Ventilatory response to high inspired carbon dioxide concentrations in anesthetized dogs

Abstract

Background:The ventilation ( ) response to inspired CO2 has been extensively studied, but rarely with concentrations >10%.Aims:These experiments were performed to determine whether would increase correspondingly to higher concentrations and according to conventional chemoreceptor time delays.Materials and Methods:We exposed anesthetized dogs acutely, with and without vagotomy and electrical stimulation of the right vagus, to 20-100% CO2-balance O2 and to 0 and 10% O2-balance N2.Results:The time delays decreased and response magnitude increased with increasing concentrations (p<0.01), but at higher concentrations the time delays were shorter than expected, i.e., 0.5 s to double at 100% CO2, with the response to 0% O2 being ~3 s slower. Right vagotomy significantly reduced baseline breathing frequency (fR), increased tidal volume (VT) and increased the time delay by ~3 s. Bilateral vagotomy further reduced baseline fR and , and reduced the response to CO2 and increased the time delay by ~12 s. Electro-stimulation of the peripheral right vagus while inspiring CO2 caused a 13 s asystole and further reduced and delayed the response, especially after bilateral vagotomy, shifting the mode from VT to fR.Conclusions:Results indicate that airway or lung receptors responded to the rapid increase in lung H+ and that vagal afferents and unimpaired circulation seem necessary for the initial rapid response to high CO2 concentrations by receptors upstream from the aortic bodies.

Isocitrate supplementation promotes breathing generation, gasping, and autoresuscitation in neonatal mice

“…Examples of such compensatory changes are common in the literature in response to pharmacological, surgical, or behavioral conditions (Foster et al, 1983; Spahija and Grassino, ; Abbott et al, ). The fact that the same effects observed after the injection of isocitrate in vivo are produced by rather diverse experimental conditions such as vagotomy (Kashani and Haig, 1975; Gratz, ; Martin‐Body and Sinclair, ; Loeppky and Risling, ); inhalation of diethyl ether, trichlorethylene, or halothane (Katz and Ngai, ; Ngai et al, ); or application of opiod‐like compounds such as methadone, dermorphin, morphine, and oxycodone (Vonhof and Siren, ; Leino et al, ; Colman and Miller, ; Lewanowitsch et al, ), clearly indicates that attributing such effects to a single cellular process or neural network is not possible. These observations make the in vitro preparation a very reliable approximation for understanding the mechanism at the level of isolated neural networks; however, it requires validation in a more complex, but more real, scenario found under in vivo conditions.…”

and T1 assessment of abdominal tissue response to graded hypoxia and hypercapnia using a controlled gas mixing circuit for small animals

“…1,2 The state of hypercapnia is associated with a number of symptoms, including shortness of breath, an elevated heart rate and blood pressure, 3,4 and hyperventilation. 5 However, hypercapnia can also be used as a stimulus for probing the health of the cerebral vasculature. This technique, known as a gas challenge, alters the inspired level of CO 2 and relies on the vasodilatory effect of CO 2 to determine the extent to which the cerebral vascular response is affected in both healthy and diseased states.…”