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  • 1
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2013
    In:  Neuro-Oncology Vol. 15, No. suppl 3 ( 2013-11-01), p. iii12-iii31
    In: Neuro-Oncology, Oxford University Press (OUP), Vol. 15, No. suppl 3 ( 2013-11-01), p. iii12-iii31
    Type of Medium: Online Resource
    ISSN: 1522-8517 , 1523-5866
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2013
    detail.hit.zdb_id: 2094060-9
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  • 2
    In: Diseases of the Colon & Rectum, Ovid Technologies (Wolters Kluwer Health), Vol. 35, No. 5 ( 1992-05), p. 1-45
    Type of Medium: Online Resource
    ISSN: 0012-3706
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1992
    detail.hit.zdb_id: 2046914-7
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  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 1994
    In:  Journal of Applied Physiology Vol. 77, No. 4 ( 1994-10-01), p. 2048-2051
    In: Journal of Applied Physiology, American Physiological Society, Vol. 77, No. 4 ( 1994-10-01), p. 2048-2051
    Abstract: This study investigated the interaction between vagal afferent input and central chemosensitivity in modulating the respiratory motor output of in vitro brain stem-spinal cord preparations from adult bullfrogs. With this preparation, the spatiotemporal distribution of respiratory-related motor output emulated that of intact bullfrogs; that is, the fictive breathing pattern was mostly episodic. Recordings from cranial motor nerves (V and X) showed that, without peripheral feedback, increasing the PCO2 of the mock cerebrospinal fluid (thereby reducing pH from 8.3 to 7.7) caused a modest increase in respiration-related burst frequency. When the pulmonary branch of a vagus nerve was stimulated phasically (2 V, 20 Hz, 0.2 ms) during each fictive breath to simulate afferent pulmonary stretch receptor feedback 1) the responsiveness of the preparation to the same changes in pH was augmented nearly threefold and 2) the breathing pattern remained episodic. It appears, therefore, that episodic breathing is an intrinsic property of the central nervous system in bullfrogs. It is concluded that there is a strong interaction between vagal feedback and central chemodetection in controlling the temporal relationships that characterize this episodic breathing pattern.
    Type of Medium: Online Resource
    ISSN: 8750-7587 , 1522-1601
    RVK:
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1994
    detail.hit.zdb_id: 1404365-8
    SSG: 12
    SSG: 31
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  • 4
    Online Resource
    Online Resource
    The Company of Biologists ; 2005
    In:  Journal of Experimental Biology Vol. 208, No. 6 ( 2005-03-15), p. 1095-1107
    In: Journal of Experimental Biology, The Company of Biologists, Vol. 208, No. 6 ( 2005-03-15), p. 1095-1107
    Abstract: Experiments were carried out to test the hypothesis that ventilatory and cardiovascular responses to hypercarbia (elevated water PCO2) in the tambaqui Colossoma macropomum are stimulated by externally oriented receptors that are sensitive to water CO2 tension as opposed to water pH. Cardiorespiratory responses to acute hypercarbia were evaluated in both the absence and presence of internal hypercarbia (elevated blood PCO2), achieved by treating fish with the carbonic anhydrase inhibitor acetazolamide. Exposure to acute hypercarbia (15 min at each level, final water CO2 tensions of 7.2,15.5 and 26.3 mmHg) elicited significant increases in ventilation frequency(at 26.3 mmHg, a 42% increase over the normocarbic value) and amplitude(128%), together with a fall in heart rate (35%) and an increase in cardiac stroke volume (62%). Rapid washout of CO2 from the water reversed these effects, and the timing of the changes in cardiorespiratory variables corresponded more closely to the fall in water PCO2(PwCO2) than to that in blood PCO2(PaCO2). Similar responses to acute hypercarbia (15 min,final PwCO2 of 13.6 mmHg) were observed in acetazolamide-treated (30 mg kg-1) tambaqui. Acetazolamide treatment itself, however, increased PaCO2 (from 4.81±0.58 to 13.83±0.91 mmHg, mean ± s.e.m.; N=8) in the absence of significant change in ventilation, heart rate or cardiac stroke volume. The lack of response to changes in blood PCO2 and/or pH were confirmed by comparing responses to the bolus injection of hypercarbic saline(5% or 10% CO2; 2 ml kg-1) into the caudal vein with those to the injection of CO2-enriched water (1%, 3%, 5% or 10%CO2; 50 ml kg-1) into the buccal cavity. Whereas injections of hypercarbic saline were ineffective in eliciting cardiorespiratory responses, changes in ventilation and cardiovascular parameters accompanied injection of CO2-laden water into the mouth. Similar injections of CO2-free water acidified to the corresponding pH of the hypercarbic water (pH 6.3, 5.6, 5.3 or 4.9, respectively) generally did not stimulate cardiorespiratory responses. These results are in agreement with the hypothesis that in tambaqui, externally oriented chemoreceptors that are predominantly activated by increases in water PCO2,rather than by accompanying decreases in water pH, are linked to the initiation of cardiorespiratory responses to hypercarbia.
