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  • American Physiological Society  (119)
  • 1
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    American Physiological Society ; 1982
    In:  Journal of Applied Physiology Vol. 53, No. 5 ( 1982-11-01), p. 1071-1079
    In: Journal of Applied Physiology, American Physiological Society, Vol. 53, No. 5 ( 1982-11-01), p. 1071-1079
    Kurzfassung: Functional residual capacity (FRC), tidal volume (VT), and frequency (f) were compared in 23 rats while either awake and unrestrained or anesthetized. FRC was determined from gas compression with closed airway inside a cone-shaped body plethysmograph. In the awake state (mean +/- SD), FRC was 1.02 +/- 0.22 ml/100 g, VT was 0.38 +/- 0.06 ml/100 g, and f was 142 +/- 22 breaths/min. During anesthesia, FRC decreased (P less than 0.01) to 52.9% of awake values, VT increased (P less than 0.01) to 147.4%, and f decreased (P less than 0.01) to 71.8%, leaving minute ventilation almost unchanged. An additional seven rats were used to examine postural effects on FRC during anesthesia, and in another seven animals pleural pressure changes were monitored. Dynamic lung compliance (0.80 ml . kg-1 X cmH2O-1) was not altered by anesthesia, but the pressure-volume curve was shifted 6 cmH2O higher. Thoracic compression, followed by a time-dependent effect of volume history, may account for the major change in FRC. The remainder of the decrease in FRC may be due to lower breathing frequency, loss of inspiratory muscle activity, and/or less airway resistance after anesthesia. Peak diaphragmatic electromyogram per unit VT was shown to increase almost linearly with FRC, indicating that diaphragmatic efficiency was decreased as lung volume was elevated. Functional residual capacity (FRC), tidal volume (VT), and frequency (f) were compared in 23 rats while either awake and unrestrained or anesthetized. FRC was determined from gas compression with closed airway inside a cone-shaped body plethysmograph. In the awake state (mean +/- SD), FRC was 1.02 +/- 0.22 ml/100 g, VT was 0.38 +/- 0.06 ml/100 g, and f was 142 +/- 22 breaths/min. During anesthesia, FRC decreased (P less than 0.01) to 52.9% of awake values, VT increased (P less than 0.01) to 147.4%, and f decreased (P less than 0.01) to 71.8%, leaving minute ventilation almost unchanged. An additional seven rats were used to examine postural effects on FRC during anesthesia, and in another seven animals pleural pressure changes were monitored. Dynamic lung compliance (0.80 ml . kg-1 X cmH2O-1) was not altered by anesthesia, but the pressure-volume curve was shifted 6 cmH2O higher. Thoracic compression, followed by a time-dependent effect of volume history, may account for the major change in FRC. The remainder of the decrease in FRC may be due to lower breathing frequency, loss of inspiratory muscle activity, and/or less airway resistance after anesthesia. Peak diaphragmatic electromyogram per unit VT was shown to increase almost linearly with FRC, indicating that diaphragmatic efficiency was decreased as lung volume was elevated. Functional residual capacity (FRC), tidal volume (VT), and frequency (f) were compared in 23 rats while either awake and unrestrained or anesthetized. FRC was determined from gas compression with closed airway inside a cone-shaped body plethysmograph. In the awake state (mean +/- SD), FRC was 1.02 +/- 0.22 ml/100 g, VT was 0.38 +/- 0.06 ml/100 g, and f was 142 +/- 22 breaths/min. During anesthesia, FRC decreased (P less than 0.01) to 52.9% of awake values, VT increased (P less than 0.01) to 147.4%, and f decreased (P less than 