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  • English  (10)
  • Biology  (10)
  • XA 52094  (10)
  • 1
    Online Resource
    Online Resource
    Effects of acute cold exposure on carotid and femoral wave intensity indexes: evidence for reflection coefficient as a measure of distal vascular resistance
    American Physiological Society ; 2011
    In:  Journal of Applied Physiology Vol. 110, No. 3 ( 2011-03), p. 738-745
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 110, No. 3 ( 2011-03), p. 738-745
    Abstract: Our aim was to investigate the effects of acute cold pressor test (CPT) on augmentation index (AI) and wave intensity (WI) indexes from right common carotid artery (RCCA) and right common femoral artery (RCFA) and to test whether the reflection coefficient (RC) from wave intensity analysis can reflect the distal vascular resistance (DVR) accurately. Forty-three healthy males were randomly selected for measurements at baseline and 1 min after CPT at RCCA or RCFA. CPT induced similar increases of heart rate and blood pressure in RCCA and RCFA groups with their pulse pressures unchanged. The W 2 (the second peak of WI) was too obscure in RCFA to be analyzed. The W 1 (the first peak of WI) of both arteries, W 1 -W 2 (interval between W 1 and W 2 ), and NA (negative area between W 1 and W 2 , indicating reflected waves) of RCCA and the R-W 1 (interval between the R wave of ECG and W 1 ) of RCFA decreased obviously, whereas the W 2 and R-W 1 of RCCA and the RC (calculated as NA/W 1 ) of RCFA increased with no changes in the RC of RCCA and the NA of RCFA during CPT compared with baseline. The AIs from both arteries increased significantly after CPT. These results suggested that acute CPT has opposing effects on cerebral and peripheral vascular resistances, with the former decreased and the latter increased. The RCs from RCCA and RCFA are more associated with the changes of cerebral and peripheral vascular resistances, respectively, than the NA and AI, and the RC is of guiding value in assessing DVR.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00863.2010
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2011
    detail.hit.zdb_id: 1404365-8
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  • 2
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    Online Resource
    Molecular control of circadian metabolic rhythms
    American Physiological Society ; 2009
    In:  Journal of Applied Physiology Vol. 107, No. 6 ( 2009-12), p. 1959-1964
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 107, No. 6 ( 2009-12), p. 1959-1964
    Abstract: Circadian metabolic rhythms are fundamental to the control of nutrient and energy homeostasis, as well as the pathogenesis of metabolic disease, such as obesity, lipid disorders, and type 2 diabetes. This temporal organization of tissue metabolism is coordinated through reciprocal cross talk between the biological timing system and the metabolic regulatory networks. In this review, we discuss the signaling mechanisms that serve to couple metabolic regulation to the circadian pacemaker, in particular the role of the peroxisome proliferator-activated receptor-γ coactivator-1 transcriptional coactivators in integrating clock and energy metabolism.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00467.2009
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 3
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    Online Resource
    Air embolism-induced lung injury in isolated rat lungs
    American Physiological Society ; 1992
    In:  Journal of Applied Physiology Vol. 72, No. 4 ( 1992-04-01), p. 1235-1242
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 72, No. 4 ( 1992-04-01), p. 1235-1242
    Abstract: Pulmonary air embolism causes physical obstruction of microvasculature and leads to permeability changes, release of mediators, and injury to lung tissue. In this study we employed an isolated perfused rat lung model to investigate the primary and secondary effects produced by infusion of air into the pulmonary artery. Infusion of various doses of air (0.10–0.25 ml) over a 1-min period produced a dose-dependent increase in pulmonary arterial pressure and lung weight gain. In contrast, when a constant air dose was administered over various periods of time (0.25 ml over 0.5–8.0 min), the pulmonary arterial pressure rose to the same extent regardless of the infusion rate, whereas the lung weight gain increased proportionately with the rate of infusion. Total vascular resistance rose from 1.41 +/- 0.04 to 5.04 +/- 0.09 mmHg.ml-1.min in rats given 0.25 ml air over 1 min (n = 14, P less than 0.001), with greater than or equal to 90% of this increase occurring in the arterial segments. Both thromboxane B2 and endothelin concentrations also increased in the perfusate, suggesting their involvement in this increased resistance. Furthermore the pulmonary filtration coefficient increased from 0.21 +/- 0.05 to 1.28 +/- 0.26 g.min-1.cmH2O–1.100 g (n = 8, P less than 0.001), and the protein concentration in lung lavage fluid also rose, indicating lung injury. Leukocyte counts in the perfusate were unaffected by embolization, but chemiluminescent activity was increased, indicating a possible role for activated leukocytes in lung injury induced by air emboli.(ABSTRACT TRUNCATED AT 250 WORDS)
