Abolition of reflex bradycardia by cardiac vagotomy has no effect on the regulation of oxygen uptake by Atlantic cod in progressive hypoxia

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Abolition of reflex bradycardia by cardiac vagotomy has no effect on the regulation of oxygen uptake by Atlantic cod in progressive hypoxia. / McKenzie, David J; Skov, Peter V; Taylor, E W Ted; Wang, Tobias; Steffensen, John F.

In: Comparative Biochemistry and Physiology A, Vol. 153, No. 3, 2009, p. 332-8.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

McKenzie, DJ, Skov, PV, Taylor, EWT, Wang, T & Steffensen, JF 2009, 'Abolition of reflex bradycardia by cardiac vagotomy has no effect on the regulation of oxygen uptake by Atlantic cod in progressive hypoxia', Comparative Biochemistry and Physiology A, vol. 153, no. 3, pp. 332-8. https://doi.org/10.1016/j.cbpa.2009.03.009

APA

McKenzie, D. J., Skov, P. V., Taylor, E. W. T., Wang, T., & Steffensen, J. F. (2009). Abolition of reflex bradycardia by cardiac vagotomy has no effect on the regulation of oxygen uptake by Atlantic cod in progressive hypoxia. Comparative Biochemistry and Physiology A, 153(3), 332-8. https://doi.org/10.1016/j.cbpa.2009.03.009

Vancouver

McKenzie DJ, Skov PV, Taylor EWT, Wang T, Steffensen JF. Abolition of reflex bradycardia by cardiac vagotomy has no effect on the regulation of oxygen uptake by Atlantic cod in progressive hypoxia. Comparative Biochemistry and Physiology A. 2009;153(3):332-8. https://doi.org/10.1016/j.cbpa.2009.03.009

Author

McKenzie, David J ; Skov, Peter V ; Taylor, E W Ted ; Wang, Tobias ; Steffensen, John F. / Abolition of reflex bradycardia by cardiac vagotomy has no effect on the regulation of oxygen uptake by Atlantic cod in progressive hypoxia. In: Comparative Biochemistry and Physiology A. 2009 ; Vol. 153, No. 3. pp. 332-8.

Bibtex

@article{23791f90e65611deba73000ea68e967b,
title = "Abolition of reflex bradycardia by cardiac vagotomy has no effect on the regulation of oxygen uptake by Atlantic cod in progressive hypoxia",
abstract = "The functional significance of chemoreflexive hypoxic bradycardia was explored in Atlantic cod Gadus morhua L. (mean mass approximately 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 (MO(2)), 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) approximately 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 MO(2), 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 P(crit) 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).",
author = "McKenzie, {David J} and Skov, {Peter V} and Taylor, {E W Ted} and Tobias Wang and Steffensen, {John F}",
note = "Keywords: Animals; Anoxia; Bradycardia; Gadus morhua; Heart; Oxygen; Vagotomy",
year = "2009",
doi = "10.1016/j.cbpa.2009.03.009",
language = "English",
volume = "153",
pages = "332--8",
journal = "Comparative biochemistry and physiology. Part A, Molecular & integrative physiology",
issn = "1095-6433",
publisher = "Elsevier",
number = "3",

}

RIS

TY - JOUR

T1 - Abolition of reflex bradycardia by cardiac vagotomy has no effect on the regulation of oxygen uptake by Atlantic cod in progressive hypoxia

AU - McKenzie, David J

AU - Skov, Peter V

AU - Taylor, E W Ted

AU - Wang, Tobias

AU - Steffensen, John F

N1 - Keywords: Animals; Anoxia; Bradycardia; Gadus morhua; Heart; Oxygen; Vagotomy

PY - 2009

Y1 - 2009

N2 - The functional significance of chemoreflexive hypoxic bradycardia was explored in Atlantic cod Gadus morhua L. (mean mass approximately 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 (MO(2)), 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) approximately 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 MO(2), 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 P(crit) 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).

AB - The functional significance of chemoreflexive hypoxic bradycardia was explored in Atlantic cod Gadus morhua L. (mean mass approximately 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 (MO(2)), 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) approximately 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 MO(2), 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 P(crit) 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).

U2 - 10.1016/j.cbpa.2009.03.009

DO - 10.1016/j.cbpa.2009.03.009

M3 - Journal article

C2 - 19303050

VL - 153

SP - 332

EP - 338

JO - Comparative biochemistry and physiology. Part A, Molecular & integrative physiology

JF - Comparative biochemistry and physiology. Part A, Molecular & integrative physiology

SN - 1095-6433

IS - 3

ER -

ID: 16239585