Tolerance of chronic hypercapnia by the European eel Anguilla anguilla.

D J McKenzie; M Piccolella; A Z Dalla Valle; E W Taylor; C L Bolis; J F Steffensen

doi:10.1242/jeb.00352

Tolerance of chronic hypercapnia by the European eel Anguilla anguilla.

D J McKenzie, M Piccolella, A Z Dalla Valle, E W Taylor, C L Bolis, J F Steffensen

Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review

67 Citationer (Scopus)

Abstract

Udgivelsesdato: 2003-May

Originalsprog	Engelsk
Tidsskrift	Journal of Experimental Biology
Vol/bind	206
Udgave nummer	Pt 10
Sider (fra-til)	1717-26
Antal sider	9
ISSN	0022-0949
DOI	https://doi.org/10.1242/jeb.00352
Status	Udgivet - 2003

Bibliografisk note

Keywords: Acid-Base Equilibrium; Aerobiosis; Anguilla; Animals; Anoxia; Epinephrine; Exertion; Hydrocortisone; Hypercapnia; Models, Biological; Norepinephrine; Oxygen

Adgang til dokumentet

10.1242/jeb.00352

Citationsformater

@article{f5686d00893011dd9c20000ea68e967b,

title = "Tolerance of chronic hypercapnia by the European eel Anguilla anguilla.",

abstract = "European eels were exposed for 6 weeks to water CO(2) partial pressures (P(CO)(2)) from ambient (approx. 0.8 mmHg), through 15+/-1 mmHg and 30+/-1 mmHg to 45+/-1 mmHg in water with a total hardness of 240 mg l(-1) as CaCO(3), pH 8.2, at 23+/-1 degrees C. Arterial plasma P(CO)(2) equilibrated at approximately 2 mmHg above water P(CO)(2) in all groups, and plasma bicarbonate accumulated up to 72 mmol l(-1) in the group at a water P(CO)(2) of 45 mmHg. This was associated with an equimolar loss of plasma Cl(-), which declined to 71 mmol l(-1) at the highest water P(CO)(2). Despite this, extracellular acid-base compensation was incomplete; all hypercapnic groups tolerated chronic extracellular acidoses and reductions in arterial blood O(2) content (Ca(O)(2)), of progressive severity with increasing P(CO)(2). All hypercapnic eels, however, regulated the intracellular pH of heart and white muscle to the same levels as normocapnic animals. Hypercapnia had no effect on such indicators of stress as plasma catecholamine or cortisol levels, plasma osmolality or standard metabolic rate. Furthermore, although Ca(O)(2) was reduced by approximately 50% at the highest P(CO)(2), there was no effect of hypercapnia on the eels' tolerance of hypoxia, aerobic metabolic scope or sustained swimming performance. The results indicate that, at the levels tested, chronic hypercapnia was not a physiological stress for the eel, which can tolerate extracellular acidosis and extremely low Cl(-) levels while compensating tissue intracellular pH, and which can meet the O(2) requirements of routine and active metabolism despite profound hypoxaemia.",

author = "McKenzie, {D J} and M Piccolella and {Dalla Valle}, {A Z} and Taylor, {E W} and Bolis, {C L} and Steffensen, {J F}",

note = "Keywords: Acid-Base Equilibrium; Aerobiosis; Anguilla; Animals; Anoxia; Epinephrine; Exertion; Hydrocortisone; Hypercapnia; Models, Biological; Norepinephrine; Oxygen",

year = "2003",

doi = "10.1242/jeb.00352",

language = "English",

volume = "206",

pages = "1717--26",

journal = "Journal of Experimental Biology",

issn = "0022-0949",

publisher = "The/Company of Biologists Ltd.",

number = "Pt 10",

}

TY - JOUR

T1 - Tolerance of chronic hypercapnia by the European eel Anguilla anguilla.