0.01) to 71.8%, leaving minute ventilation almost unchanged. An additional seven rats were used to examine postural effects on FRC during anesthesia, and in another seven animals pleural pressure changes were monitored. Dynamic lung compliance (0.80 ml . kg-1 X cmH2O-1) was not altered by anesthesia, but the pressure-volume curve was shifted 6 cmH2O higher. Thoracic compression, followed by a time-dependent effect of volume history, may account for the major change in FRC. The remainder of the decrease in FRC may be due to lower breathing frequency, loss of inspiratory muscle activity, and/or less airway resistance after anesthesia. Peak diaphragmatic electromyogram per unit VT was shown to increase almost linearly with FRC, indicating that diaphragmatic efficiency was decreased as lung volume was elevated. Functional residual capacity (FRC), tidal volume (VT), and frequency (f) were compared in 23 rats while either awake and unrestrained or anesthetized. FRC was determined from gas compression with closed airway inside a cone-shaped body plethysmograph. In the awake state (mean +/- SD), FRC was 1.02 +/- 0.22 ml/100 g, VT was 0.38 +/- 0.06 ml/100 g, and f was 142 +/- 22 breaths/min. During anesthesia, FRC decreased (P less than 0.01) to 52.9% of awake values, VT increased (P less than 0.01) to 147.4%, and f decreased (P less than 0.01) to 71.8%, leaving minute ventilation almost unchanged. An additional seven rats were used to examine postural effects on FRC during anesthesia, and in another seven animals pleural pressure changes were monitored. Dynamic lung compliance (0.80 ml . kg-1 X cmH2O-1) was not altered by anesthesia, but the pressure-volume curve was shifted 6 cmH2O higher. Thoracic compression, followed by a time-dependent effect of volume history, may account for the major change in FRC. The remainder of the decrease in FRC may be due to lower breathing frequency, loss of inspiratory muscle activity, and/or less airway resistance after anesthesia. Peak diaphragmatic electromyogram per unit VT was shown to increase almost linearly with FRC, indicating that diaphragmatic efficiency was decreased as lung volume was elevated.
    Materialart: Online-Ressource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 1982
    ZDB Id: 1404365-8
    SSG: 12
    SSG: 31
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
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    American Physiological Society ; 1979
    In:  Journal of Applied Physiology Vol. 47, No. 2 ( 1979-08-01), p. 352-359
    In: Journal of Applied Physiology, American Physiological Society, Vol. 47, No. 2 ( 1979-08-01), p. 352-359
    Kurzfassung: Receptor sites for the ventilatory response to isoproterenol were investigated in anesthetized rabbits with bolus injections in the common carotid artery (ia) and in the vena cava (iv). The delay from injection to the increase in ventilation (TVE) was significantly shorter following ia (1.5 s) compared to iv injections (about 5 s). The delay to the increase in heart rate (THR) was significantly shorter after iv (about 4.5 s) than after ia injections (12.5 s). When isoproterenol and NaCN injections were compared, there was no difference in TVE. Following carotid body resection, the VE response to isoproterenol was greatly reduced after iv and ia injections; however, THR was unaffected. In intact animals breathing 100% O2 the VE response to isoproterenol was significantly reduced with no change in TVE or in the heart rate response. We conclude that the ventilatory increase following the injection of isoproterenol is due primarily to direct stimulation of the carotid bodies.
