Santiago T V, Edelman N H
J Clin Invest. 1976 Apr;57(4):977-86. doi: 10.1172/JCI108374.
The effects of carbon monoxide on ventilation were studied in unanesthetized goats. Responses to single breaths of 10-25% CO in O2, 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 O2, 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 less than 0.001) beginning 5-6 min after onset of 1% CO in O2 inhalation when COHb saturation reached 50-60%. In eight studies of six animals HCO3- concentration fell (from 21.3 to 15.8 meq/liter; P less than 0.001) and lactate concentration rose (from 2.5 to 4.2 meq/liter; P less than 0.05) in the cisternal cerebrospinal fluid during the CO-induced hyperpnea. Additional studies ruled out ventilatory stimulation from left heart failure or enhanced chemo-sensitivity 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 brain-cerebrospinal fluid acidosis; (c) mobilization of body CO2 stores due to the circulatory response to CO may obscure an initial depression of ventilation by CO.
在未麻醉的山羊身上研究了一氧化碳对通气的影响。对在氧气中单次呼吸10% - 25%一氧化碳的反应，可使碳氧血红蛋白（COHb）迅速从5%升至60%，被认为反映了外周化学感受器介导的反射；而对在氧气中持续吸入1%一氧化碳的反应，可使COHb缓慢从0%升至60%，被认为反映了外周化学感受器和非外周化学感受器机制。在六只山羊中，每只单次呼吸一氧化碳均未引发任何即时通气反应。然而，在同一动物中，当吸入含1%一氧化碳的氧气后，随着碳氧血红蛋白血症缓慢形成，当COHb饱和度达到50% - 60%时，在开始吸入后5 - 6分钟总是引发通气刺激（从平均7.43升/分钟增至16.02升/分钟，P < 0.001）。在对六只动物进行的八项研究中，在一氧化碳诱发的呼吸急促期间，脑池脑脊液中的HCO₃⁻浓度下降（从21.3降至15.8毫当量/升；P < 0.001），乳酸浓度上升（从2.5升至4.2毫当量/升；P < 0.05）。进一步的研究排除了左心衰竭引起的通气刺激或对二氧化碳化学敏感性增强的因素。尽管延迟性呼吸急促与一氧化碳引起的高动力性心血管反应有关，但用普萘洛尔（2毫克/千克）阻断这些循环效应并不能消除延迟性呼吸急促；然而，普萘洛尔确实揭示了在呼吸急促之前存在的通气抑制成分。结论是：（a）吸入一氧化碳后的过度通气不是由颈动脉体介导的；（b）吸入一氧化碳后的延迟性呼吸急促主要是由于脑 - 脑脊液酸中毒；（c）一氧化碳引起的循环反应导致体内二氧化碳储备的调动可能掩盖了一氧化碳对通气的初始抑制作用。
