Acute intermittent hypoxia evokes ventilatory long-term facilitation and active expiration in unanesthetized rats

Author(s)

Mendonca-Junior, Bolival A. ^[1] ; Fernandes, V, Marcos ; Zoccal, Daniel B. ^[2]

Affiliation

^[1] Sao Paulo State Univ, Sch Dent Araraquara, Dept Physiol & Pathol, UNESP, Rua Humaita 1680, BR-14801903 Araraquara, SP - Brazil

^[2] Fernandes, Marcos, V, Sao Paulo State Univ, Sch Dent Araraquara, Dept Physiol & Pathol, UNESP, Rua Humaita 1680, BR-14801903 Araraquara, SP - Brazil

• Document type: Journal article
• Source: Respiratory Physiology & Neurobiology; v. 294, DEC 2021.
• Web of Science Citations: 0

Abstract

Acute intermittent hypoxia (AIH) modifies the functioning of the respiratory network, causing respiratory motor facilitation in anesthetized animals and a compensatory increase in pulmonary ventilation in freely behaving animals. However, it is still unclear whether the ventilatory facilitation induced by AIH in unanesthetized animals is associated with changes in the respiratory pattern. We found that Holtzman male rats (80-150 g) exposed to AIH (10 x 6% O2 for 30-40 s every 5 min, n = 9) exhibited a prolonged (30 min) increase in baseline minute ventilation (P < 0.05) compared to control animals (n = 13), combined with the occurrence of late expiratory peak flow events, suggesting the presence of active expiration. The increase in ventilation after AIH was also accompanied by reductions in arterial CO2 and body temperature (n = 5-6, P < 0.05). The systemic treatment with ketanserin (a 5-HT2 receptor antagonist) before AIH prevented the changes in ventilation and active expiration (n = 11) but potentiated the hypothermic response (n = 5, P < 0.05) when compared to appropriate control rats (n = 13). Our findings indicate that the ventilatory long-term facilitation elicited by AIH exposure in unanesthetized rats is linked to the generation of active expiration by mechanisms that may depend on the activation of serotonin receptors. In contrast, the decrease in body temperature induced by AIH may not require 5-HT2 receptor activation. (AU)

• FAPESP's process: 13/17251-6 - Neural mechanisms generating the respiratory pattern and the respiratory-sympathetic coupling in conditions of hypoxia
• Grantee: Daniel Breseghello Zoccal
• Support Opportunities: Research Grants - Young Investigators Grants
• FAPESP's process: 18/21000-2 - Ionic mechanisms underlying the ATP-mediated respiratory stimulation: understanding the interaction between central oxygen sensors and rhythm-generating neurons
• Grantee: Daniel Breseghello Zoccal
• Support Opportunities: Scholarships abroad - Research