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  • American Physiological Society  (6)
  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 2012
    In:  Journal of Applied Physiology Vol. 113, No. 4 ( 2012-08-15), p. 595-601
    In: Journal of Applied Physiology, American Physiological Society, Vol. 113, No. 4 ( 2012-08-15), p. 595-601
    Abstract: We have previously shown that heat acclimation provides protection against central nervous system oxygen toxicity (CNS-OT). This was well correlated with increased levels of heat shock protein 72 (HSP72). We now examine other antioxidative defenses against CNS-OT that are correlated with heat acclimation. Two groups of male Sprague-Dawley rats were used. The heat-acclimated group (HA) was exposed for 4 wk to 32°C, and the control group (C) was maintained at 24°C. At the end of the acclimation period, rats were exposed to oxygen at 608 kPa. EEG was recorded continuously until appearance of the first electrical discharge. Brain samples were taken from each group after exposure to pressure. Levels of the antioxidant enzymes CuZnSOD, MnSOD, catalase, and glutathione peroxidase, as well as levels of HSP72, were quantified by Western blot. Comparative proteome analysis of the brains of HA and C rats was carried out using two-dimensional electrophoresis and mass spectrometry to define protein spot alterations. Levels of HSP72 and CuZnSOD were higher in HA rats. Levels of the other antioxidant enzymes were not affected significantly by heat acclimation. Differences in the levels of four protein spots identified as α-synuclein, valosin-containing protein, adenylate kinase 1 (AK1), and the mitochondrial H+-ATP synthase α subunit were found between HA and C rats. We conclude that elevation of HSP72, CuZnSOD, AK1, and the mitochondrial H+-ATP synthase α subunit and possible phosphorylation of α-synuclein—all proteins involved in oxidative stress or energy conservation—might contribute to the prolongation of latency to CNS-OT induced by heat acclimation.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
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    Language: English
    Publisher: American Physiological Society
    Publication Date: 2012
    detail.hit.zdb_id: 1404365-8
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    SSG: 31
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 2002
    In:  Journal of Applied Physiology Vol. 93, No. 6 ( 2002-12-01), p. 2095-2104
    In: Journal of Applied Physiology, American Physiological Society, Vol. 93, No. 6 ( 2002-12-01), p. 2095-2104
    Abstract: Based on our observations of energy sparing in heat-acclimated (AC) rat hearts, we investigated whether changes in preischemic glycogen level, glycolytic rate, and plasma thyroxine level mediate cardioprotection induced in these hearts during ischemia-reperfusion insults. Control (C) (24°C), AC (34°C, 30 days), acclimated-euthyroid (34°C + 3 ng/ml l-thyroxine), and control hypothyroid (24°C + 0.02% 6- n-propyl-2-thiouracil) groups were studied. Preischemic glycogen was higher in AC than in C hearts [39.0 ± 8.5 vs. 19.2 ± 4.2 (SE) μmol glucose/g wet wt; P 〈 0.0006], and the lactate produced vs. glycogen level during total ischemia ( 13 C-NMR spectroscopy) was markedly slower (AC: −0.82 x, r = 0.98 vs. C: −4.7 x, r = 0.9). Time to onset of ischemic contracture was lengthened, and the fraction of hearts experiencing ischemic contracture was lowered. Pulse pressure recovery was improved in AC compared with C animals before, but not after, absolute sodium iodoacetate-induced glycolysis inhibition. Acclimated-euthyroid hearts exhibited decreased ischemic tolerance, whereas induced hypothyroidism in C improved cardiotolerance. Thus higher preischemic glycogen and slowed glycolysis are associated with hypothyroidism and are likely important mediators of the improved ischemic tolerance exhibited by AC hearts.
