Tourniquet hyperpnea and its modification by agents which alter cerebral blood flow.

When CO2 is added to the inspired gas of a normal resting subject, the PCO2 of arterial blood rises quickly, but the ventilation rate increases gradually. The lag of ventilation behind change in arterial Pco2 has been ascribed to the time required for the tissues of the respiratory center to come into balance with the altered Pco2 of the perfusing blood (1-3). The response of ventilation to change in arterial Po2 is more prompt, presumably because the peripheral chemoreceptors are more richly perfused (2, 4-7). These relationships have been well established, but there is little information about factors which can affect the rate at which ventilation responds to a bloodborne stimulus. It is possible to produce an abrupt increase in arterial Pco2, as well as other arterial blood changes, by releasing tourniquets which have occluded blood flow through the legs for several minutes (8-11). A few seconds after the rise in arterial PCO2 begins, there is an abrupt increase in ventilation rate (Figure 1). It is found that the time of onset and the magnitude of this ventilation increase can be markedly altered by a variety of procedures which also have the common property of changing the rate of cerebral blood flow. It is, however, difficult to explain all of the observations satisfactorily in terms of our present understanding of the control of ventilation. It is the purpose of this report to present data on the production and modification of tourniquet hyperpnea with particular reference to apparent variations in the stimulus-response time of ventilation, and to speculate on the meaning of these data.