Abstract
Systemic changes of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), neutrophil elastase (ELT) and myeloperoxidase (MPO) during mechanical ventilation (MV) in horses anaesthetized for surgery are evaluated. Thirty-four client-owned ASA I-II horses randomly received mechanical ventilation (MV) with either a peak inspiratory pressure (PIP) of 30 cm H2O and tidal volume (VT)>10 mL kg-1 (high pressure-volume MV) or PIP of 15 cm H2O and VT ≤ 10 mL kg-1 (low pressure-volume MV) in dorsal or lateral recumbency. Horses were premedicated with acepromazine (0.1 mg kg-1 IM) and xylazine (0.6 mg kg-1 IV), induced with midazolam (0.06 mg kg-1 IV) and ketamine (2.2 mg kg-1 IV) and maintained with isoflurane in oxygen 70% plus ketamine-midazolam infusion (1 and 0.02 mg kg-1 h-1, respectively). Anti-inflammatory drug and antibiotics were administered before surgery. Plasmatic proinflammatory mediator concentrations were estimated by ELISA at the beginning (T0) and after 60 minutes (T1) of MV. Mean plasmatic TNF-α, MPO, and ELT concentrations at T1 were significantly (p<0.05) lower than T0. Mean plasmatic concentration of IL-6 did not significantly change with time. The reduction in plasmatic concentration of proinflammatory mediators at T1 was not linked to ventilation strategy or recumbency. None of the ventilation protocols enhanced systemic inflammatory response during surgery after 1 hour of MV. The anti-inflammatory properties of drugs included in the anaesthesia protocol may have contributed to the overall decreased systemic inflammatory mediator concentrations, despite MV and surgery.
Highlights
Mechanical ventilation (MV) may be responsible for lung damage, a phenomenon referred as ventilator-induced lung injury (VILI)
We investigated the plasmatic change of IL-6, TNF-α, MPO and ELT during mechanical ventilation (MV) in systemically healthy horses anesthetized for surgery
respiratory rate (RR), PaCO2 and end-tidal concentration of CO2 (ETCO2) were significantly higher in low pressure-volume than in high pressurevolume MV, irrespective of recumbency
Summary
Mechanical ventilation (MV) may be responsible for lung damage, a phenomenon referred as ventilator-induced lung injury (VILI). Repeated airway closure and reopening takes place during the tidal cycle when insufficient positive end-expiratory pressure (PEEP) is applied and has been associated with intense shearing forces [4]. PEEP is known to exacerbate the reduction in cardiac output [21] This is largely mediated by a reduction in venous return, stroke volume, and blood pressure associated with positive pressure MV, and should be taken into account whenever PEEP is applied. Increased levels of both IL-6 and TNF-α were found in isolated perfused murine lungs [22] and after in vivo ventilation of healthy rats with 20 mL kg-1 of VT [23]. The aim of the study was to investigate if conventional MV acts as priming insult to trigger an inflammatory
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