Objective: To investigate the diaphragmatic contractile function and mitochondrial ultrastructure in rats with acute lung injury.
Methods: Twenty-eight Sprague-Dawley (SD) rats were allocated randomly into three groups: a control group (n = 10), a lipopolysaccharide (LPS, endotoxins) 4 h group (n =9) and aLPS 24 h group (n =9). Diaphragmatic samples were taken at 4 h and 24 h after 100 microg/kg LPS was instilled into the trachea of the rats. Normal saline (0.5 ml/kg) was instilled in the control group. Then the contractile function of the diaphragmatic samples, including the peak twitch tension, frequency depended force and fatigue index (FI), was tested in vitro. The diaphragmatic ultrastructure was also measured by electron microscopy. SPSS version 15.0 was used for statistical analysis. Data were presented as x +/- s, and means were compared with analysis of variance.
Results: The diaphragmatic force-generating capacity and peak twitch tension in LPS4 h group [(3.4 +/- 1.9); (0.9 +/- 0.4) N/cm2 ] decreased significantly compared to the control group [(6.7 +/- 4.3); (2.2 +/- 1.7) N/cm2, F = 3.59 and 3.78 respectively, P <0.05], but a marked recovery was observed in LPS 24 h group [(4.1 +/- 1.2) and (1.2 +/- 0.7) N/cm), P <0.05]. The FI was also reduced remarkably in LPS 4 h and LPS 24 h adL group (0.07 +/- 0.06; 0.12 +/- 0.07) compared to the control group (0.26 +/- 0.14, F = 9.27, P < 0.01. Ultrastructural examination showed mitochondria derangement at LPS 4 h and LPS 24 h groups, including swollen mitochondria with abnormal cristae, and disrupted external membrane of mitochondria.
Conclusion: Diaphragmatic contractile force-generating capacity decreased remarkably in rats treated with 100 microg/kg LPS, and the diaphragm was susceptible to developing fatigue. These changes may result in respiratory failure.