Effects of hypoxemia on phrenic nerve responses to static lung inflation in anesthetized dogs

doi:10.1016/0034-5687(87)90040-5

Respiration Physiology

Volume 67, Issue 2, February 1987, Pages 183-195

Respiration Physiolo...

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Abstract

To study interactions between hypoxemia and lung stretch in modulating ventilatory activity, an experimental preparation was used that allows independent control of static airway pressure (Paw) and arterial P_O₂ in anesthetized dogs. Phrenic burst frequency (f) and integrated amplitude (Phr)_were monitored while Paw was varied between 2 and 12 cm H₂O at levels of Pa_O₂ between 30 and 200 mm Hg. Experiments were repeated in intact (n = 8) and carotid denervated dogs (CBX; n = 7). In intact dogs, f decreased with increasing Paw through an effect on the expiratory duration (Te). Hypoxia increased f by decreasing both the inspiratory duration (Ti)_and (Te). Hypoxia had no effect on the slope of the f vs Paw relationship, but attenuated the effect of Pa on Te. Phr was increased by hypoxia, but Paw had little effect. After CBX, f was still inhibited by Paw, but Pa_O₂ had no consistent effect on f, Ti or Te at any level of Paw. Phr was inhibited by hypoxia after CBX, but Paw had no effect. The results indicate that Paw and Pa_O₂ exert additive effects on f in anesthetized dogs. Hypoxia attenuates the effet of Paw on Te, which alone would attenuate the slope of the f vs Paw relationship. However, the effect of hypoxia on Ti enhances the slope of the f vs Paw relationship, restoring a parallel shift. These effects are abolished by carotid denervation.

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Effects of prolonged inflation on pulmonary stretch receptor discharge in turtles
1989, Respiration Physiology
The tonic and phasic discharge characteristics of single, slowly adapting pulmonary stretch receptors (SAR) were examined before and after 1 h periods of constant pressure inflation to normal resting ( $V_{Lr}, pressure = 0 cm H_{2} O$ ) and elevated ( $V_{Le}, pressure = 10 cm H_{2} O$ ) lung volumes in turtles (Chrysemys sp.). Based on their discharge at V_Lr, SAR were classified as either low (n = 13) or high threshold (n = 4) receptors. Inflations were performed with both air and 5% CO₂ in air. Lung gas composition and arterial P_CO₂ and pH were measured during the maintained inflations. In animals ventilated with air, low and high threshold receptors adapted by 57 and 30% respectively over the first 3 min at V_Le. During the remainder of the 1 h period, the discharge of low threshold SAR fell an additional 20% while that of the high threshold SAR remained relatively constant. There were significant increases in both alveolar and arterial P_CO₂ during the maintained inflations. Ventilation with 5% CO₂ reduced the static discharge levels of low and high threshold SAR by 10 and 25% respectively, suggesting that a part of the apparent adaptation of these receptors to maintained inflation for 1 h with air was due to the accumulation of metabolic CO₂. Following 1 h of maintained inflation, the phasic responses to pump ventilation were decreased in low threshold SAR but remained unchanged in high threshold SAR. The static discharge associated with step inflation was unchanged in both receptor groups. The data suggest that increased SAR discharge is sustained indefinitely during increased lung volume and may account for persistent changes in breathing pattern previously observed during chronic changes in lung volume.
Effects of carotid denervation on interactions between lung inflation and Pa<inf>CO<inf>2</inf></inf> in modulating phrenic activity
1987, Respiration Physiology
Hypercapnia attenuates the effects of static airway pressure (Paw) on phrenic burst frequency (f) and the expiratory duration. We examined the role of carotid chemoreceptors in this response using an experimental preparation that allowed independent control of lung inflation and CO₂ reflexes. Experiments were conducted in intact (n = 6) and carotid denervated (CBX;n = 12) chloralose/urethane anesthetized dogs. Integrated phranic amplitude (Phr), f, and the inspiratory (Ti) and expiratory durations (Te) were measured as a function of Paw (2–12 cm H₂O) at levels of Pa_CO₂ between 30 and 80 mm Hg. In intact dogs: (1) f decreased as Paw increased, and elevated Pa_CO₂ decreased the slope of this relationship; (2) neither Pa_CO₂ nor Paw affected Ti; and (3) Te increased hyperbolically with Paw, and elevated Pa_CO₂ attenuated this relationship. In CBX dogs: (1) f decreased as Paw increased, but this relationship was not affected by Pa_CO₂; (2) Ti increased as Pa_CO₂ increased but was unaffected by Paw; and (3) Te increased as Paw increased but was unaffected by Pa_CO₂. The results indicate that carotid chemoreceptors are necessary in the mechanism whereby hypercapnia attenuates the effects of Paw on f and Te. Furthermore, carotid denervation reveals an effect of hypercapnia on Ti, a effect that is not evident in dogs with functional carotid chemoreceptors.
Phrenic nerve responses to lung inflation and hypercapnia in decerebrate dogs
1990, Pflügers Archiv European Journal of Physiology

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Effects of hypoxemia on phrenic nerve responses to static lung inflation in anesthetized dogs

Abstract

Respir. Physiol.

Respir. Physiol.

Respir. Physiol.

Respir. Physiol.

Respir. Physiol.

Respir. Physiol.

Respir. Physiol.

Studies of the pulmonary vagal control of central respiratory rhythm in the absence of breathing movements

J. Physiol. (London)

Brain hypoxia and control of breathing: neuromechanical control

J. Appl. Physiol.

Effects of lung volume changes on respiratory drive during hypoxia and hypercapnia

J. Appl. Physiol.

Models of respiratory phase switching

Possible alterations in brain monoamine metabolism during hypoxia induced tachypnea in cats

J. Appl. Physiol.

Adaptation of reflex effects of prolonged lunf inflation

J. Appl. Physiol.