    Type of Medium: Online Resource
    ISSN: 1477-9145 , 0022-0949
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2005
    detail.hit.zdb_id: 1482461-9
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  • 5
    Online Resource
    Online Resource
    The Company of Biologists ; 1999
    In:  Journal of Experimental Biology Vol. 202, No. 24 ( 1999-12-15), p. 3647-3658
    In: Journal of Experimental Biology, The Company of Biologists, Vol. 202, No. 24 ( 1999-12-15), p. 3647-3658
    Abstract: Central vascular blood flows and ventilation were measured in conscious toads (Bufo marinus) at 15 and 25 °C. The animals were exposed to hypoxia ( and 0.05, where is the fractional oxygen concentration of inspired air) at both temperatures. In addition, the cardiorespiratory responses to hypercapnia and atropine injection (5mgkg−1; 7.4 μmol kg−1) were studied at 25 °C. At 25 °C, systemic blood flow (Q̇sys) exceeded pulmocutaneous blood flow (Q̇pc), indicating a large net right-to-left shunt (Q̇pc/Q̇sys was 0.39). Q̇pc/Q̇sys was reduced significantly to 0.22 at 15 °C. At both temperatures, Q̇pc increased significantly during hypoxia (from 26.2 to 50.8ml min−1 kg−1 at 25 °C and from 11.2 to 18.9 ml min−1 kg−1 at 15 °C), whereas Q̇sys changed little (from 77.2 to 66.2ml min−1 kg−1 at 25 °C and from 54.3 to 50.1 ml min−1 kg−1 at 15 °C). As a result, the net right-to-left shunt was greatly reduced, while total cardiac output remained almost unaffected. The ventilatory response was more pronounced during hypercapnia but, since Q̇pc and Q̇sys were affected similarly, there was no change in the shunt pattern. In undisturbed toads at 25 °C, atropine injection increased Q̇pc and eliminated the net right-to-left shunt. This is consistent with the known vagal innervation of the pulmonary artery. The present study shows that the cardiac right-to-left shunt that prevails in undisturbed and resting toads is reduced with increased temperature and during hypoxia. These findings are consistent with the general view that the cardiac right-to-left shunt is regulated and reduced whenever oxygen delivery is compromised or metabolic rate is increased.
    Type of Medium: Online Resource
    ISSN: 0022-0949 , 1477-9145
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 1999
    detail.hit.zdb_id: 1482461-9
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    American Physiological Society ; 2004
    In:  American Journal of Physiology-Regulatory, Integrative and Comparative Physiology Vol. 287, No. 1 ( 2004-07), p. R188-R197
    In: American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, American Physiological Society, Vol. 287, No. 1 ( 2004-07), p. R188-R197
    Abstract: Experiments were performed to assess the afferent and efferent limbs of the hypoxia-mediated humoral adrenergic stress response in selected hypoxia-tolerant tropical fishes that routinely experience environmental O 2 depletion. Plasma catecholamine (Cat) levels and blood respiratory status were measured during acute aquatic hypoxia [water Po 2 (Pw O 2 ) = 10–60 mmHg] in three teleost species, the obligate water breathers Hoplias malabaricus (traira) and Piaractus mesopotamicus (pacu) and the facultative air breather Hoplerythrinus unitaeniatus (jeju). Traira displayed a significant increase in plasma Cat levels (from 1.3 ± 0.4 to 23.3 ± 15.1 nmol/l) at Pw O 2 levels below 20 mmHg, whereas circulating Cat levels were unaltered in pacu at all levels of hypoxia. In jeju denied access to air, plasma Cat levels were increased markedly to a maximum mean value of 53.6 ± 19.1 nmol/l as Pw O 2 was lowered below 40 mmHg. In traira and jeju, Cat release into the circulation occurred at abrupt thresholds corresponding to arterial Po 2 (Pa O 2 ) values of approximately 8.5–12.5 mmHg. A comparison of in vivo blood O 2 equilibration curves revealed low and similar P 50 values (i.e., Pa O 2 at 50% Hb-O 2 saturation) among the three species (7.7–11.3 mmHg). Thus Cat release in traira and jeju occurred as blood O 2 concentration was reduced to approximately 50–60% of the normoxic value. Intravascular injections of nicotine (600 nmol/kg) elicited pronounced increases in plasma Cat levels in traira and jeju but not in pacu. Thus the lack of Cat release during hypoxia in pacu may reflect an inoperative or absent humoral adrenergic stress response in this species. When allowed access to air, jeju did not release Cats into the circulation at any level of aquatic hypoxia. The likeliest explanation for the absence of Cat release in these fish was that air breathing, initiated by aquatic hypoxia, prevented Pa O 2 values from falling to the critical threshold required for Cat secretion. The ventilatory responses to hypoxia in each species were similar, consisting generally of increases in both frequency and amplitude. These responses were not synchronized with or influenced by plasma Cat levels. Thus the acute humoral adrenergic stress response does not appear to stimulate ventilation during acute hypoxia in these tropical species.
