A lowest oxygen level acceptable (LOLA) standard should apply to All ages

A lowest oxygen level acceptable (LOLA) standard should apply to All ages Correspondence | 803 A lowest oxygen level acceptable (LOLA) standard should apply to All ages V. J. Kopp* and M. W. Koenig Chapel Hill, North Carolina, USA *E-mail: vkopp@aims.unc.edu Editor—We appreciate Habre and Petak for addressing age- tensions exceeding the threshold may contribute less to oxygen– related oxygen supplementation in anaesthesia. We write to ATP homeostasis than to pro-oxidant kinetics. Even assuming highlight three issues that they do not address and which we be- being ‘middle age’ confers oxygen resistance greater than that lieve are worthy of all anaesthetists’ attention. mustered by the very young and the very old, the logic of exces- First, ample concern exists about oxygen’s involvement in sive arbitrary oxygen exposure seems unfounded simply on a biological processes outside the anaesthetist’sarena.Lane the- physical chemistry basis. orizes that an uneven continuum exists in susceptibility or re- In summary, Habre and Petak deserve credit for their contri- sistance to oxidative damage due to genetic variability that bution to reassessment of anaesthesia’s ‘oxygen culture’.Like makes it impossible to predict who will be affected by oxidative all drugs, oxygen has specific indications, dosing requirements, stress exposure and when they might be most vulnerable. Non- and toxic potentials. As the most potent drug anaesthetists use, anaesthetists like Gupta and colleagues argue contemporary oxygen use deserves restraint at every age. In this spirit we advo- oxygen research is biased for ‘hypoxia’ and oxidative stress ef- cate adoption of a ‘lowest oxygen level acceptable’ (LOLA) stand- fects over ‘the impact of oxygen on the basic biological processes ard coupled with objective monitoring during anaesthesia and of life such as transcription, DNA replication, cell cycle progres- sedation in any setting. sion, protein folding, apoptosis, senescence, and cellular motil- ity’ that shape health under normal and abnormal conditions. Embedded in their critique is the supposition that patients Declaration of interest exposed to supplemental oxygen experience deviations from None declared. normoxia with potential age-independent consequences. By way of illustration, the example of bone marrow stem cell niche oxygen handling underscores how ‘middle age’ alone References might not confer oxygen resistance at every relevant biological site. 1. Habre W, Petak F. Perioperative use of oxygen: variabilities Second, ‘middle age’ is ill defined in Habre and Petak’s review. across age. Br J Anaesth 2014; 113(Suppl 2): ii2–36 While oxygen use is being re-evaluated in a number of clinical 2. Lane N. A unifying view of ageing and disease: the double- settings, we see oxygen supplementation by anaesthetists dur- agent theory. J Theor Biol 2003; 225: 531–40 ing parturition for ‘non-reassuring foetal status’ as a salient ex- 3. Gupta K, Madan E, Sayyid M, et al. Oxygen regulates molecular ample where ambiguity exists. Here the parturient in ‘middle mechanisms of cancer progression and metastasis. Cancer age’ carries the oxygen-vulnerable foetus. Hamel and colleagues Metastasis Rev 2014; 33: 183–215 suggest insufficient evidence exists to support administering 4. Spencer JA, Ferraro F, Roussakis E, et al. Direct measurement of oxygen to a non-hypoxic mother in order to convert her into an local oxygen concentration in bone marrow of live animals. oxygen conduit for her stressed foetus. They urge ceasing this Nature 2014; 508: 269–73 practice with limited objective efficacy and potential dual harm- 5. O’Driscoll BR, Howard LS, Davison AG. BTS guidelines for fulness until rigorous controlled trials are conducted. emergency oxygen use in adult patients. Thorax 2008; 63 Third, it is known that anaesthesia reduces oxygen consump- (Suppl VI): vi1–68 tion. So, why increase tissue oxygen levels above what is neces- 6. Hamel MS, Anderson BL, Rouse DJ. Oxygen for intrauterine re- sary or can be used? Different anaesthetics disrupt respiratory suscitation: of unproved benefit and potentially harmful. Am J chain function enough to disturb intra-mitochondrial reactive Obstet Gynecol 2014; 211: 124–7 oxygen and nitrogen species (RONS) ecology. A reduction in oxy- 7. Venancio C, Felix L, Almeida V, et al. Acute ketamine gen requirement accompanied by altered RONS ecology can lead impairs mitochondrial function and promotes superoxide to mass action effects engendered by intra-mitochondrial hyper- dismutase activity in rat brain. Anesth Analg 2015; 120: oxia, which can overwhelm antioxidant defences, even briefly, 320–8 and further contribute to baseline oxidative damage. Because 8. Kuper M, Soni NC. Oxygen transfer: cascade or whirlpool? Curr supply limitation thresholds are very low, mitochondrial oxygen Anaesth Crit Care 2003; 14:58–65 doi:10.1093/bja/aev322 Downloaded from https://academic.oup.com/bja/article-abstract/115/5/803/230633 by Ed 'DeepDyve' Gillespie user on 03 February 2018 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png BJA: British Journal of Anaesthesia Oxford University Press