    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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  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 1999
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 276, No. 2 ( 1999-02-01), p. R550-R558
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 276, No. 2 ( 1999-02-01), p. R550-R558
    Abstract: The involvement of reduced thyroxine level in the emergence of heat acclimation-induced negative lusitropic effect was examined. Experiments were carried out on 1) control rat hearts maintained at 24 ± 1°C (C); 2) rat hearts acclimated at 34°C for 1 mo (AC); 3) AC-euthyroid rat hearts, via administration of thyroxine in the drinking water (AT); and 4) hypothyroid rat hearts, maintained at 24 ± 1°C, via administration of thiouracil in the drinking water (CP). Systolic pressure and velocities of contraction (dP/d t ⋅ P) and relaxation (−dP/d t ⋅ P) were measured using the Langendorff perfusion system. The steady-state levels of Ca 2+ -ATPase and phospholamban mRNAs and the expression of the encoded proteins Ca 2+ -ATPase (SERCA) and phospholamban (PLB) were measured, using semi-quantitative RT-PCR and Western immunoblotting, respectively. Rat thyroxine levels were measured using RIA. Heat acclimation, which brought about a reduced thyroxine level, led to downregulation of Ca 2+ -ATPase mRNA expression and translation and upregulation of phospholamban mRNA and PLB. Consequently, the PLB-to-SERCA ratio (PLB/SERCA) of the AC hearts showed a significant increase. These changes, as well as the greater pressure generation and the reduced dP/d t ⋅ P and −dP/d t ⋅ P observed in AC hearts were blunted in the AT hearts. Our data suggest that sustained heat acclimation-induced low thyroxine level has a decisive effect on the contractile machinery of the AC heart. Elevated PLB/SERCA apparently explains the negative lusitropic effect observed in these hearts.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1477297-8
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  • 4
    Online Resource
    Online Resource
    American Physiological Society ; 2005
    In:  Journal of Applied Physiology Vol. 98, No. 5 ( 2005-05), p. 1653-1659
    In: Journal of Applied Physiology, American Physiological Society, Vol. 98, No. 5 ( 2005-05), p. 1653-1659
    Abstract: Elevated arterial Pco 2 (hypercapnia) has a major effect on central nervous system oxygen toxicity in diving with a closed-circuit breathing apparatus. The purpose of the present study was to follow up the ability of divers to detect CO 2 and to determine the CO 2 retention trait after 1 year of active oxygen diving with closed-circuit apparatus. Ventilatory and perceptual responses to variations in inspired CO 2 (range: 0–5.6 kPa, 0–42 Torr) during moderate exercise were assessed in Israeli Navy combat divers on active duty. Tests were carried out on 40 divers during the novice oxygen diving phase (ND) and the experienced oxygen diving phase. No significant changes were found between the two phases for the minimal mean inspired Pco 2 that could be detected. The mean (with SD in parentheses) end-tidal Pco 2 during exposure to an inspired Pco 2 of 5.6 kPa (42 Torr) was significantly higher in the novice diving phase than in the experienced diving phase [8.1 kPa (SD 0.7), 62 Torr (SD 5) and 7.8 kPa (SD 0.6), 59 Torr (SD 4), respectively; P ≤ 0.001]. One year of shallow oxygen diving activity with a closed-circuit apparatus does not affect the ability to detect CO 2 nor does it lead to increased CO 2 retention; rather, it may even bring about a decrease in this trait. This finding suggests that acquiring experience in oxygen diving with a closed-circuit apparatus at shallow depths does not place the diver at a greater risk of central nervous system oxygen toxicity due to CO 2 retention.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2005
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 5
    Online Resource
    Online Resource
    American Physiological Society ; 2000
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 279, No. 1 ( 2000-07-01), p. R77-R85
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 279, No. 1 ( 2000-07-01), p. R77-R85
