest and during exercise on a cycle ergometer at 40, 60, and 90% of a previously determined maximal O2 consumption. Subjects at rest were subjected to two-dimensional and M-mode echocardiograms and a standard 12-lead electrocardiogram. Hemoglobin and hematocrit were measured on arrival at sea level by use of a Coulter Stacker S+ analyzer. After a 6-wk deacclimation period, all variables were remeasured using the identical methodology. Hemoglobin values decreased significantly over the deacclimation period (15.7 +/- 1.1 to 13.5 +/- 1.2 g/dl; P less than 0.01). The results indicate that the removal of these high-altitude-adapted natives from 4,300 m to sea level for 6 wk results in only minor changes to the cardiac structure and function as measured by these noninvasive techniques.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
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    Language: English
    Publisher: American Physiological Society
    Publication Date: 1991
    detail.hit.zdb_id: 1404365-8
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    SSG: 31
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  • 4
    Online Resource
    Online Resource
    American Physiological Society ; 1986
    In:  Journal of Applied Physiology Vol. 60, No. 4 ( 1986-04-01), p. 1116-1120
    In: Journal of Applied Physiology, American Physiological Society, Vol. 60, No. 4 ( 1986-04-01), p. 1116-1120
    Abstract: Lactate metabolism was studied in six normal males using a primed continuous infusion of lactate tracer during continuous graded supine cycle ergometer exercise. Subjects exercised at 49, 98, 147, and 196 W for 6 min at each work load. Blood was sampled from the brachial artery, the iliac vein, and the brachial vein. Arteriovenous differences were determined for chemical lactate concentration and L-[1–14C]-lactate. Tracer-measured lactate extraction was determined from the decrease in lactate radioactivity per volume of blood perfusing the tissue bed. Net lactate release was determined from the change in lactate concentration across the tissue bed. Total lactate release was taken as the sum of tracer-measured lactate extraction and net (chemical) release. At rest the arms and legs showed tracer-measured lactate extraction, as determined from the isotope extraction, despite net chemical release. Exercise elicited an increase in both net lactate release and tracer-measured lactate extraction by the legs. For the legs the total lactate release (net lactate release + tracer-measured lactate extraction) was roughly equal to twice the net lactate release under all conditions. The tracer-measured lactate extraction by the exercising legs was positively correlated to arterial lactate concentration (r = 0.81, P less than 0.001) at the lower two power outputs. The arms showed net lactate extraction during exercise, which was correlated to the arterial concentration (r = 0.86). The results demonstrate that exercising skeletal muscle extracts a significant amount of lactate during net lactate release and that the working skeletal muscle appears to be a major site of blood lactate removal during exercise.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1986
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 5
    Online Resource
    Online Resource
    American Physiological Society ; 1985
    In:  American Journal of Physiology-Endocrinology and Metabolism Vol. 249, No. 6 ( 1985-12-01), p. E595-E602
    In: American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 249, No. 6 ( 1985-12-01), p. E595-E602
    Abstract: To investigate the relationships between oxygen consumption (VO2) and the rates of systemic lactate appearance (Ra) and disappearance (Rd), six healthy males were studied at rest and during continuous graded exercise using a primed continuous infusion of lactate tracer. Subjects exercised for 6 min at 300, 600, 900, and 1,200 kg . m . min-1. L-(+)-[1-14C]lactate was infused intravenously, and arterial samples were drawn at rest and every 2 min throughout the exercise period. Ra and Rd were calculated using nonsteady-state equations. At rest Ra and Rd were 14.4 +/- 1.8 and 15.1 +/- 2.2 mumol . kg-1 . min-1, respectively. Near steady-state values were observed toward the end of the first two work loads. Ra and Rd values were 32.8 +/- 2.3 and 37.4 +/- 1.3 mumol . kg-1 . min-1 during min 5 and 6 at 300 kg . m . min-1 and were 59.1 +/- 2.6 and 55.4 +/- 2.3 mumol . kg-1 . min-1 during min 5 and 6 at 600 kg . m . min-1. Ra was significantly greater than Rd at both 900 and 1,200 kg . m . min-1. Ra and Rd averaged 145.4 +/- 10.5 and 110.2 +/- 5.6 mumol . kg-1 . min-1, respectively, during the last 2 min at 900 kg . m . min-1, and 309.4 +/- 20.8 and 169.7 +/- 10.6 mumol . kg-1 . min-1, respectively, at 1,200 kg . m . min-1.(ABSTRACT TRUNCATED AT 250 WORDS)
