The effect of bilateral block of vagus and glossopharyngeal nerves on the ventilatory response to CO2 of conscious man

The activity of lung irritant receptors during pneumothorax, hyperpnoea and pulmonary vascular congestion

“…In man bilateral anaesthetization of the vagus and glossopharyngeal nerves approximately halves the ventilatory response to breathing a CO2 in 02 mixture (Guz et al 1966). Thus in both species there can be, in certain experimental conditions, a vagal reflex drive during hypercapnia which potentiates the hyperpnoeic response.…”

“…The hyperpnoea due to severe hypercapnia or asphyxia can be decreased by vagotomy in experimental animals (Scott, 1908;Sasaki, 1927;Wiemer & Kiwull, 1965;Richardson & Widdicombe, 1965 and by vagal blockade in man (Guz, Noble, Widdicombe, Trenchard & Mushin, 1966). A third condition which induces reflex hyperpnoea by a vagal afferent pathway is pulmonary vascular congestion (Schwiegk, 1935;Daly, Luda6ny, Todd & Verney, 1937;Aviado, Li, Kalow, Schmidt, Turnbull, Peskin, Hess & Weiss, 1951;Downing, 1957).…”

On the regulation of depth and rate of breathing

“…The same might also be true for man judging from experiments of Guz, Noble, Widdicombe, Trenchard & Mushin (1966) where the vagus nerves were blocked in human subjects. Volume information from the lungs is known also to play an important role in the adjustment of tidal volume in animals, but its importance for man has been questioned (Campbell, Dickinson, Dinnick & Howell, 1961; Widdicombe, 1961;Guz et al 1966). The nature of this volume feed-back mechanism is not understood, nor is it known whether the difference between man and several other species in this respect reflects a fundamental species difference or is primarily quantitative in nature.…”

Relationship between sensitivity to carbon dioxide and clinical features in patients with chronic airways obstruction

“…Observations in unanaesthetized human subjects are confined to those on one individual (Guz, Noble, Widdicombe, Trenchard, and Mushin, 1966 The interplay between mechanical factors and CO2 sensitivity is also important in determining the resting level of arterial Pco2, although again other ventilatory drives may also be involved. This has been examined by Lane, Howell, and Giblin (1968) No positive correlation emerged between arterial saturation and CO2 sensitivity, although polycythaemia, which is generally thought to be secondary to chronic hypoxia, was seen significantly more often in patients with a reduced sensitivity to CO2.…”