    Materialart: Online-Ressource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 1979
    ZDB Id: 1404365-8
    SSG: 12
    SSG: 31
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
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    American Physiological Society ; 1973
    In:  Journal of Applied Physiology Vol. 35, No. 1 ( 1973-07), p. 58-67
    In: Journal of Applied Physiology, American Physiological Society, Vol. 35, No. 1 ( 1973-07), p. 58-67
    Materialart: Online-Ressource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 1973
    ZDB Id: 1404365-8
    SSG: 12
    SSG: 31
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 4
    Online-Ressource
    Online-Ressource
    American Physiological Society ; 1973
    In:  Journal of Applied Physiology Vol. 35, No. 1 ( 1973-07), p. 68-76
    In: Journal of Applied Physiology, American Physiological Society, Vol. 35, No. 1 ( 1973-07), p. 68-76
    Materialart: Online-Ressource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 1973
    ZDB Id: 1404365-8
    SSG: 12
    SSG: 31
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 5
    Online-Ressource
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    American Physiological Society ; 1977
    In:  Journal of Applied Physiology Vol. 43, No. 2 ( 1977-08-01), p. 379-381
    In: Journal of Applied Physiology, American Physiological Society, Vol. 43, No. 2 ( 1977-08-01), p. 379-381
    Kurzfassung: A semicontinuous but noninvasive blood pressure monitoring system is described. It consists of a commercial electronic sphygmomanometer which utilizes a microphone under an occluding arm cuff to detect the Korotkoff sounds, a pressure transducer, and a simple gating circuit. The gate passes the cuff pressure signal to a recorder only when a proper Korotkoff sound is detected. The cuff is rapidly inflated to just above the anticipated systolic pressure, then deflated at a steady rate of 2–6 Torr/heartbeat. When diastolic pressure is passed, the cuff is fully deflated momentarily before repeating the cycle. Systolic and diastolic pressures can be recorded up to 3 or 4 times/min. Spurious signals are rejected by the electronics which process the output of the microphone. This allows the use of the system in experiments on exercising man and in environments where unwanted signals exist. The system offers greater versatility than commercial semiautomatic pressure monitors, at less than half the cost.
    Materialart: Online-Ressource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 1977
    ZDB Id: 1404365-8
    SSG: 12
    SSG: 31
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 6
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    American Physiological Society ; 1995
    In:  American Journal of Physiology-Cell Physiology Vol. 268, No. 4 ( 1995-04-01), p. C944-C951
    In: American Journal of Physiology-Cell Physiology, American Physiological Society, Vol. 268, No. 4 ( 1995-04-01), p. C944-C951
    Kurzfassung: Muscarinic receptor-mediated changes in intracellular pH (pHi) were measured in isolated 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein-loaded cells, suspended in bicarbonate-containing media, from the exocrine nasal gland of freshwater-fed ducklings (Anas platyrhynchos). The pHi recovery from an acid load was sensitive to amiloride, required sodium ions in the external medium, and was independent of added bicarbonate. These findings are consistent with the hypothesis that the pHi recovery was mediated by a Na+/H+ exchanger. Muscarinic activation of cells resulted in a sustained cytosolic alkalinization that was sensitive to atropine and that was blocked by amiloride. Activation of protein kinase C (PKC) or inhibition of protein phosphatases mimicked the effect of receptor activation on pHi, whereas inhibitors of PKC blocked the response, indicating that phosphorylation of a major pHi control mechanism results in a shift of pHi to more alkaline values. In contrast, fully differentiated salt gland cells isolated from nasal glands of salt-stressed ducklings responded to muscarinic receptor activation with a transient cytosolic acidification. These findings raise the question whether the cytosolic alkalinization in muscarinic acetylcholine receptor-activated naive cells may serve as a signal or a permissive factor for the initiation of adaptive growth and/or differentiation processes observed in the salt glands of salt-stressed birds.