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/jappl.1992.72.4.1235
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1992
    detail.hit.zdb_id: 1404365-8
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  • 4
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    Online Resource
    Heat stress attenuates air bubble-induced acute lung injury: a novel mechanism of diving acclimatization
    American Physiological Society ; 2003
    In:  Journal of Applied Physiology Vol. 94, No. 4 ( 2003-04-01), p. 1485-1490
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 94, No. 4 ( 2003-04-01), p. 1485-1490
    Abstract: Diving acclimatization refers to a reduced susceptibility to acute decompression sickness (DCS) in individuals undergoing repeated compression-decompression cycles. We postulated that mechanisms responsible for the acclimatization are similar to that of a stress preconditioning. In this study, we investigated the protective effect of prior heat shock treatment on air embolism-induced lung injury and on the incidence of DCS in rats. We exposed rats ( n = 31) to a pressure cycle that induced signs of severe DCS in 48% of the rats, greater wet-to-dry ratio (W/D) of lung weight compared with the control group (5.48 ± 0.69 vs. 4.70 ± 0.17), and higher protein concentration in bronchoalveolar lavage (BAL) fluid (362 ± 184 vs. 209 ± 78 mg/l) compared with the control group. Rats with DCS expressed more heat shock protein 70 (HSP70) in the lungs than those without signs of disease. Prior heat shock ( n = 12) increased the expression of HSP70 in the lung and attenuated the elevation of W/D of lung weight (5.03 ± 0.17) after the identical decompression protocol. Prior heat shock reduced the incidence of severe DCS by 23%, but this failed to reach statistical significant (χ 2 = 1.94, P = 0.163). Venous air infusion (1.0 ml/40 min) caused profound hypoxemia (54.5 ± 3.8 vs. 83.8 ± 3.2 Torr at baseline; n = 6), greater W/D of lung weight (5.98 ± 0.45), and high protein concentration in BAL fluid (595 ± 129 mg/l). Prior heat shock ( n = 6) did not alter the level of hypoxemia caused by air embolism, but it accelerated the recovery to normoxemia after air infusion was stopped. Prior heat shock also attenuated the elevation of W/D of lung weight (5.19 ± 0.40) and the increase in BAL protein (371 ± 69 mg/l) in air embolism group. Our results showed that the occurrence of DCS after rapid decompression is associated with increased expression of a stress protein (HSP70) and that prior heat shock exposure attenuates the air bubble-induced lung injury. These results suggest that bubble formation in tissues activates a stress response and that stress preconditioning attenuates lung injury on subsequent stress, which may be the mechanism responsible for diving acclimatization.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00952.2002
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2003
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 5
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    Online Resource
    Airway mechanoreceptor deactivation
    American Physiological Society ; 2007
    In:  Journal of Applied Physiology Vol. 103, No. 2 ( 2007-08), p. 600-607
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 103, No. 2 ( 2007-08), p. 600-607
    Abstract: Airway sensors play an important role in control of breathing. Recently, it was found that pulmonary slowly adapting stretch receptors (SARs) cease after a brief excitation following sodium pump blockade by ouabain. This deactivation can be explained by overexcitation. If this is true, mechanical stimulation of the SARs should also lead to a deactivation. In this study, we recorded unit activity of the SARs in anesthetized, open-chest, and mechanically ventilated rabbits and examined their responses to lung inflation at different constant pressures. Forty-seven of 137 units had a clear deactivation during the lung inflation. The deactivation threshold varied from unit to unit. For a given unit, the higher the inflation pressure, the sooner the deactivation occurs. For example, the SARs deactivated at 3.0 ± 0.3 and 4.8 ± 0.4 s when the lungs were inflated to constant pressures of 30 and 20 cmH 2 O, respectively ( n = 25, P 〈 0.0001). The units usually ceased after a brief intense discharge. In some units, their activity shifted to a lower level, indicating a pacemaker switching. Our results support the notion that SARs deactivate due to overexcitation.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.01286.2006
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2007
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 6
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    Online Resource
    Contrasting effects of simulated microgravity with and without daily −G x gravitation on structure and function of cerebral and mesenteric small arteries in rats
    American Physiological Society ; 2009
    In:  Journal of Applied Physiology Vol. 107, No. 6 ( 2009-12), p. 1710-1721
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 107, No. 6 ( 2009-12), p. 1710-1721
