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Mechanical ventilation of healthy rats suppresses peripheral immune function

¹ Paediatric Intensive Care Unit, and ² Laboratory for Psychoneuroimmunology, University Medical Centre, Utrecht, ³ Paediatric Intensive Care Unit, VU Medical Centre, Amsterdam, and ⁴ Dept of Anaesthesiology, Erasmus MC-Faculty, Rotterdam, the Netherlands

CORRESPONDENCE: A.J. van Vught, Paediatric Intensive Care Unit, University Medical Centre Utrecht, KG.02.307.0, Lundlaan 6, 3584 EA Utrecht, The Netherlands. Fax: 31 302505340. E-mail: a.vanvught@wkz.azu.nl

Keywords: cytokine production, mechanical ventilation, mitogen-induced splenocyte proliferation, natural killer cell activity, rat, ventilator-induced lung injury

Received: March 28, 2003
Accepted July 21, 2003

This study was financially supported by the "Catharne Stichting Utrecht".

This study was designed to investigate the possible effect of injurious mechanical ventilation on peripheral immune function of healthy rats. Three ventilation strategies were compared: 1) low peak inspiratory pressure (PIP)/positive end-expiratory pressure (PEEP); 2) high PIP/PEEP; and 3) high PIP/zero PEEP (ZEEP). As a reference group, healthy, nonventilated, sham-operated, anaesthetised rats were used.

After 4 h, rats were sacrificed and macrophage inflammatory protein (MIP)-2 levels in lung and plasma were determined. Peripheral immune function was determined by measurement of splenic natural killer (NK) activity, mitogen-induced splenocyte proliferation and in vitro cytokine production. All immune measurements in the low PIP/PEEP group did not differ from the immune measurements in the reference group. High PIP strategies, irrespective of applied PEEP, enhanced MIP-2 levels in lung and plasma.

NK cell activity, mitogen-induced splenocyte proliferation and MIP-2 and interleukin (IL)-10 production significantly decreased after high PIP/PEEP ventilation. In the high PIP/ZEEP-ventilated group, the decrease in splenocyte proliferation, MIP-2 and IL-10 production and NK cell activity was more pronounced and interferon- production was also significantly lower than in the low PIP/PEEP group.

These data show that high positive inspiratory pressure ventilation induces an inflammatory response in the lung, whereas at the same time the peripheral immune response is downregulated. Ventilator-induced peripheral immune suppression may contribute to poor outcome in acute respiratory distress syndrome patients.

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