    Materialart: Online-Ressource
    ISSN: 0363-6143 , 1522-1563
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 1995
    ZDB Id: 1477334-X
    SSG: 12
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 7
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    American Physiological Society ; 2020
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 318, No. 4 ( 2020-04-01), p. H1018-H1027
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 318, No. 4 ( 2020-04-01), p. H1018-H1027
    Kurzfassung: Preeclampsia is a pregnancy-related disorder characterized by hypertension, vascular dysfunction and an increase in circulating inflammatory factors including the cytokine, tumor necrosis factor-α (TNF-α). Studies have shown that placental ischemia is associated with 1) increased circulating TNF-α, 2) attenuated pressure-induced cerebral vascular tone, and 3) suppression of β-epithelial Na + channel (βENaC) protein in cerebral vessels. In addition to its role in epithelial Na + and water transport, βENaC is an essential signaling element in transduction of pressure-induced (aka “myogenic”) constriction, a critical mechanism of blood flow autoregulation. While cytokines inhibit expression of certain ENaC proteins in epithelial tissue, it is unknown if the increased circulating TNF-α associated with placental ischemia mediates the loss of cerebrovascular βENaC and cerebral blood flow regulation. Therefore, the purpose of this study was to test the hypothesis that increasing plasma TNF-α in normal pregnant rats reduces cerebrovascular βENaC expression and impairs cerebral blood flow (CBF) regulation. In vivo TNF-α infusion (200 ng/day, 5 days) inhibited cerebrovascular expression of βENaC and impaired CBF regulation in pregnant rats. To determine the direct effects of TNF-α and underlying pathways mediating vascular smooth muscle cell βENaC reduction, we exposed cultured VSMCs (A10 cell line) to TNF-α (1–100 ng/mL) for 16–24 h. TNF-α reduced βENaC protein expression in a concentration-dependent fashion from 0.1 to 100 ng/mL, without affecting cell death. To assess the role of canonical MAPK signaling in this response, VSMCs were treated with p38MAPK or c-Jun kinase (JNK) inhibitors in the presence of TNF-α. We found that both p38MAPK and JNK blockade prevented TNF-α-mediated βENaC protein suppression. These data provide evidence that disorders associated with increased circulating TNF-α could lead to impaired cerebrovascular regulation, possibly due to reduced βENaC-mediated vascular function. NEW & NOTEWORTHY This manuscript identifies TNF-α as a possible placental-derived cytokine that could be involved in declining cerebrovascular health observed in preeclampsia. We found that infusion of TNF-α during pregnancy impaired cerebral blood flow control in rats at high arterial pressures. We further discovered that cerebrovascular β-epithelial sodium channel (βENaC) protein, a degenerin protein involved in mechanotransduction, was reduced by TNF-α in pregnant rats, indicating a potential link between impaired blood flow and this myogenic player. We next examined this effect in vitro using a rat vascular smooth muscle cell line. TNF-α reduced βENaC through canonical MAPK-signaling pathways and was not dependent on cell death. This study demonstrates the pejorative effects of TNF-α on cerebrovascular function during pregnancy and warrants future investigations to study the role of cytokines on vascular function during pregnancy.
    Materialart: Online-Ressource
    ISSN: 0363-6135 , 1522-1539
    RVK:
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2020
    ZDB Id: 1477308-9
    SSG: 12
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 8
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    American Physiological Society ; 2007
    In:  Journal of Applied Physiology Vol. 103, No. 2 ( 2007-08), p. 710-716
    In: Journal of Applied Physiology, American Physiological Society, Vol. 103, No. 2 ( 2007-08), p. 710-716
    Kurzfassung: CO 2 regulation of lung compliance is currently explained by pH- and CO 2 -dependent changes in alveolar surface forces and bronchomotor tone. We hypothesized that in addition to, but independently of, those mechanisms, the parenchyma tissue responds to hypercapnia and hypocapnia by relaxing and contracting, respectively, thereby improving local matching of ventilation (V̇a) to perfusion (Q̇). Twenty adult rats were slowly ventilated with modified Krebs solution (rate = 3 min −1 , 37°C, open chest) to produce unperfused living lung preparations free of intra-airway surface forces. The solution was gassed with 21% O 2 , balance N 2 , and CO 2 varied to produce alveolar hypocapnia (Pco 2 = 26.1 ± 2.4 mmHg, pH = 7.56 ± 0.04) or hypercapnia (Pco 2 = 55.0 ± 2.3 mmHg, pH = 7.23 ± 0.02). The results show that lung recoil, as indicated from airway pressure measured during a breathhold following a large volume inspiration, is reduced ∼30% when exposed to hypercapnia vs. hypocapnia ( P 〈 0.0001, paired t-test), but stress relaxation and flow-dependent airway resistance were unaltered. Increasing CO 2 from hypo- to hypercapnic levels caused a substantial, significant decrease in the quasi-static pressure-volume relationship, as measured after inspiration and expiration of several tidal volumes, but hysteresis was unaltered. Furthermore, addition of the glycolytic inhibitor NaF abolished CO 2 effects on lung recoil. The results suggest that lung parenchyma tissue relaxation, arising from active elements in response to increasing alveolar CO 2 , is independent of (and apparently in parallel with) passive tissue elements and may actively contribute to V̇a/Q̇ matching.
