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Auteur (up) Iversen, N.K.; McKenzie, D.J.; Malte, H.; Wang, T.
Titre Reflex bradycardia does not influence oxygen consumption during hypoxia in the European eel (Anguilla anguilla) Type Article scientifique
Année 2010 Publication Revue Abrégée J. Comp. Physiol. B-Biochem. Syst. Environ. Physiol.
Volume 180 Numéro 4 Pages 495-502
Mots-Clés Anguilla anguilla; Cardiac output; Critical oxygen tension; Hypoxic bradycardia; Oxygen; Teleost; atlantic cod; cardiac vagotomy; circulation; consumption; dogfish scyliorhinus-canicula; fish; heart-rate; rainbow-trout; responses; temperature; tolerance
Résumé Most teleost fish reduce heart rate when exposed to acute hypoxia. This hypoxic bradycardia has been characterised for many fish species, but it remains uncertain whether this reflex contributes to the maintenance of oxygen uptake in hypoxia. Here we describe the effects of inhibiting the bradycardia on oxygen consumption (MO(2)), standard metabolic rate (SMR) and the critical oxygen partial pressure for regulation of SMR in hypoxia (Pcrit) in European eels Anguilla anguilla (mean +/- A SEM mass 528 +/- A 36 g; n = 14). Eels were instrumented with a Transonic flow probe around the ventral aorta to measure cardiac output (Q) and heart rate (f (H)). MO(2) was then measured by intermittent closed respirometry during sequential exposure to various levels of increasing hypoxia, to determine Pcrit. Each fish was studied before and after abolition of reflex bradycardia by intraperitoneal injection of the muscarinic antagonist atropine (5 mg kg(-1)). In the untreated eels, f (H) fell from 39.0 +/- A 4.3 min(-1) in normoxia to 14.8 +/- A 5.2 min(-1) at the deepest level of hypoxia (2 kPa), and this was associated with a decline in Q, from 7.5 +/- A 0.8 mL min(-1) kg(-1) to 3.3 +/- A 0.7 mL min(-1) kg(-1) in normoxia versus deepest hypoxia, respectively. Atropine had no effect on SMR, which was 16.0 +/- A 1.8 mu mol O(2) kg(-1) min(-1) in control versus 16.8 +/- A 0.8 mu mol O(2) kg(-1) min(-1) following treatment with atropine. Atropine also had no significant effect on normoxic f (H) or Q in the eel, but completely abolished the bradycardia and associated decline in Q during progressive hypoxia. This pharmacological inhibition of the cardiac responses to hypoxia was, however, without affect on Pcrit, which was 11.7 +/- A 1.3 versus 12.5 +/- A 1.5 kPa in control versus atropinised eels, respectively. These results indicate, therefore, that reflex bradycardia does not contribute to maintenance of MO(2) and regulation of SMR by the European eel in hypoxia.
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ISSN 0174-1578 ISBN Médium
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Numéro d'Appel MARBEC @ isabelle.vidal-ayouba @ collection 805
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Auteur (up) McKenzie, D.J.; Skov, P.V.; Taylor, E.W.T.; Wang, T.; Steffensen, J.F.
Titre Abolition of reflex bradycardia by cardiac vagotomy has no effect on the regulation of oxygen uptake by Atlantic cod in progressive hypoxia Type Article scientifique
Année 2009 Publication Revue Abrégée Comp. Biochem. Physiol. A-Mol. Integr. Physiol.
Volume 153 Numéro 3 Pages 332-338
Mots-Clés Cranial nerve X; Gas exchange; Heart rate; Hypoxia; Sodium cyanide; Vagus; blood; channel catfish; dogfish scyliorhinus-canicula; fish; fish hearts; gadus-morhua; performance; pressure; rainbow-trout; respiration; responses; ventilation
Résumé The functional significance of chemoreflexive hypoxic bradycardia was explored in Atlantic cod Gadus morhua L. (mean mass similar to 800 g, acclimated to a seawater temperature of 11 degrees C) by investigating responses to progressive hypoxia following section of the cardiac branches of cranial nerve X Cardiac denervation had no effect on oxygen uptake rate (M(O2)), gill ventilation rate (f(G)) or opercular pressure amplitude (P(OP)) under normoxic conditions, but caused a significant increase in heart rate (f(H)), to 50 +/- 1 beats min(-1) by comparison to 40 +/- 2 beats min(-1) in sham-operated cod (mean +/- s.e.m., n=9). Sham-operated cod exhibited transient profound bradycardia following oxygen chemoreceptor stimulation by bolus injection of sodium cyanide into the buccal cavity (2 mg in 2 ml seawater), but this cardiac chemoreflex was abolished in denervated cod. Both groups, however, exhibited similar marked transient chemoreflexive hyperventilation following NaCN. When exposed from normoxia (PO(2)similar to 18 kPa) to progressive hypoxia at nominal water PO(2)'S of 8, 6, 5, 4 and 3 kPa, both groups exhibited the same pattern of homeostatic regulation of M(O2), with no significant difference in their mean critical PO(2) (P(crit)) values, which were 7.40 +/- 0.81 kPa and 8.73 +/- 0.71 kPa, respectively (n=9). Both groups exhibited significant bradycardia during progressive hypoxia, although denervated fish always had higher mean f(H). The incipient threshold for bradycardia coincided with P(crit) in sham-operated cod whereas, in denervates, the threshold was below their P(crit) and bradycardia presumably reflected direct effects of hypoxia on the myocardium. The sham-operated group displayed a significantly more pronounced ventilatory response than denervates in hypoxia, in particular for P(OP). In sham-operated cod, peak ventilatory responses occurred in deep hypoxia below P(crit) whereas, in denervates, more modest peak responses coincided with Pit and, in deep hypoxia, they exhibited a significant decline in f(G) below their normoxic rate. Only a minority of shams lost equilibrium in hypoxia whereas a majority of denervates did, some of which failed to recover. The results indicate that chemoreflexive bradycardia plays no role in the homeostatic regulation of oxygen uptake by cod in hypoxia, but does contribute to maintenance of overall functional integrity below P(crit). (C) 2009 Elsevier Inc. All rights reserved.
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Langue English Langue du Résumé Titre Original
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Volume de collection Numéro de collection Edition
ISSN 1095-6433 ISBN Médium
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Numéro d'Appel MARBEC @ isabelle.vidal-ayouba @ collection 431
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