    Abstract: This study was designed to test the hypothesis that a 28-day tail suspension (SUS) could induce hypertrophy and enhanced myogenic and vasoconstrictor reactivity in middle cerebral arteries (MCAs), whereas atrophy and decreased myogenic and vasoconstrictor responses in mesenteric third-order arterioles (MSAs). Also, in addition to the functional enhancement in MCAs, structural changes in both kinds of arteries and functional decrement in MSAs could all be prevented by the intervention of daily 1-h dorsoventral (−G x ) gravitation by restoring to standing posture. To test this hypothesis, vessel diameters to pressure alterations and nonreceptor- and receptor-mediated agonists were determined using a pressure arteriograph with a procedure to measure in vivo length and decrease hysteresis of vessel segments and longitudinal middlemost sections of vessels fixed at maximally dilated state were examined using electron microscopy and histomorphometry. Functional studies showed that 28-day tail-suspended, head-down tilt (SUS) resulted in enhanced and decreased myogenic tone and vasoconstrictor responses, respectively, in MCAs and MSAs. Histomorphometric data revealed that SUS-induced hypertrophic changes in MCAs characterized by increases in thickness (T) and cross-sectional area (CSA) of the media and the number of vascular smooth-muscle-cell layers (N CL ), whereas in MSAs, it induced decreases in medial CSA and T and N CL . Daily 1-h −G x over 28 days can fully prevent these differential structural changes in both kinds of small arteries and the functional decrement in MSAs, but not the augmented myogenic tone and increased vasoreactivity in the MCAs. These findings have revealed special features of small resistance arteries during adaptation to microgravity with and without gravity-based countermeasure.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00493.2009
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 7
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    Online Resource
    7,8-dihydroxyflavone exhibits therapeutic efficacy in a mouse model of Rett syndrome
    American Physiological Society ; 2012
    In:  Journal of Applied Physiology Vol. 112, No. 5 ( 2012-03-01), p. 704-710
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 112, No. 5 ( 2012-03-01), p. 704-710
    Abstract: Rett syndrome (RTT), caused by mutations in the methyl-CpG binding protein 2 gene ( MECP2), is a debilitating autism spectrum developmental disorder predominantly affecting females. Mecp2 mutant mice have reduced levels of brain-derived neurotrophic factor (BDNF) in the brain; conditional deletion and overexpression of BDNF in the brain accelerates and slows, respectively, disease progression in Mecp2 mutant mice. Thus we tested the hypothesis that 7,8-dihydroxyflavone (7,8-DHF), a small molecule reported to activate the high affinity BDNF receptor (TrkB) in the CNS, would attenuate disease progression in Mecp2 mutant mice. Following weaning, 7,8-DHF was administered in drinking water throughout life. Treated mutant mice lived significantly longer compared with untreated mutant littermates (80 ± 4 and 66 ± 2 days, respectively). 7,8-DHF delayed body weight loss, increased neuronal nuclei size and enhanced voluntary locomotor (running wheel) distance in Mecp2 mutant mice. In addition, administration of 7,8-DHF partially improved breathing pattern irregularities and returned tidal volumes to near wild-type levels. Thus although the specific mechanisms are not completely known, 7,8-DHF appears to reduce disease symptoms in Mecp2 mutant mice and may have potential as a therapeutic treatment for RTT patients.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.01361.2011
    RVK:
    WA 15000
    RVK:
    XA 52094
    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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  • 8
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    Mitochondrial antioxidative capacity regulates muscle glucose uptake in the conscious mouse: effect of exercise and diet
    American Physiological Society ; 2012
    In:  Journal of Applied Physiology Vol. 113, No. 8 ( 2012-10-15), p. 1173-1183
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 113, No. 8 ( 2012-10-15), p. 1173-1183
    Abstract: The objective of this study was to test the hypothesis that exercise-stimulated muscle glucose uptake (MGU) is augmented by increasing mitochondrial reactive oxygen species (mtROS) scavenging capacity. This hypothesis was tested in genetically altered mice fed chow or a high-fat (HF) diet that accelerates mtROS formation. Mice overexpressing SOD2 ( sod2 Tg ), mitochondria-targeted catalase ( mcat Tg ), and combined SOD2 and mCAT (mtAO) were used to increase mtROS scavenging. mtROS was assessed by the H 2 O 2 emitting potential ( JH 2 O 2 ) in muscle fibers. sod2 Tg did not decrease JH 2 O 2 in chow-fed mice, but decreased JH 2 O 2 in HF-fed mice. mcat Tg and mtAO decreased JH 2 O 2 in both chow- and HF-fed mice. In parallel, the ratio of reduced to oxidized glutathione (GSH/GSSG) was unaltered in sod2 Tg in chow-fed mice, but was increased in HF-fed sod2 Tg and both chow- and HF-fed mcat Tg and mtAO. Nitrotyrosine, a marker of NO-dependent, reactive nitrogen species (RNS)-induced nitrative stress, was decreased in both chow- and HF-fed sod2 Tg , mcat Tg , and mtAO mice. This effect was not changed with exercise. Kg, an index of MGU was assessed using 2-[ 14 C]-deoxyglucose during exercise. In chow-fed mice, sod2 Tg , mcat Tg , and mtAO increased exercise Kg compared with wild types. Exercise Kg was also augmented in HF-fed sod2 Tg and mcat Tg mice but unchanged in HF-fed mtAO mice. In conclusion, mtROS scavenging is a key regulator of exercise-mediated MGU and this regulation depends on nutritional state.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.01344.2011
