Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2014;69(5):360-6.
doi: 10.6061/clinics/2014(05)11.

Effect of chronic ethanol exposure on rat ventilatory responses to hypoxia and hypercapnia

Affiliations

Effect of chronic ethanol exposure on rat ventilatory responses to hypoxia and hypercapnia

João Paulo J Sabino et al. Clinics (Sao Paulo). 2014.

Abstract

Objective: The effect of chronic ethanol exposure on chemoreflexes has not been extensively studied in experimental animals. Therefore, this study tested the hypothesis that known ethanol-induced autonomic, neuroendocrine and cardiovascular changes coincide with increased chemoreflex sensitivity, as indicated by increased ventilatory responses to hypoxia and hypercapnia.

Methods: Male Wistar rats were subjected to increasing ethanol concentrations in their drinking water (first week: 5% v/v, second week: 10% v/v, third and fourth weeks: 20% v/v). At the end of each week of ethanol exposure, ventilatory parameters were measured under basal conditions and in response to hypoxia (evaluation of peripheral chemoreflex sensitivity) and hypercapnia (evaluation of central chemoreflex sensitivity).

Results: Decreased respiratory frequency was observed in rats exposed to ethanol from the first until the fourth week, whereas minute ventilation remained unchanged. Moreover, we observed an increased tidal volume in the second through the fourth week of exposure. The minute ventilation responses to hypoxia were attenuated in the first through the third week but remained unchanged during the last week. The respiratory frequency responses to hypoxia in ethanol-exposed rats were attenuated in the second through the third week but remained unchanged in the first and fourth weeks. There was no significant change in tidal volume responses to hypoxia. With regard to hypercapnic responses, no significant changes in ventilatory parameters were observed.

Conclusions: Our data are consistent with the notion that chronic ethanol exposure does not increase peripheral or central chemoreflex sensitivity.

PubMed Disclaimer

Conflict of interest statement

No potential conflict of interest was reported.

Figures

Figure 1
Figure 1
Baseline values of respiratory frequency (f, top), tidal volume (VT, middle) and minute ventilation (VE, bottom) in rats receiving water (control group) or ethanol (ETOH) in increasing concentrations (first week: 5% v/v, second week: 10% v/v, third and fourth weeks: 20% v/v). Values are expressed as the mean±SEM. *, p<0.05 (two-way ANOVA) compared to control rats.
Figure 2
Figure 2
Changes during the first (left panel) and second (right panel) weeks in respiratory frequency (f, top), tidal volume (VT, middle) and minute ventilation (VE, bottom) in response to 10% O2-mediated hypoxia in rats receiving water (control group) or ethanol (ETOH) in increasing concentrations (first week: 5% v/v, second week: 10% v/v, third and fourth weeks: 20% v/v). Values are expressed as the mean±SEM. *, p<0.05 (two-way ANOVA) compared to control rats.
Figure 3
Figure 3
Changes during the third (left panel) and fourth (right panel) weeks in respiratory frequency (f, top), tidal volume (VT, middle) and minute ventilation (VE, bottom) in response to 10% O2-mediated hypoxia in rats receiving water (control group) or ethanol (ETOH) in increasing concentrations (first week: 5% v/v, second week: 10% v/v, third and fourth weeks: 20% v/v). Values are expressed as the mean±SEM. *, p<0.05 (two-way ANOVA) compared to control rats.
Figure 4
Figure 4
Changes during the first (left panel) and second (right panel) weeks in respiratory frequency (f, top), tidal volume (VT, middle) and minute ventilation (VE, bottom) in response to 7% CO2-mediated hypercapnia in rats receiving water (control group) or ethanol (ETOH) in increasing concentrations (first week: 5% v/v, second week: 10% v/v, third and fourth weeks: 20% v/v). Values are expressed as the mean±SEM.
Figure 5
Figure 5
Changes during the third (left panel) and fourth (right panel) weeks in respiratory frequency (f, top), tidal volume (VT, middle) and minute ventilation (VE, bottom) in response to 7% CO2-mediated hypercapnia in rats receiving water (control group) or ethanol (ETOH) in increasing concentrations (first week: 5% v/v, second week: 10% v/v, third and fourth weeks: 20% v/v). Values are expressed as the mean±SEM.

Similar articles

Cited by

References

    1. Clarck LT. Alcohol induced hypertension: mechanisms, complications, and clinical implications. J Natl Med Assoc. 1985;77(5):385–9. - PMC - PubMed
    1. Resstel LB, Tirapelli CR, Lanchote VL, Uyemura AS, De Oliveira AM, Corrêa FM. Chronic ethanol consumption alters cardiovascular functions in conscious rats. Life Sci. 2006;78(19):2179–87. - PubMed
    1. Resstel LB, Scopinho AA, Lopes da Silva A, Antunes-Rodrigues J, Corrêa FM. Increased circulating vasopressin may account for ethanol-induced hypertension in rats. Am J Hypertens. 2008;21(8):930–5. - PubMed
    1. Abdel-Rahman AA, Wooles WR. Ethanol induced hypertension involves impairment of baroreceptors. Hypertension. 1987;10(1):1965–73. - PubMed
    1. Chan TC, Sutter MC. Ethanol consumption and blood pressure. Life Sci. 1983;33(20):1965–73. - PubMed

Publication types

LinkOut - more resources