    Type of Medium: Online Resource
    ISSN: 0193-1849 , 1522-1555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1985
    detail.hit.zdb_id: 1477331-4
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    American Physiological Society ; 2002
    In:  Journal of Applied Physiology Vol. 93, No. 4 ( 2002-10-01), p. 1235-1242
    In: Journal of Applied Physiology, American Physiological Society, Vol. 93, No. 4 ( 2002-10-01), p. 1235-1242
    Abstract: In immature dogs after pneumonectomy (PNX), pulmonary viscous resistance is persistently elevated predominantly as a result of a high airway resistance (Raw). We examined the anatomical basis for this observation by using computerized tomography scans obtained from foxhounds 4–10 mo after right PNX. Airways of the left lower lobe were followed from generations z = 0 (trachea) to z = 12. By 4 mo post-PNX, airway length increased significantly relative to sham-operated dogs, but airway cross-sectional area (CSA) did not. By 10 mo post-PNX, average airway CSA was 24% above that in controls. Theoretically, the increased airway length and CSA should reduce lobar Raw by 50%. However, post-PNX airway dilatation did not normalize total CSA, and estimated resistance due to turbulence and convective acceleration increased threefold; i.e., the 50% reduction in lobar Raw would be offset by the loss of four of seven lobes. Thus the expected reduction in work of breathing in the whole animal is only ∼30%, consistent with previously measured work of breathing in pneumonectomized dogs. We conclude that airway structure adapts slowly and incompletely, resulting in limited functional compensation.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2002
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 7
    Online Resource
    Online Resource
    American Physiological Society ; 1988
    In:  Journal of Applied Physiology Vol. 64, No. 1 ( 1988-01-01), p. 115-119
    In: Journal of Applied Physiology, American Physiological Society, Vol. 64, No. 1 ( 1988-01-01), p. 115-119
    Abstract: To examine the effects of increased O2 utilization on the glutathione antioxidant system in blood, eight moderately trained male volunteers were exercised to peak O2 consumption (VO2peak) and for 90 min at 65% of VO2peak on a cycle ergometer. Blood samples were taken during exercise, and for up to 4 days of recovery from submaximal exercise. During exercise to VO2peak, blood reduced glutathione (GSH) and total glutathione [GSH + oxidized glutathione (GSSG)] did not change significantly. Lactate (L), pyruvate (P), and L/P increased significantly from rest values (P less than 0.01). During prolonged submaximal exercise, GSH decreased 60% from control, and GSSG increased 100%. Total glutathione, glucose, pyruvate, and lactate concentrations and L/P did not change significantly during sustained exercise. During recovery, GSH and GSH/GSSG increased from exercise levels and significantly overshot preexercise levels, reaching maximum values after 3 days. Oxidation of GSH during submaximal exercise and its reduction in recovery suggest increased formation of active O2-. species in blood during physical exercise in moderately trained males.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1988
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 8
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 325, No. 4 ( 2023-10-01), p. H687-H701
