@article{
 title = {Tolerance of acute hypercapnic acidosis by the European eel ( Anguilla anguilla).},
 type = {article},
 year = {2002},
 identifiers = {[object Object]},
 keywords = {Acid-Base Equilibrium,Acid-Base Equilibrium: physiology,Acidosis, Respiratory,Acidosis, Respiratory: physiopathology,Anguilla,Anguilla: physiology,Animals,Carbon Dioxide,Carbon Dioxide: blood,Cardiac Output,Cardiac Output: physiology,Europe,Hypercapnia,Hypercapnia: physiopathology,Oxygen,Oxygen Consumption,Oxygen Consumption: physiology,Oxygen: blood,Respiration},
 pages = {339-46},
 volume = {172},
 websites = {http://www.ncbi.nlm.nih.gov/pubmed/12037596},
 month = {5},
 id = {6f71eeeb-8038-3497-ac03-9d133cd961c1},
 created = {2012-12-06T09:13:40.000Z},
 accessed = {2012-11-07},
 file_attached = {true},
 profile_id = {0b777e31-8c9d-39dd-97a3-3e054bd99cfe},
 group_id = {764582e8-5773-3a66-8d6b-9b40e4fb5a88},
 last_modified = {2017-03-14T17:27:14.020Z},
 read = {false},
 starred = {false},
 authored = {false},
 confirmed = {true},
 hidden = {false},
 citation_key = {McKenzie2002},
 abstract = {European eels ( Anguilla anguilla) were exposed sequentially to partial pressures of CO(2) in the water ( PwCO(2)) of 5, 10, 20, 40, 60 then 80 mm Hg (equivalent to 0.66-10.5 kPa), for 30 min at each level. This caused a profound drop in arterial plasma pH, from 7.9 to below 7.2, an increase in arterial PCO(2) from 3.0 mm Hg to 44 mm Hg, and a progressive decline in arterial blood O(2) content (caO(2)) from 10.0% to 1.97% volume. Gill ventilation rate increased significantly at water PwCO(2)s of 10, 20 and 40 mm Hg, followed by a decline at PwCO(2)s of 60 and 80 mm Hg, due to periodic breathing. Mean opercular pressure amplitude increased steadily throughout hypercapnic exposure and was significantly elevated at a PwCO(2) of 80 mm Hg. Hypercapnia caused a tachycardia between PwCO(2)s of 5 mmHg and 10 mm Hg, followed by a progressive decline in heart rate. Cardiac output (CO) remained unchanged throughout, as a consequence of a significant increase in stroke volume at PwCO(2)s of 40, 60 and 80 mm Hg. The eels maintained O(2) uptake at routine normocapnic levels throughout hypercapnic exposure. A comparison of the rates of blood O(2) delivery (calculated from CO and caO(2)) against O(2) consumption at PwCO(2)s of 60 mm Hg and 80 mm Hg indicated that a portion of O(2) uptake was due to cutaneous respiration. Thus, the European eel's exceptional tolerance of acute hypercapnia is probably a consequence of the tolerance of its heart to acidosis and hypoxia, and a contribution to O(2) uptake from cutaneous respiration.},
 bibtype = {article},
 author = {McKenzie, D J and Taylor, E W and Dalla Valle, a Z and Steffensen, J F},
 journal = {Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology},
 number = {4}
}

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This caused a profound drop in arterial plasma pH, from 7.9 to below 7.2, an increase in arterial PCO(2) from 3.0 mm Hg to 44 mm Hg, and a progressive decline in arterial blood O(2) content (caO(2)) from 10.0% to 1.97% volume. Gill ventilation rate increased significantly at water PwCO(2)s of 10, 20 and 40 mm Hg, followed by a decline at PwCO(2)s of 60 and 80 mm Hg, due to periodic breathing. Mean opercular pressure amplitude increased steadily throughout hypercapnic exposure and was significantly elevated at a PwCO(2) of 80 mm Hg. Hypercapnia caused a tachycardia between PwCO(2)s of 5 mmHg and 10 mm Hg, followed by a progressive decline in heart rate. Cardiac output (CO) remained unchanged throughout, as a consequence of a significant increase in stroke volume at PwCO(2)s of 40, 60 and 80 mm Hg. The eels maintained O(2) uptake at routine normocapnic levels throughout hypercapnic exposure. A comparison of the rates of blood O(2) delivery (calculated from CO and caO(2)) against O(2) consumption at PwCO(2)s of 60 mm Hg and 80 mm Hg indicated that a portion of O(2) uptake was due to cutaneous respiration. Thus, the European eel's exceptional tolerance of acute hypercapnia is probably a consequence of the tolerance of its heart to acidosis and hypoxia, and a contribution to O(2) uptake from cutaneous respiration.","bibtype":"article","author":"McKenzie, D J and Taylor, E W and Dalla Valle, a Z and Steffensen, J F","journal":"Journal of comparative physiology. 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