Comments for:

Critical role for CXCR2 and CXCR2 ligands during the pathogenesis of ventilator-induced lung injury

John A. Belperio, … , Roderick J. Phillips, Robert M. Strieter

John A. Belperio, … , Roderick J. Phillips, Robert M. Strieter

Published December 1, 2002
Citation Information: J Clin Invest. 2002;110(11):1703-1716. https://doi.org/10.1172/JCI15849.

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Neutrophils in ventilator-induced lung injury: Is CO2 important?

Submitter: Scott E. Sinclair, M.D. | ssincla1@utmem.edu

University of Tennessee

Published February 10, 2003

I read with great interest the study by Belperio and colleagues in which their well designed experiments revealed the critical role of neutrophils in ventilator-induced lung injury and the mechanisms by which they are recruited in a murine model of high versus low peak pressure ventilation.
In their experimental model, both group were mechanically ventilated at a respiratory rate of 100 breaths per minute and appropriately so. When comparing which ventilation strategy causes the most lung injury, the potential injurious insults (i.e. number of breaths) should be kept equal between experimental groups, as was done in this study. I am concerned, however, that no arterial blood gas values were presented in the paper.
Recent studies have shown that the presence of hypercapnic acidosis can ameliorate the severity of ventilator-induced lung injury in an isolated perfused lung (1) as well as an intact animal model (2) of ventilator-induced lung injury. In the latter study, a significant reduction in neutrophils was observed in the bronchoalveolar lavage fluid of hypercapnic compared to eucapnic subjects both exposed to high tidal volume ventilation. The mechanisms for the potential protective effects of CO2 in critical illness are many (3) and have been the subject of increasing reserarch interest.
Given the 50% reduction in inflation pressure in the low pressure/low stretch group, there is potential for at least relative hypercapnia to develop, which may have contributed to the observed reduction in lung injury in this group. I am aware of the difficulties of routine blood gas analysis in mice given their small circulating blood volume but the potential for CO2 to impact lung injury makes it imperative that they be measured and controlled for in experimental models of injury. I bring this to the authors attention only as a potential confounding factor and do not wish to detract from their excellent study in any way.
1) Broccard AF, Hotchkiss JR, Vannay C, Markert M, Sauty A, Feihl F, Schaller MD. Protective effects of hypercapnic acidosis on ventilator-induced lung injury. Am J Respir Crit Care Med 2001;164:802-806
2) Sinclair SE, Kregnow DA, Lamm WJE, Starr IR, Chi EY, Hlastala MP. Hypercapnic acidosis is protective in an in vivo model of ventilator-induced lung injury. Am J Resp Crit Care Med 2002;166:403-408.
3) Laffey JG and Kavanagh BP. Biological effects of hypercapnia. Intensive Care Med 2000;26:133-138.