    Abstract: The involvement of adrenergic signaling and sarcoplasmic calcium regulatory proteins in the development of heat acclimation-induced adaptations in cardiac mechanics was studied in heat-acclimated (34°C) rats for 2, 5, and 30 days (AC 2 , AC 5 , and AC 30 , respectively). Control (C) rats were held at 24 ± 1°C. Systolic pressure (LVP) and velocities of contraction (dP/d t/P) and relaxation (−dP/d t/P) were measured using a Langendorff system. For adrenergic signaling, β-adrenoreceptor (AR) density and affinity (Scatchard plots) and cardiac inotropic response to norepinephrine (10 − 7 mM, ± 10 − 6 mM propranolol) were measured. For the regulatory proteins, steady-state levels of Ca 2+ -ATPase and phospholamban (PLB) mRNAs and the encoded proteins Ca 2+ -ATPase [sarco(endo)plasmic reticulum Ca 2+ -ATPase (SERCA)] and PLB were measured using semiquantitative RT-PCR and Western immunoblotting, respectively. Both short (STHA; AC 2 and AC 5 )- and long-term heat acclimation (LTHA; AC 30 ) enhanced LVP. However, dP/d t ⋅ P and −dP/d t ⋅ P in STHA hearts resembled that of the controls, whereas on LTHA, both parameters decreased ( P 〈 0.05), implying decreased velocity of contraction and relaxation. β-AR density remained unchanged with their affinity markedly decreased ( P 〈 0.05). AR responsiveness, however, diminished in AC 2 but was markedly enhanced on LTHA. During STHA, PLB and sarcoplasmic reticulum Ca 2+ -ATPase transcripts were upregulated with no change in the encoded proteins except for SERCA downregulation on AC 5 , leading to an increased PLB/SERCA ratio ( P 〈 0.05). This mismatched preacclimation lusitropic state on STHA and increased PLB/SERCA ratio was evident ( P 〈 0.05) due to downregulation of SERCA and upregulation of PLB. Our data fit a biphasic acclimation model in which desensitized adrenergic signaling is dominant during STHA, whereas on LTHA, the contractile machinery is influenced by altered expression of the calcium regulatory proteins leading to both augmented adrenergic inotropic response (via PLB elevation) and decreased velocity of relaxation. The sustained low thyroxin measured on LTHA causally associates with this response.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1477297-8
    SSG: 12
    Location Call Number Limitation Availability
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  • 6
    Online Resource
    Online Resource
    American Physiological Society ; 2015
    In:  Journal of Applied Physiology Vol. 119, No. 5 ( 2015-09-01), p. 463-467
    In: Journal of Applied Physiology, American Physiological Society, Vol. 119, No. 5 ( 2015-09-01), p. 463-467
    Abstract: Findings regarding blood glucose level (BGL) on exposure to hyperbaric oxygen (HBO) are contradictory. We investigated the influence of HBO on BGL, and of BGL on latency to central nervous system oxygen toxicity (CNS-OT). The study was conducted on five groups of rats: Group 1, exposure to oxygen at 2.5 atmospheres absolute (ATA), 90 min/day for 7 days; Group 2, exposure to oxygen once a week from 2 to 6 ATA in increments of 1 ATA/wk, for a period of time calculated as 60% of the latency to CNS-OT (no convulsions); Group 3, exposure to 6 ATA breathing a gas mixture with a pO 2 of 0.21; Group 4, received 10 U/kg insulin to induce hypoglycemia before exposure to HBO; Group 5, received 33% glucose to induce hyperglycemia before exposure to HBO. Blood samples were drawn before and after exposures for measurement of BGL. No change was observed in BGL after exposure to oxygen at 2.5 ATA, 90 min/day for 7 days. BGL was significantly elevated after exposure to oxygen at 6 ATA until the appearance of convulsions, and following exposure to 4, 5, and 6 ATA without convulsions ( P 〈 0.01). No change was observed in BGL after exposure to 6 ATA breathing a gas mixture with a pO 2 of 0.21. Hypoglycemia shortened latency to CNS oxygen toxicity, whereas hyperglycemia had no effect. Our results demonstrate an influence of HBO exposure on elevation of BGL, starting at 4 ATA. This implies that BGL may serve as a marker for the generation of CNS-OT.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2015
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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