AU - McKenzie, D J

AU - Piccolella, M

AU - Dalla Valle, A Z

AU - Taylor, E W

AU - Bolis, C L

AU - Steffensen, J F

N1 - Keywords: Acid-Base Equilibrium; Aerobiosis; Anguilla; Animals; Anoxia; Epinephrine; Exertion; Hydrocortisone; Hypercapnia; Models, Biological; Norepinephrine; Oxygen

PY - 2003

Y1 - 2003

N2 - European eels were exposed for 6 weeks to water CO(2) partial pressures (P(CO)(2)) from ambient (approx. 0.8 mmHg), through 15+/-1 mmHg and 30+/-1 mmHg to 45+/-1 mmHg in water with a total hardness of 240 mg l(-1) as CaCO(3), pH 8.2, at 23+/-1 degrees C. Arterial plasma P(CO)(2) equilibrated at approximately 2 mmHg above water P(CO)(2) in all groups, and plasma bicarbonate accumulated up to 72 mmol l(-1) in the group at a water P(CO)(2) of 45 mmHg. This was associated with an equimolar loss of plasma Cl(-), which declined to 71 mmol l(-1) at the highest water P(CO)(2). Despite this, extracellular acid-base compensation was incomplete; all hypercapnic groups tolerated chronic extracellular acidoses and reductions in arterial blood O(2) content (Ca(O)(2)), of progressive severity with increasing P(CO)(2). All hypercapnic eels, however, regulated the intracellular pH of heart and white muscle to the same levels as normocapnic animals. Hypercapnia had no effect on such indicators of stress as plasma catecholamine or cortisol levels, plasma osmolality or standard metabolic rate. Furthermore, although Ca(O)(2) was reduced by approximately 50% at the highest P(CO)(2), there was no effect of hypercapnia on the eels' tolerance of hypoxia, aerobic metabolic scope or sustained swimming performance. The results indicate that, at the levels tested, chronic hypercapnia was not a physiological stress for the eel, which can tolerate extracellular acidosis and extremely low Cl(-) levels while compensating tissue intracellular pH, and which can meet the O(2) requirements of routine and active metabolism despite profound hypoxaemia.

AB - European eels were exposed for 6 weeks to water CO(2) partial pressures (P(CO)(2)) from ambient (approx. 0.8 mmHg), through 15+/-1 mmHg and 30+/-1 mmHg to 45+/-1 mmHg in water with a total hardness of 240 mg l(-1) as CaCO(3), pH 8.2, at 23+/-1 degrees C. Arterial plasma P(CO)(2) equilibrated at approximately 2 mmHg above water P(CO)(2) in all groups, and plasma bicarbonate accumulated up to 72 mmol l(-1) in the group at a water P(CO)(2) of 45 mmHg. This was associated with an equimolar loss of plasma Cl(-), which declined to 71 mmol l(-1) at the highest water P(CO)(2). Despite this, extracellular acid-base compensation was incomplete; all hypercapnic groups tolerated chronic extracellular acidoses and reductions in arterial blood O(2) content (Ca(O)(2)), of progressive severity with increasing P(CO)(2). All hypercapnic eels, however, regulated the intracellular pH of heart and white muscle to the same levels as normocapnic animals. Hypercapnia had no effect on such indicators of stress as plasma catecholamine or cortisol levels, plasma osmolality or standard metabolic rate. Furthermore, although Ca(O)(2) was reduced by approximately 50% at the highest P(CO)(2), there was no effect of hypercapnia on the eels' tolerance of hypoxia, aerobic metabolic scope or sustained swimming performance. The results indicate that, at the levels tested, chronic hypercapnia was not a physiological stress for the eel, which can tolerate extracellular acidosis and extremely low Cl(-) levels while compensating tissue intracellular pH, and which can meet the O(2) requirements of routine and active metabolism despite profound hypoxaemia.

U2 - 10.1242/jeb.00352

DO - 10.1242/jeb.00352

M3 - Journal article

C2 - 12682103

SN - 0022-0949

VL - 206

SP - 1717

EP - 1726

JO - Journal of Experimental Biology

JF - Journal of Experimental Biology

IS - Pt 10

ER -