Document Detail

Cardiovascular effects of hypercarbia in rainbow trout (Oncorhynchus mykiss): a role for externally oriented chemoreceptors.
MedLine Citation:
PMID:  11104715     Owner:  NLM     Status:  MEDLINE    
In situ and in vivo experiments were performed on rainbow trout (Oncorhynchus mykiss) to examine (i) the direct effect of CO(2) on the systemic vasculature and (ii) the influence of internal versus external hypercapnic acidosis on cardiovascular variables including blood pressure, cardiac output and systemic vascular resistance. Results from in situ saline-perfused trunk preparations indicated that CO(2) (0.6, 1.0 or 2.0% CO(2)) elicited a significant vasodilation, but only in the presence of pre-existing humoral adrenergic tone. In the absence of pre-existing vascular tone, CO(2) was without effect on systemic resistance. In contrast, hypercarbia in vivo triggered a statistically significant increase in systemic resistance (approximately 70 %) that was associated with elevated ventral aortic (approximately 42 %) and dorsal aortic (approximately 43 %) blood pressures and with a significant bradycardia (approximately 12 %); cardiac output was not significantly affected. To determine the potential roles of internal versus external chemoreceptors in mediating the cardiovascular responses to hypercarbia, experiments were performed to elevate the endogenous arterial partial pressure of CO(2) (Pa(CO2)) without an accompanying increase in external P(CO2) (Pw(CO2)). In one series, trout were given a bolus injection of the carbonic anhydrase inhibitor acetazolamide (30 mg kg(-1)) to inhibit CO(2) excretion, and thus raise Pa(CO2), 5-7 h prior to being exposed to an acute increase in Pw(CO2) (maximum Pw(CO2)=6.3+/-0.4 mmHg; 1 mmHg=0.133 kPa). Despite a marked increase in Pa(CO2) (approximately 7 mmHg) after injection of acetazolamide, there was no increase in dorsal aortic blood pressure (P(DA)) or systemic resistance (R(S)). The ensuing exposure to hypercarbia, however, significantly increased P(DA) (by approximately 20 %) and R(S) (by approximately 35 %). A second series of experiments used a 5-7 h period of exposure to hyperoxia (Pw(O2)=643+/-16 mmHg) to establish a new, elevated baseline Pa(CO2) (7.8+/-1.1 mmHg) without any change in Pw(CO2). Despite a steadily increasing Pa(CO2) during the 5-7 h of hyperoxia, there was no associated increase in P(DA) or R(S). Ensuing exposure to hypercarbia, however, significantly increased P(DA) (by approximately 20 %) and R(S) (by approximately 150 %). Plasma adrenaline levels were increased significantly during exposure to hypercarbia and, therefore, probably contributed to the accompanying cardiovascular effects. These findings demonstrate that the cardiovascular effects associated with hypercarbia in rainbow trout are unrelated to any direct constrictory effects of CO(2) on the systemic vasculature and are unlikely to be triggered by activation of internally oriented receptors. Instead, the data suggest that the cardiovascular responses associated with hypercarbia are mediated exclusively by externally oriented chemoreceptors.
J E McKendry; S F Perry
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of experimental biology     Volume:  204     ISSN:  0022-0949     ISO Abbreviation:  J. Exp. Biol.     Publication Date:  2001 Jan 
Date Detail:
Created Date:  2001-01-31     Completed Date:  2001-02-15     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0243705     Medline TA:  J Exp Biol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  115-25     Citation Subset:  IM    
Department of Biology, University of Ottawa, Ottawa, Ontario, Canada K1N 6N5.
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MeSH Terms
Acetazolamide / pharmacology
Blood Pressure
Carbon Dioxide / blood*
Carbonic Anhydrase Inhibitors / pharmacology
Cardiovascular Physiological Phenomena*
Chemoreceptor Cells / physiology*
Epinephrine / blood
Oncorhynchus mykiss / physiology*
Oxygen / blood
Vascular Resistance
Reg. No./Substance:
0/Carbonic Anhydrase Inhibitors; 124-38-9/Carbon Dioxide; 51-43-4/Epinephrine; 59-66-5/Acetazolamide; 7782-44-7/Oxygen

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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