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  • Medicine  (2)
  • WA 15000  (2)
  • XA 52094  (2)
  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 2002
    In:  Journal of Applied Physiology Vol. 92, No. 4 ( 2002-04-01), p. 1524-1530
    In: Journal of Applied Physiology, American Physiological Society, Vol. 92, No. 4 ( 2002-04-01), p. 1524-1530
    Abstract: The cardiac sarcoplasmic reticulum calcium-ATPase (SERCA2a), Na + /Ca 2+ exchanger (NCX1), and ryanodine receptor (RyR2) are proteins involved in the regulation of myocyte calcium. We tested whether exercise training (ET) alters those proteins during development of chronic heart failure (CHF). Ten dogs were chronically instrumented to permit hemodynamic measurements. Five dogs underwent 4 wk of cardiac pacing (210 beats/min for 3 wk and 240 beats/min for the 4th wk), whereas five dogs underwent the same pacing regimen plus daily ET (5.1 ± 0.3 km/h, 2 h/day). Paced animals developed CHF characterized by hemodynamic abnormalities and reduced ejection fraction. ET preserved resting hemodynamics and ejection fraction. Left ventricular samples were obtained from all dogs and another five normal dogs for mRNA (Northern analysis, band intensities normalized to glyceraldehyde-3-phosphate dehydrogenase) and protein level (Western analysis, band intensities normalized to tubulin) measurements. In failing hearts, SERCA2a was decreased by 33% ( P 〈 0.05) and 65% ( P 〈 0.05) in mRNA and protein level, respectively, compared with normal hearts; there was only an 8.6% reduction in mRNA and a 32% reduction in protein in exercised animals ( P 〈 0.05 from CHF). mRNA expression of NCX1 increased by 44% in paced-only dogs compared with normal ( P 〈 0.05) but only by 22% in trained dogs ( P 〈 0.05 vs. CHF); protein level of NCX1 was elevated in paced-only dogs (71%, P 〈 0.05) but partially normalized by ET (33%, P 〈 0.05 from CHF). RyR2 was not altered in any of the dogs. In conclusion, long-term ET may ameliorate cardiac deterioration during development of CHF, in part via normalization of myocardial calcium-handling proteins.
    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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  • 2
    In: Journal of Applied Physiology, American Physiological Society
    Abstract: CO 2 inhalation has been previously reported as a treatment for central sleep apnea both when associated with heart failure or where the cause is unknown. Here we evaluated a novel CO 2 supply system using a novel open mask capable of comfortably delivering a constantly inspired fraction of CO 2 (FiCO 2 ) during sleep. We recruited eighteen patients with central sleep apnea (13 patients with cardiac disease, and 5 patients idiopathic) diagnosed by diaphragm EMG recordings made during overnight full polysomnography (Night 1). In each case the optimal FiCO 2 was determined by an overnight manual titration with PSG (Night 2). Titration commenced at 1% CO 2 and increased by 0.2% increments until CSA disappeared. Patients were then treated on the third night (Night 3) with the lowest therapeutically effective concentration of CO 2 derived from night 2. Comparing night 1 and night 3, both AHI (31±14 vs. 6±3 events/h, p 〈 0.01) and arousal index (22±8 vs. 15±8 events/h, p 〈 0.01) were significantly improved during CO 2 treatment. Sleep efficiency improved from 71±18 to 80±11%, p 〈 0.05, and sleep latency was shorter (23±18 vs. 10±10 min, p 〈 0.01). Heart rate was not different between night 1 and night 3. Our data confirm the feasibility of our CO 2 delivery system and indicate that individually titrated CO 2 supplementation with a novel device including a special open mask can reduce sleep disordered breathing severity and improve sleep quality. Randomized controlled studies should now be undertaken to assess therapeutic benefit for patients with CSA.
    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
    Location Call Number Limitation Availability
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