A lowest oxygen level acceptable (LOLA) standard should apply to All ages

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Publisher
Oxford University Press
Copyright
© The Author 2015. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: journals.permissions@oup.com
ISSN
0007-0912
eISSN
1471-6771
D.O.I.
10.1093/bja/aev322
Publisher site
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Abstract

Correspondence | 803 A lowest oxygen level acceptable (LOLA) standard should apply to All ages V. J. Kopp* and M. W. Koenig Chapel Hill, North Carolina, USA *E-mail: vkopp@aims.unc.edu Editor—We appreciate Habre and Petak for addressing age- tensions exceeding the threshold may contribute less to oxygen– related oxygen supplementation in anaesthesia. We write to ATP homeostasis than to pro-oxidant kinetics. Even assuming highlight three issues that they do not address and which we be- being ‘middle age’ confers oxygen resistance greater than that lieve are worthy of all anaesthetists’ attention. mustered by the very young and the very old, the logic of exces- First, ample concern exists about oxygen’s involvement in sive arbitrary oxygen exposure seems unfounded simply on a biological processes outside the anaesthetist’sarena.Lane the- physical chemistry basis. orizes that an uneven continuum exists in susceptibility or re- In summary, Habre and Petak deserve credit for their contri- sistance to oxidative damage due to genetic variability that bution to reassessment of anaesthesia’s ‘oxygen culture’.Like makes it impossible to predict who will be affected by oxidative all drugs, oxygen has specific indications, dosing requirements, stress exposure and when they might be most vulnerable. Non- and toxic potentials. As the most potent drug anaesthetists use, anaesthetists like Gupta and colleagues argue contemporary oxygen use deserves restraint at every age. In this spirit we advo- oxygen research is biased for ‘hypoxia’ and oxidative stress ef- cate adoption of a ‘lowest oxygen level acceptable’ (LOLA) stand- fects over ‘the impact of oxygen on the basic biological processes ard coupled with objective monitoring during anaesthesia and of life such as transcription, DNA replication, cell cycle progres- sedation in any setting. sion, protein folding, apoptosis, senescence, and cellular motil- ity’ that shape health under normal and abnormal conditions. Embedded in their critique is the supposition that patients Declaration of interest exposed to supplemental oxygen experience deviations from None declared. normoxia with potential age-independent consequences. By way of illustration, the example of bone marrow stem cell niche oxygen handling underscores how ‘middle age’ alone References might not confer oxygen resistance at every relevant biological site. 1. Habre W, Petak F. Perioperative use of oxygen: variabilities Second, ‘middle age’ is ill defined in Habre and Petak’s review. across age. Br J Anaesth 2014; 113(Suppl 2): ii2–36 While oxygen use is being re-evaluated in a number of clinical 2. Lane N. A unifying view of ageing and disease: the double- settings, we see oxygen supplementation by anaesthetists dur- agent theory. J Theor Biol 2003; 225: 531–40 ing parturition for ‘non-reassuring foetal status’ as a salient ex- 3. Gupta K, Madan E, Sayyid M, et al. Oxygen regulates molecular ample where ambiguity exists. Here the parturient in ‘middle mechanisms of cancer progression and metastasis. Cancer age’ carries the oxygen-vulnerable foetus. Hamel and colleagues Metastasis Rev 2014; 33: 183–215 suggest insufficient evidence exists to support administering 4. Spencer JA, Ferraro F, Roussakis E, et al. Direct measurement of oxygen to a non-hypoxic mother in order to convert her into an local oxygen concentration in bone marrow of live animals. oxygen conduit for her stressed foetus. They urge ceasing this Nature 2014; 508: 269–73 practice with limited objective efficacy and potential dual harm- 5. O’Driscoll BR, Howard LS, Davison AG. BTS guidelines for fulness until rigorous controlled trials are conducted. emergency oxygen use in adult patients. Thorax 2008; 63 Third, it is known that anaesthesia reduces oxygen consump- (Suppl VI): vi1–68 tion. So, why increase tissue oxygen levels above what is neces- 6. Hamel MS, Anderson BL, Rouse DJ. Oxygen for intrauterine re- sary or can be used? Different anaesthetics disrupt respiratory suscitation: of unproved benefit and potentially harmful. Am J chain function enough to disturb intra-mitochondrial reactive Obstet Gynecol 2014; 211: 124–7 oxygen and nitrogen species (RONS) ecology. A reduction in oxy- 7. Venancio C, Felix L, Almeida V, et al. Acute ketamine gen requirement accompanied by altered RONS ecology can lead impairs mitochondrial function and promotes superoxide to mass action effects engendered by intra-mitochondrial hyper- dismutase activity in rat brain. Anesth Analg 2015; 120: oxia, which can overwhelm antioxidant defences, even briefly, 320–8 and further contribute to baseline oxidative damage. Because 8. Kuper M, Soni NC. Oxygen transfer: cascade or whirlpool? Curr supply limitation thresholds are very low, mitochondrial oxygen Anaesth Crit Care 2003; 14:58–65 doi:10.1093/bja/aev322 Downloaded from https://academic.oup.com/bja/article-abstract/115/5/803/230633 by Ed 'DeepDyve' Gillespie user on 03 February 2018

Journal

BJA: British Journal of AnaesthesiaOxford University Press

Published: Oct 16, 2015

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