Pulmonary apoptosis after supraceliac aorta clamping in a rat model

Lungs are a major target in several models of systemic inflammation. We investigated the effect of gut ischemia reperfusion on lung injury as apoptotic histological changes and pulmonary dysfunction.

Sixteen Wistar male rats were randomized in two equal groups: a control group and a gut ischemia-reperfusion (IR) group for which gut IR was performed by clamping the supraceliac aorta during 40 min. After 60 min of reperfusion, blood gas, bronchoalveolar liquid (BAL) and pulmonary tissue were sampled for measurements. Acidosis status was used to assess the importance of gut IR. Tumor necrosis factor-alpha in the BAL reflected the inflammatory pulmonary response. A terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling method was used to quantify the percentage of apoptotic cells in BAL and to visualize apoptotic cells on tissue samples. Pulmonary dysfunction was assessed by PaO(2) measure.

Gut IR caused an important metabolic acidosis (pH = 7.19 +/- 0.05 versus 7.32 +/- 0.02, P = 0.032 and HCO(3-) = 10.8 +/- 2.54 versus 21.1 +/- 1.72 mmol/L, P = 0.027). At the pulmonary level, there was yet no hypoxemia (paO(2) = 18.1 +/- 1.85 versus 12.3 +/- 1.1 kPa, P = 0.005) but a significant inflammatory response (tumor necrosis factor-alpha in BAL = 7.5 +/- 5 versus 0 pg/mL). The number of apoptotic cell in BAL more than doubled in the gut IR group (51.3 +/- 8 versus 23 +/- 4.3%, P = 0.046). Apoptose involved pneumocytes and bronchiolar epithelial cells.

Our rat models of gut IR induced a significant pulmonary injury characterized by a doubling in apoptotic cells but not yet by a functional pulmonary impairment.