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2012
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 9
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    Effects of different stresses on cardiac autonomic control and cardiovascular coupling
    American Physiological Society ; 2017
    In:  Journal of Applied Physiology Vol. 122, No. 3 ( 2017-03-01), p. 435-445
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 122, No. 3 ( 2017-03-01), p. 435-445
    Abstract: The objective of this study was to investigate the impacts of different stresses on time-varying autonomic reactivity and cardiovascular coupling. In total, 25 male subjects were recruited. RR intervals (RRI), systolic and diastolic blood pressure (SBP, DBP), stroke volume (SV), cardiac output (CO), and systemic vascular resistance (SVR) values were collected during rest, mental arithmetic task (MAT), and cold pressor test (CPT). Baroreflex sensitivity (BRS) was derived using the transfer function method. Continuous wavelet transformation of RRI was used to describe the time-variant patterns of autonomic neural activities. Wavelet cross correlation and phase synchronization were used to estimate the amplitude and phase coupling between RRI and SBP. MAT was characterized by increased heart rate (HR), SBP, DBP, and CO with decreased BRS attributable to prolonged parasympathetic withdrawal. Moreover, cardiovascular coupling was disrupted in MAT. These results indicated that baroreflex was depressed, and the top-down system started to take action under mental stress. In CPT, SBP, DBP, and SVR increased significantly, whereas HR and BRS remained unchanged. The increase of sympathetic activity was transient, and cardiovascular coupling did not change in CPT. Intriguingly, the frequency of the maximum cross-correlation coefficient in the low-frequency band (0.04–0.15 Hz) was significantly decreased in CPT, which may be due to the change of resonance frequency of the baroreflex loop. NEW & NOTEWORTHY The study is the first to compare the time-variant pattern of autonomic nervous activities and cardiovascular coupling between the mental arithmetic task (MAT) and the cold pressor test (CPT). Our results demonstrated that MAT and CPT elicited different time-varying patterns of autonomic neural activities and cardiovascular synchronization. Both the amplitude and phase consistency of blood pressure and heart rate decreased in MAT. CPT may affect the harmonic frequency of the baroreflex loop.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.00245.2016
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2017
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 10
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    CapZ and actin capping dynamics increase in myocytes after a bout of exercise and abates in hours after stimulation ends
    American Physiological Society ; 2013
    In:  Journal of Applied Physiology Vol. 114, No. 11 ( 2013-06-01), p. 1603-1609
    Details
    In: Journal of Applied Physiology, American Physiological Society, Vol. 114, No. 11 ( 2013-06-01), p. 1603-1609
    Abstract: The time course of the response and recovery after acute activity seen in exercise is not well understood. The goal of this work is to address how proteins of the thin filament (actin and its capping protein CapZ) are changed by 1 h of mechanical stimulation and return to baseline over time. Neonatal rat ventricular myocytes in culture were subjected to cyclic 10% strain at 1 Hz for 1 h to mimic increased mechanical loading during exercise. CapZ and actin dynamics were analyzed by fluorescence recovery after photobleaching (FRAP) using CapZβ1-GFP, actin-GFP, or actin-RFP. After cyclic strain, CapZ dynamics increased above resting controls and abated 2–3 h after cessation of the cyclic strain. Similarly, actin dynamics initially increased and abated 1.5–2 h after the end of stimulation. Neurohormonal hypertrophic stimulation by phenylephrine or norepinephrine treatments also elevated actin dynamics but required a much longer time of treatment (24–48 h) to be detectable. The actin capping mechanism was explored by use of expression of CapZβ1 with a COOH-terminal deletion (CapZβ1ΔC). Increased dynamics of actin seen with CapZβ1ΔC was similar to the response to cyclic strain. Thus it is possible that mechanical stimulation alters the dynamics for CapZ capping of the actin filament through the CapZβ1 COOH terminus, known as the β tentacle, thereby remodeling sarcomeres in cardiac myocytes. This adaptive mechanism, which is probably regulating thin-filament addition, declines a few hours after the end of a bout of exercise.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    URL: Article
    DOI: 10.1152/japplphysiol.01283.2012
    RVK:
    WA 15000
    RVK:
    XA 52094
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2013
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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