    Type of Medium: Online Resource
    ISSN: 0363-6119 , 1522-1490
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2004
    detail.hit.zdb_id: 1477297-8
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 1984
    In:  Journal of Comparative Physiology B Vol. 154, No. 2 ( 1984), p. 167-174
    In: Journal of Comparative Physiology B, Springer Science and Business Media LLC, Vol. 154, No. 2 ( 1984), p. 167-174
    Type of Medium: Online Resource
    ISSN: 0174-1578 , 1432-136X
    RVK:
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 1984
    detail.hit.zdb_id: 231245-1
    detail.hit.zdb_id: 1459302-6
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  • 8
    Online Resource
    Online Resource
    The Company of Biologists ; 2001
    In:  Journal of Experimental Biology Vol. 204, No. 8 ( 2001-04-15), p. 1519-1527
    In: Journal of Experimental Biology, The Company of Biologists, Vol. 204, No. 8 ( 2001-04-15), p. 1519-1527
    Abstract: Adult Pacific spiny dogfish (Squalus acanthias) were exposed to acute (approximately 20 min) hypercarbia while we monitored arterial blood pressure, systemic vascular resistance (RS), cardiac output and frequency (fH) as well as ventilatory amplitude (VAMP) and frequency (fV). Separate series of experiments were conducted on control, atropinized (100 nmol kg−1 ) and branchially denervated fish to investigate putative CO2-chemoreceptive sites on the gills and their link to the autonomic nervous system and cardiorespiratory reflexes. In untreated fish, moderate hypercarbia (water CO2 partial pressure; mmHg) (1 mmHg= 0.133 kPa) elicited significant increases in VAMP (of approximately 92 %) and fV (of approximately 18 %) as well as decreases in fH (of approximately 64 %), (approximately 29 %) and arterial blood pressure (of approximately 11 %); RS did not change significantly. Denervation of the branchial branches of cranial nerves IX and X to the pseudobranch and each gill arch eliminated all cardiorespiratory responses to hypercarbia. Prior administration of the muscarinic receptor antagonist atropine also abolished the hypercarbia-induced ventilatory responses and virtually eliminated all CO2-elicited cardiovascular adjustments. Although the atropinized dogfish displayed a hypercarbic bradycardia, the magnitude of the response was significantly attenuated (36±6 % decrease in fH in controls versus 9±2 % decrease in atropinized fish; means ± S.E.M.). Thus, the results of the present study reveal the presence of gill CO2 chemoreceptors in dogfish that are linked to numerous cardiorespiratory reflexes. In addition, because all cardiorespiratory responses to hypercarbia were abolished or attenuated by atropine, the CO2 chemoreception process and/or one or more downstream elements probably involve cholinergic (muscarinic) neurotransmission.
    Type of Medium: Online Resource
    ISSN: 0022-0949 , 1477-9145
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2001
    detail.hit.zdb_id: 1482461-9
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    The Company of Biologists ; 1980
    In:  Journal of Experimental Biology Vol. 87, No. 1 ( 1980-08-01), p. 53-63
    In: Journal of Experimental Biology, The Company of Biologists, Vol. 87, No. 1 ( 1980-08-01), p. 53-63
    Abstract: The normal breathing pattern of the turtle, Chrysemys picta (Schneider), consists of periods of continuous breathing interspersed with periods of breath holding. During each ventilatory period respiratory frequency and tidal volume are controlled independently. There is a large variability in inspiratory and expiratory gas-flow rates yet tidal volumes are maintained within narrow limits by adjustments of the lengths of the active inspiratory and expiratory intervals. Lung volume information carried within the vagus nerve is responsible for the careful regulation of tidal volume as well as for modulation of the air flow rates and lowering of the threshold of the mechanism initiating expiration following breath holding. Increases in pulmonary minute ventilation during hypercapnia are caused by increases in respiratory frequency due solely to a shortening of the periods of breath holding. There is some increase in tidal volume but the breath length remains constant and thus the frequency of breathing within each ventilatory period also remains constant. After vagotomy, changes in minute ventilation due to hypercapnia stem primarily from changes in tidal volume while changes in respiratory frequency are greatly reduced.
    Type of Medium: Online Resource
    ISSN: 0022-0949 , 1477-9145
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 1980
    detail.hit.zdb_id: 1482461-9
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    Wiley ; 1979
    In:  The Journal of Physiology Vol. 291, No. 1 ( 1979-06-01), p. 37-49
    In: The Journal of Physiology, Wiley, Vol. 291, No. 1 ( 1979-06-01), p. 37-49
    Type of Medium: Online Resource
    ISSN: 0022-3751
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 1979
    detail.hit.zdb_id: 1475290-6
    SSG: 12
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