Endotoxemia accelerates diaphragm dysfunction in ventilated rabbits

Ventilators may induce diaphragm dysfunction, and most of the septic population who are admitted to the intensive care unit require mechanical ventilation. However, there is no evidence that sepsis accelerates the onset of ventilator-induced diaphragm dysfunction or affects the microcirculation. Our study investigated whether lipopolysaccharide (LPS)-induced endotoxemia accelerated diaphragm dysfunction in ventilated rabbits by evaluating microcirculation, lipid accumulation, and diaphragm contractility.

After anesthesia and tracheostomy, 25 invasively monitored and mechanically ventilated New Zealand white rabbits were randomized to control (n = 5), controlled mechanical ventilation (CMV) (n = 5), pressure support ventilation (PSV; n = 5), CMV or PSV with LPS-induced endotoxemia (CMV-LPS and PSV-LPS, respectively; n = 5 for each). Rabbits were anesthetized and ventilated for 24 h, except the control rabbits (30 min). Diaphragmatic contractility was evaluated using neuromechanical and neuroventilatory efficiency. We evaluated the following at the end of the protocol: (1) diaphragm microcirculation; (2) lipid accumulation; and (3) diaphragm muscular fibers structure.

Diaphragm contractility, microcirculation, lipid accumulation, and fiber structures were severely compromised in endotoxemic animals after 24 h compared to nonendotoxemic rabbits. Moreover, a slight but significant increase in lipid accumulation was observed in CMV and PSV groups compared with controls (P < 0.05).

Endotoxemia accelerates the diaphragm dysfunction process in ventilated rabbits, affects the microcirculation, and results in diaphragmatic lipid accumulation and contractility impairment.