Abstract
BackgroundCarotid body O2-chemosensitivity determines the hypoxic ventilatory response (HVR) as part of crucial regulatory reflex within oxygen homeostasis. Nicotine has been suggested to attenuate HVR in neonates of smoking mothers. However, whether smoking affects HVR in adulthood has remained unclear and probably blurred by acute ventilatory stimulation through cigarette smoke. We hypothesized that HVR is substantially reduced in smokers when studied after an overnight abstinence from cigarettes i.e. after nicotine elimination.MethodsWe therefore determined the isocapnic HVR of 23 healthy male smokers (age 33.9 ± 2.0 years, BMI 24.2 ± 0.5 kg m−2, mean ± SEM) with a smoking history of >8 years after 12 h of abstinence and compared it to that of 23 healthy male non-smokers matched for age and BMI.ResultsSmokers and non-smokers were comparable with regard to factors known to affect isocapnic HVR such as plasma levels of glucose and thiols as well as intracellular levels of glutathione in blood mononuclear cells. As a new finding, abstinent smokers had a significantly lower isocapnic HVR (0.024 ± 0.002 vs. 0.037 ± 0.003 l min−1 %−1BMI−1, P = 0.002) compared to non-smokers. However, upon re-exposure to cigarettes the smokers’ HVR increased immediately to the non-smokers’ level.ConclusionsThis is the first report of a substantial HVR reduction in abstinent adult smokers which appears to be masked by daily smoking routine and may therefore have been previously overlooked. A low HVR may be suggested as a novel link between smoking and aggravated hypoxemia during sleep especially in relevant clinical conditions such as COPD.Electronic supplementary materialThe online version of this article (doi:10.1186/s12890-016-0323-0) contains supplementary material, which is available to authorized users.
Highlights
Carotid body O2-chemosensitivity determines the hypoxic ventilatory response (HVR) as part of crucial regulatory reflex within oxygen homeostasis
Evidence for an impaired chemoreceptor O2-sensing through nicotine exposure appears to be preliminary and restricted to studies in infants of smoking mothers in the context of sudden infant death: Healthy, ≤3 months old, term or preterm infants exposed to maternal cigarette smoking/nicotine revealed a weakened HVR and awakening response [18, 24, 25]
Large reduction of isocapnic HVR in healthy male adult SM compared to NSM, which was virtually completely masked by acute enhancement through smoking a single cigarette
Summary
Carotid body O2-chemosensitivity determines the hypoxic ventilatory response (HVR) as part of crucial regulatory reflex within oxygen homeostasis. Whether smoking affects HVR in adulthood has remained unclear and probably blurred by acute ventilatory stimulation through cigarette smoke. Evidence for an impaired chemoreceptor O2-sensing through nicotine exposure appears to be preliminary and restricted to studies in infants of smoking mothers in the context of sudden infant death: Healthy, ≤3 months old, term or preterm infants exposed to maternal cigarette smoking/nicotine revealed a weakened (poikilocapnic) HVR and awakening response [18, 24, 25]. One earlier study by Kawakami et al [26] in smokers (SM) and their non-smoking (NSM) homozygote twins failed to demonstrate a smokingrelated HVR attenuation after a 3-h-abstinence which is insufficient to eliminate nicotine with an in-vivo half-life of 2 h, as already speculated by these authors themselves. Subsequent studies, including one from the same group, have shown an acute HVR-increase through smoking in both, SM and NSM probably mediated through carotid chemoreceptors [27,28,29,30] which might have masked a possible HVR attenuation in the elegant study by Kawakami et al [26] in twins
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