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Mechanical ventilation (MV) with high tidal volumes (Vt) leads to enormous biophysical lung damage, both in patients and in experimental animal models. From a biological point of view, however, the inflammatory response triggered by high Vt-MV and its association with the development of multisystem organ failure is still under study.
Based on an acute model (3 hr) of MV with high Vt in rats, we intend to characterize the clinical and histopathological pattern of cardiac injury resulting from injurious MV.
8 male Wistar rats were mechanically ventilated during an initial stabilization period of 20 min with Vt = 8 ml/kg, PEEP = 5 cmH2O and FiO2 = 0.4, followed by Vt = 25 ml/kg and ZEEP for 3 hr (HVt group). A sham group (n = 6) was maintained with spontaneous ventilation during the same period. Arterial blood gases, mean arterial pressure (MAP) and lung weight gain were measured. Lung injury (ATS score) and pathology of the apex was evaluated histologically. The data were analysed by t-test (* p < 0.05).
No statistically significant changes were observed in hemodynamic and respiratory oxygenation between groups. The HVt group showed pulmonary oedema, worsening of the pulmonary histological consisting in benign vascular damage, and myocyte injury. (Table (Table11)
Under these experimental conditions, animals ventilated with high Vt had pulmonary oedema and worsening of ATS score, associated to cardiac structural changes compatible with myositis and necrosis.