Pulmonary mechanical and vascular responses after acute hyperbaric oxygen exposure

Abstract

Pulmonary mechanical and vascular responses were studied in Sprague–Dawley rats exposed to hyperbaric oxygen (HBO, 100% O2 at 2.8 atm (1 atm = 101.325 kPa) for 6 h). Two groups of animals were examined after HBO exposure: group HBO comprised rats examined immediately after exposure and group R consisted of rats left recovering while breathing air for 24 h before being studied. Both groups were compared with control rats, group C, not exposed to HBO. Pulmonary mechanical responses were measured by quantitating static lung compliance (Cs), wet to dry weight ratio (W/D) of lung tissue, and surface tension (ST) of broncho-alveolar lavage as a measurement of lung surfactant. Cs and W/D did not change significantly after exposure to HBO. ST was slightly lower in group R compared with group C (18.46 ± 1.46 vs. 22.47 ± 0.91 dynes/cm (1 dyne = 10 μN); p < 0.05). The effects of HBO on the pulmonary vasculature were studied in an isolated perfused lung preparation. Pulmonary vascular responses to hypoxia were recorded repeatedly over a period of 1 h. The percent increase in pulmonary vascular resistance (PVR) with hypoxia was blunted in group HBO and returned to the normal level in group R (8.2 ± 2.4% in group HBO vs. 44.2 ± 7.2% in group C and 42.9 ± 11.2% in group R; p < 0.001). In a subgroup of rats, to assess the vascular smooth muscle contractility, 0.1 mL of KCl (15 mmol/L) was added to the perfusate and the pulmonary vascular responses were also recorded. The vascular response to KCl was less in group R (86.6 ± 10.1% in R vs. 162.6 ± 12.2% in C and 179.0 ± 23.2% in HBO; p < 0.01). Our study shows that acute HBO exposure induces only minor pulmonary mechanical changes, while pulmonary vascular responses are markedly altered.Key words: hyperbaric oxygen, oxygen toxicity, lung mechanics, surfactant, pulmonary vasculature.