Dynamics of brain extracellular fluid pH and phrenic nerve activity in cats after end-tidal CO2 forcing

Section: Introductionmentioning

confidence: 75%

Differential effects of carbon dioxide and pH on central chemoreceptors in the rat in vitro.

Harada¹,

Kuno²,

Wang³

1985

“…In cats there is evidence of considerable neuronal dynamics in the ventilatory response to changes in PETC0, (Teppema, Vis, Evers & Folgering, 1982). Our empirical two-compartment model leads to the conclusion, provided the central time constant does not change appreciably with cerebral blood flow, that in a rebreathing experiment the steady-state CO2 sensitivity should be obtained.…”

Section: Comparison With the Rebreathing Methods In The Humanmentioning

confidence: 86%

A pseudo‐rebreathing technique for assessing the ventilatory response to carbon dioxide in cats.

Berkenbosch¹,

DeGoede²,

Olievier³

et al. 1986

SUMMARY1. The ventilatory sensitivity to CO2 obtained from a non-steady-state step-ramp CO2 challenge (analogous to the Read rebreathing method) was compared with the one of the steady-state method.2. Experiments were performed during normoxia on twenty cats anaesthetized with chloralose-urethane. In eight of these cats additional measurements were carried out during metabolic acidosis and alkalosis.3. The slope of the non-steady-state ventilatory response curve to CO2 was not significantly different from the steady-state one only if the ratio of the step-wise increase in end-tidal PCO2 (PET,Co2) (A) above its resting value and the subsequent rate ofrise of the PET, C02 (R) was equal to the time constant ofthe central chemoreflex pathway (,r). This also held true during metabolic acidosis and alkalosis.4. It is predicted that in human beings during hyperoxia the ventilatory response line obtained with Read's rebreathing method is to a fair approximation shifted to the right by a value of A with respect to the steady-state response line, provided A/R = rC 5. We argue that Read's prescription that a PETC02 equilibrium should be established between mixed venous blood, arterial blood and end-tidal gas has to be regarded as an experimental condition leading to stable experiments rather than dictated by physiological mechanisms.

“…It is usually assumed that the central chemoreceptors react instantaneously to the neighbouring tissue Pco2 In that case the dynamics of the central ventilatory response to changes in PET, co2 are governed by the loading and unloading of a brain compartment, which in its turn is essentially determined by the cerebral blood flow. The rate of the central respiratory response may also be modulated by central neuronal dynamics as reported in adult cats (Teppema, Vis, Evers & Folgering, 1982;Wagner & Eldridge, 1991). Although Lawson & Long (1984) reported an after-discharge phenomenon by electrically stimulating the cut sinus nerve in the newborn piglet, it is not known to what extent this mechanism would influence the dynamics of the central ventilatory response.…”

Section: Discussionmentioning

confidence: 98%

The effects of hypoxia on the ventilatory response to sudden changes in CO2 in newborn piglets.

Wolsink

Berkenbosch

DeGoede

et al. 1992

SUMMARY1. The ventilatory response to square-wave challenges in end-tidal partial pressure of CO2 (Pc02) was investigated at three levels of arterial Po0 (Pa°2) in nineteen anaesthetized 2-to 11-day-old piglets.2. The ventilatory responses, measured on a breath-to-breath basis, were separated into a peripheral and a central component using a two-compartment model. Both components were described by a CO2 sensitivity, a time constant, a time delay and a single offset.3. Fifty-six responses were analysed against a background ofnormoxaemia (Pa°2 = 12 70 +0O72 kPa, mean + S.D.), fifty-three against a background of moderate hypoxaemia (Pao = 8-63 +034 kPa) and fifty-one against a background of severe hypoxaemia (Pa,02 = 4-98 +030 kPa).4. The sensitivity of the peripheral chemoreceptors in mediating the response to C02 increased from 38-3 + 17-0 ml min-kPa-1 kg-1 during normoxaemia to 48-8 + 15-3 ml min-kPa-1 kg-' during moderate hypoxaemia and to 72-9 + 24-0 ml min-1 kPa-1 kg-1 at severe hypoxaemia.5. As compared with the central CO2 sensitivity during moderate hypoxaemia and normoxaemia (1040± 39-0 and 1008 + 41 6 ml min' kPa-1 kg-', respectively) it decreased to 85 9 + 54-1 ml min-' kPa-1 kg-1 at severe hypoxaemia. 6. We conclude that in newborn piglets there is a positive interaction between hypoxia and hypercapnia at the level of the peripheral chemoreceptors while severe hypoxaemia reduced the C02 sensitivity centrally.