Evidence for pulmonary CO2 chemosensitivity: effects on ventilation

Abstract

To determine whether there is a pulmonary chemoreceptor for CO2 that influences spontaneous ventilation (VE), we separated the systemic and pulmonary circulations and controlled partial pressure of CO2 (PCO2) independently in each circuit under hyperoxic conditions and measured VE. Dogs were anesthetized with ketamine and maintained with 1% halothane. Systemic venous return was drained from the right atrium and passed through an oxygenator and heat exchanger; blood was returned to the ascending aorta. An identical bypass was established for the pulmonary circulation, draining blood from the left atrium and returning it to the pulmonary artery. The heart was fibrillated; all cannulas were brought through the chest wall; and the median sternotomy was closed. Blood flow through both circuits was maintained at 0.080 l . kg-1 . min-1. Systemic PCO2 (PSCO2) was held constant at three different nonoscillatory levels. At each level, pulmonary PCO2 (PpCO2) was randomly varied between approximately 7 and 85 Torr. With PSCO2 at 43.5 +/- 0.4 Torr, VE increased 2.67 +/- 0.61 l . min-1 as PpCO2 was varied between these limits. With PSCO2 at 63.8 +/- 2.5 Torr, VE increased 3.95 +/- 0.73 l . min-1 over these same limits of PpCO2. With PSCO2 below 25--30 Torr, the dogs were apneic and no longer responded to changes in PpCO2. The effect of PpCO2 on VE was abolished by vagotomy. These results suggest the presence of a CO2 chemoreceptor in the lung that interacts with the nonpulmonary chemoreceptors in the control of VE.

Cardiodynamic factors affecting hyperpnea during steady-state exercise in man.

“…has been suggested that a C02-sensitive chemoreceptor may be present in the lung parenchyma in an isolated preparation of the pulmonary and systemic circulation of dogs (SHELDON and GREEN, 1982). The observed increase in VE was, however, only 75% when pulmonary Pco2 rose to 80 mmHg and arterial Pco2 remained constant.…”

“…The cardiorespiratory variables determined at rest and during direct mechanisms linking Cv~o2 to ventilation, since hitherto no chemoreceptor has been identified anatomically, either on the venous side of the systemic circulation or in the pulmonary circulation, although several investigators suggest such a possibility (SHELDON and GREEN, 1982). JONES et al (1982) found in dogs that right atrium strain caused by an increase in Q correlated linearly with VE.…”

Hypoventilation during Hemodialysis

“…In deed these authors based their conclusions mainly on the observed hyperventilation during dialysis with addition of C 0 2. There is no doubt that any change in C 0 2 tension in the pulmonary circulation can lead to a change in minute ventilation due to the presence of slowly adapting pulmonary chemoreceptors [2].…”

Blood Pressure, Ventilation and Lipid Imbalance during Hemodialysis: Effect of Dialysate Composition

“…A common feature leading to the hypoventilation observed in both settings appears to be related to gaseous CO2 losses across the dialyzer [3,5,41,56,59,60,73,74,77,97,102,103], In the case of acetate dialysis, such intradialytic losses of carbon dioxide may be further compounded by the consumption of carbon dioxide during the metabolism of acetate [5,78,81,92], The actual mcchanism(s) by which CO2 losses could result in hypoventilation, has yet to be clarified. Inactivation of prepulmonary re ceptors by a low venous pCCL is an attractive possibility [79,80], Such a postulate is sup ported by the observation that minimizing gaseous COj losses during either acetate [3, 59, 73, 74. 102] or bicarbonate [3,41,56,60,70,97] dialysis generally prevents the oc currence of hypoventilation.…”