    Abstract: The ductus arteriosus (DA) is a vascular shunt that allows oxygenated blood to bypass the developing lungs in utero. Fetal DA patency requires vasodilatory signaling via the prostaglandin E 2 (PGE 2 ) receptor EP 4 . However, in humans and mice, disrupted PGE 2 -EP 4 signaling in utero causes unexpected patency of the DA (PDA) after birth, suggesting another role for EP 4 during development. We used EP 4 -knockout (KO) mice and acute versus chronic pharmacological approaches to investigate EP 4 signaling in DA development and function. Expression analyses identified EP 4 as the primary EP receptor in the DA from midgestation to term; inhibitor studies verified EP 4 as the primary dilator during this period. Chronic antagonism recapitulated the EP 4 KO phenotype and revealed a narrow developmental window when EP 4 stimulation is required for postnatal DA closure. Myography studies indicate that despite reduced contractile properties, the EP 4 KO DA maintains an intact oxygen response. In newborns, hyperoxia constricted the EP 4 KO DA but survival was not improved, and permanent remodeling was disrupted. Vasomotion and increased nitric oxide (NO) sensitivity in the EP 4 KO DA suggest incomplete DA development. Analysis of DA maturity markers confirmed a partially immature EP 4 KO DA phenotype. Together, our data suggest that EP 4 signaling in late gestation plays a key developmental role in establishing a functional term DA. When disrupted in EP 4 KO mice, the postnatal DA exhibits signaling and contractile properties characteristic of an immature DA, including impairments in the first, muscular phase of DA closure, in addition to known abnormalities in the second permanent remodeling phase. NEW & NOTEWORTHY EP 4 is the primary EP receptor in the ductus arteriosus (DA) and is critical during late gestation for its development and eventual closure. The “paradoxical” patent DA (PDA) phenotype of EP 4 -knockout mice arises from a combination of impaired contractile potential, altered signaling properties, and a failure to remodel associated with an underdeveloped immature vessel. These findings provide new mechanistic insights into women who receive NSAIDs to treat preterm labor, whose infants have unexplained PDA.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2023
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    American Physiological Society ; 2017
    In:  Journal of Neurophysiology Vol. 118, No. 2 ( 2017-08-01), p. 1141-1150
    In: Journal of Neurophysiology, American Physiological Society, Vol. 118, No. 2 ( 2017-08-01), p. 1141-1150
    Abstract: This work represents an automated method for accessing subcortical neural tissue for intracellular electrophysiology in vivo. We have implemented a novel algorithm to detect obstructions during regional pipette localization and move around them while minimizing lateral displacement within brain tissue. This approach leverages computer control of pressure, manipulator position, and impedance measurements to create a closed-loop platform for pipette navigation in vivo. This technique enables whole cell patching studies to be performed throughout the living brain.
    Type of Medium: Online Resource
    ISSN: 0022-3077 , 1522-1598
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2017
    detail.hit.zdb_id: 80161-6
    detail.hit.zdb_id: 1467889-5
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  • 10
    Online Resource
    Online Resource
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 280, No. 2 ( 2001-02-01), p. G209-G215
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 280, No. 2 ( 2001-02-01), p. G209-G215
    Abstract: Mechanisms underlying the circadian rhythmicity in intestinal sugar absorption remain unclear. To test whether this rhythmicity is caused by changes in Na + -glucose cotransporter 1 (SGLT-1) function, we measured phloridzin-inhibitable sugar fluxes as an index of SGLT-1 activity. Jejunum obtained from rats killed at 6-h intervals during a 12-h light-dark cycle (CT0 is circadian time 0 h, time of light onset) were mounted in Ussing chambers, and 3- O-methylglucose (3-OMG) fluxes were calculated before and after addition of phloridzin. 3-OMG-induced change in short-circuit current and absorptive flux were significantly greater at CT9 than at CT3. This increase was phloridzin inhibitable. Kinetic studies indicated a significant increase in SGLT-1 maximal velocity ( V max ) at CT9. Food intake between CT3 and CT9 was 〈 10% of the daily total, indicating that the increased SGLT-1 activity was anticipatory. Diurnicity of SGLT-1 mRNA was confirmed by Northern blotting. Expression topography analyzed by in situ hybridization revealed more intense labeling along the entire villus axis at CT9 and CT15 compared with CT3 and CT21. We conclude that diurnicity in intestinal sugar absorption is caused by periodicity in SGLT-1 V max .
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1477329-6
    SSG: 12
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