    Materialart: Online-Ressource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2007
    ZDB Id: 1404365-8
    SSG: 12
    SSG: 31
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 9
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    American Physiological Society ; 2010
    In:  American Journal of Physiology-Renal Physiology Vol. 299, No. 5 ( 2010-11), p. F1040-F1047
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 299, No. 5 ( 2010-11), p. F1040-F1047
    Kurzfassung: The zebrafish is a valuable vertebrate model for kidney research. The majority of previous studies focused on the zebrafish pronephros, which comprises only two nephrons and is structurally simpler than the mesonephros of adult fish and the metanephros of mammals. To evaluate the zebrafish system for more complex studies of kidney development and regeneration, we investigated the development and postinjury regeneration of the mesonephros in adult zebrafish. Utilizing two transgenic zebrafish lines ( wt1b::GFP and pod::NTR-mCherry), we characterized the developmental stages of individual mesonephric nephrons and the temporal-spatial pattern of mesonephrogenesis. We found that mesonephrogenesis continues throughout the life of zebrafish, with a rapid growth phase during the juvenile period and a slower phase in adulthood such that the total nephron number of juvenile and adult fish linearly correlates with body mass. Following gentamicin-induced renal injury, the zebrafish mesonephros can undergo de novo regeneration of mesonephric nephrons, a process known as neonephrogenesis. We found that wt1b expression was induced in individually dispersed cells in the mesonephric interstitium as early as 48 h following injury. These wt1b-expressing cells formed aggregates by 72–96 h following injury which proceeded to form nephrons. This suggests that wt1b may serve as an early marker of fated renal progenitor cells. The synchronous nature of regenerative neonephrogenesis suggests that this process may be useful for studies of nephron development.
    Materialart: Online-Ressource
    ISSN: 1931-857X , 1522-1466
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2010
    ZDB Id: 1477287-5
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 10
    Online-Ressource
    Online-Ressource
    American Physiological Society ; 2012
    In:  American Journal of Physiology-Renal Physiology Vol. 302, No. 10 ( 2012-05-15), p. F1305-F1312
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 302, No. 10 ( 2012-05-15), p. F1305-F1312
    Kurzfassung: Endothelial progenitor cells (EPCs) protect the kidney from acute ischemic injury. The aim of this study was to analyze whether pretreatment of murine “early outgrowth” EPCs (eEPCs) with the hormone melatonin increases the cells' renoprotective effects in the setting of murine acute ischemic renal failure. Male (8–12 wk old) C57Bl/6N mice were subjected to unilateral ischemia-reperfusion injury postuninephrectomy (40 min). Postischemic animals were injected with either 0.5×10 6 untreated syngeneic murine eEPCs or with cells, pretreated with melatonin for 1 h. Injections were performed shortly after reperfusion of the kidney. While animals injected with untreated cells developed acute renal failure, eEPC pretreatment with melatonin dramatically improved renoprotective actions of the cells. These effects were completely reversed after cell pretreatment with melatonin and the MT-1/-2 antagonist luzindole. In vitro analysis revealed that melatonin reduced the amount of tumor growth factor-β-induced eEPC apoptosis/necrosis. Secretion of vascular endothelial growth factor by the cells was markedly stimulated by the hormone. In addition, migratory activity of eEPCs was enhanced by melatonin and supernatant from melatonin-treated eEPCs stimulated migration of cultured mature endothelial cells. In summary, melatonin was identified as a new agonist of eEPCs in acute ischemic kidney injury.
    Materialart: Online-Ressource
    ISSN: 1931-857X , 1522-1466
    Sprache: Englisch
    Verlag: American Physiological Society
    Publikationsdatum: 2012
    ZDB Id: 1477287-5
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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