Mechanism of the ventilatory response to carbon monoxide.

Abstract

A B S T R A C T The effects of carbon monoxide on ventilation were studied in unanesthetized goats. Responses to single breaths of 10-25% CO in 02, which rapidly raised carboxyhemoglobin (COHb) from 5 to 60%, were considered to reflect peripheral chemoreceptor-mediated reflexes whereas responses to continuous inhalation of 1% CO in 02, which slowly raised COHb from 0 to 60%, were considered to reflect both peripheral chemoreceptor and nonperipheral chemoreceptor mechanisms. In each of six goats, single breaths of CO failed to elicit any immediate ventilatory response.However, slow buildup of carboxyhemoglobinemia in the same animals always elicited ventilatory stimulation (from a mean of 7.43 to 16.02 liter/min, P < 0.001) beginning 5-6 min after onset of 1% CO in 02 inhalation when COHb saturation reached 50-60%. In eight studies of six animals HCOs-concentration fell (from 21.3 to 15.8 meq/liter; P <0.001) and lactate concentration rose (from 2.5 to 4.2 meq/liter; P < 0.05) in the cisternal cerebrospinal fluid during the CO-induced hyperpnea. Additional studies ruled out ventilatory stimulation from left heart failure or enhanced chemosensitivity to carbon dioxide. Although the delayed hyperpnea was associated with a hyperdynamic cardiovascular response to CO, blockade of these circulatory effects with propranolol (2 mg/kg) failed to abolish the delayed hyperpnea; however, the propranolol did unmask an element of ventilatory depression which preceded the hyperpnea. Conclusions were: (a) hyperventilation in response to CO inhalation is not mediated by the carotid bodies; (b) the delayed hyperpnea in response to CO inhalation is primarily due to braincerebrospinal fluid acidosis; (c) mobilization of body CO2 stores due to the circulatory response to CO may obscure an initial depression of ventilation by CO. INTRODUCTIONThe increase in ventilation caused by reduction in arterial 02 tension is well known and clearly ascribed

Mechanisms of hypoxia‐induced periodic breathing during sleep in humans.

“…sleep, the possibility exists that a direct effect of hypoxia on the central nervous system (Santiago & Edelman, 1976;Gautier & Bonora, 1980) or an effect of hypoxia and/or hypocapnia on upper airway resistance (England, Bartlett & Knuth, 1982) may also exert an influence on hypoxia-induced periodic breathing.…”

A mathematical model of ventilation response to inhaled carbon monoxide

“…Researchers at the Rutgers Medical School have provided the most complete set of data describing the ventilatory and blood chemistry response to acute exposures of carbon monoxide (19,50). Unanesthetized goats were exposed to single breaths of carbon monoxide, as well as continuous inhalation.…”

“…In transient breathing tests, animals were exposed to 40% oxygen and then one or more breaths of either pure nitrogen or 1-2.5% carbon monoxide (50). The changes in ventilation and arterial oxygen saturation were recorded.…”

“…Total ventilation demonstrates a rapid ventilatory depression following the hyperventilation peak. Although this behavior was not included in the quantitative data reported, it was mentioned as occurring in all goat studies (50) and was the overwhelming response to central lactic acidosis seen in cats (43).…”

“…We assume that flow to the tissues remains constant, but that blood flow to the brain increases during hypoxia, based on the data of Ref. 50, shown in Fig. 2A.…”