The effect of heat shock on immediate post-preservation lung function

Exposure of animals to transient hyperthermia causes the induction of highly conserved proteins, heat shock proteins (HSPs), which are thought to be cytoprotective against a variety of injuries, including ischemia. We tested the hypothesis that heating donor animals prior to harvest would improve pulmonary preservation. Anaesthetized New Zealand White rabbits underwent radiant heating to 42.5-43.5°C (rectal) 8 h prior to harvest of the lungs. The lungs were harvested without flush and stored for 18 h at 4°C. The left lung was perfused ex vivo with fresh blood for 10 min. Blood gases, pulmonary artery (P(pa)) and airway (P(aw)) pressures, and wet/dry ratios (W/D) were measured. Control animals were treated identically except without heating. All heated animals had HSP72 at lung harvest and 18 h later, whereas no control had detectable levels of HSP72 at either time. In Experiment 1 (n = 12, V(T) 20 ml, F₁O₂ 0.21, 30 bpm, PEEP 0.5 cm H₂O), PO₂ in the heated group was 57.6 ± 7.3 mmHg (mean ± SEM) vs. 51.6 ± 5.7 in the controls (NS). In Experiment 2 (n = 8, V(T) 15 ml, F₁O₂ 0.21, 35 bpm, PEEP 2 cm H₂O), PO₂ of the heated group was 63.5 ± 6.5 vs. 83.1 ± 9.5 in the controls (NS). P(pa) after 10 min was not significantly different in the heated group in Experiment 1 (16.7 ± 0.9 mmHg vs. 24.2 ± 3.7 in controls) or in Experiment 2 (19.5 ± 1.8 vs. 11.3 ± 2.9 in controls). Wet/dry ratios were not different in either Experiment 1 (6.4 ± 0.4 vs. 5.8 ± 0.2 in controls) or Experiment 2 (5.0 ± 0.2 vs. 5.0 ± 0.5). We conclude that heating rabbits leads to the induction of heat shock proteins, but is not beneficial for immediate post-preservation lung function under these conditions.