Abstract
Exposure to chronic sustained hypoxia (SH), as experienced in high altitudes, elicits an increase in ventilation, named ventilatory acclimatization to hypoxia (VAH). We previously showed that rats exposed to short-term (24 h) SH exhibit enhanced abdominal expiratory motor activity at rest, accompanied by augmented baseline sympathetic vasoconstrictor activity. In the present study, we investigated whether the respiratory and sympathetic changes elicited by short-term SH are accompanied by carotid body chemoreceptor sensitization. Juvenile male Holtzman rats (60–80 g) were exposed to SH (10% O2 for 24 h) or normoxia (control) to examine basal and hypoxic-induced ventilatory parameters in unanesthetized conditions, as well as the sensory response of carotid body chemoreceptors in artificially perfused in situ preparations. Under resting conditions (normoxia/normocapnia), SH rats (n = 12) exhibited higher baseline respiratory frequency, tidal volume, and minute ventilation compared to controls (n = 11, P < 0.05). SH group also showed greater hypoxia ventilatory response than control group (P < 0.05). The in situ preparations of SH rats (n = 8) exhibited augmented baseline expiratory and sympathetic activities under normocapnia, with additional bursts in abdominal and thoracic sympathetic nerves during late expiratory phase that were not seen in controls (n = 8, P < 0.05). Interestingly, basal and potassium cyanide-induced afferent activity of carotid sinus nerve (CSN) was similar between SH and control rats. Our findings indicate that the maintenance of elevated resting ventilation, baseline sympathetic overactivity, and enhanced ventilatory responses to hypoxia in rats exposed to 24 h of SH are not dependent on increased basal and sensorial activity of carotid body chemoreceptors.
Highlights
In mammals, a prompt increase in pulmonary ventilation emerges at the onset of hypoxia due to the reduction of arterial partial pressure of oxygen (PO2) and the consequent stimulation of peripheral chemosensitive cells, mainly located in the carotid bodies (Lahiri et al, 2006)
Under resting conditions, rats exposed to short-term sustained hypoxia (SH) (n = 12) exhibited elevated respiratory frequency (109 ± 2 vs. 98 ± 4 cpm, 95% CI: 105–113 vs. 90–107, P = 0.0161; Figure 2A), tidal volume (1.42 ± 0.11 vs. 1.01 ± 0.12 ml. 100 g−1, 95% CI: 1.15–1.68 vs. 0.74–1.28, P = 0.0277; Figure 2B), and minute ventilation (155.0 ± 13.8 vs. 97.9 ± 11.4 ml. 100 g−1.min−1, 95% CI: 124.7–185.5 vs. 72.8–123.1, P = 0.0042; Figure 2C) compared to control rats (n = 11)
We report for the first time that 24 h of SH (10% O2) is able to elevate baseline pulmonary ventilation under normoxic and normocapnic conditions, as well as to potentiate the hypoxic ventilatory response in juvenile rats
Summary
A prompt increase in pulmonary ventilation emerges at the onset of hypoxia due to the reduction of arterial partial pressure of oxygen (PO2) and the consequent stimulation of peripheral chemosensitive cells, mainly located in the carotid bodies (Lahiri et al, 2006). The pFRG neurons are activated when peripheral chemoreceptors are stimulated (Moraes et al, 2012), allowing us to speculate that 24 h of chronic SH may enhance the afferent activity of carotid body chemoreceptors and contribute to stimulate the pFRG neurons under resting conditions Based upon these observations, in the present study we considered the hypothesis that the maintenance of elevated abdominal expiratory motor output and sympathetic activities of rats exposed to chronic SH for 24 h are mainly dependent on baseline and sensory afferent hyperactivity of carotid body peripheral chemoreceptors. In the present study we considered the hypothesis that the maintenance of elevated abdominal expiratory motor output and sympathetic activities of rats exposed to chronic SH for 24 h are mainly dependent on baseline and sensory afferent hyperactivity of carotid body peripheral chemoreceptors To explore this possibility, we examined pulmonary ventilation and body temperature of unanesthetized, SH-conditioned rats under normoxic/normocapnic conditions and during a new challenge of hypoxia. We evaluated basal and hypoxic-induced afferent activity of carotid sinus nerve (CSN) of in situ preparations of rats previously exposed to SH for 24 h
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