Bosentan prevents hypoxia-reoxygenation–induced pulmonary hypertension and improves pulmonary function Jeffrey M Pearl, MD, Scott A Wellmann, MD, Jerri.

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Bosentan prevents hypoxia-reoxygenation–induced pulmonary hypertension and improves pulmonary function Jeffrey M Pearl, MD, Scott A Wellmann, MD, Jerri L McNamara, John P Lombardi, Connie J Wagner, BS, Jenni L Raake, David P Nelson, MD The Annals of Thoracic Surgery Volume 68, Issue 5, Pages 1714-1721 (November 1999) DOI: 10.1016/S0003-4975(99)00988-1

Fig 1 Pulmonary vascular resistance rapidly increased in the onset of hypoxia in both groups. However, pulmonary vascular resistance began to decrease by 30 minutes of hypoxia in the Bosentan-treated animals and remained lower than controls at all time points thereafter. ∗p < 0.05 Bosentan versus controls. The Annals of Thoracic Surgery 1999 68, 1714-1721DOI: (10.1016/S0003-4975(99)00988-1)

Fig 2 Mean pulmonary arterial pressures doubled by 30 minutes of hypoxia in the controls. Animals treated with Bosentan throughout hypoxia and recovery had lower mean pulmonary arterial pressure than controls at 30 minutes and later. ∗p < 0.05 Bosentan versus controls. The Annals of Thoracic Surgery 1999 68, 1714-1721DOI: (10.1016/S0003-4975(99)00988-1)

Fig 3 (Top) Endothelin-1 levels in the treated group rapidly increased after the administration of Bosentan because of the release of receptor-bound ET-1. (Bottom) Arterial endothelin-1 increased only slightly in control animals during hypoxia but increased more dramatically after reoxygenation. ∗p < 0.05 Bosentan versus controls; ‡p < 0.05 time point versus baseline. The Annals of Thoracic Surgery 1999 68, 1714-1721DOI: (10.1016/S0003-4975(99)00988-1)

Fig 4 Pulmonary tissue endothelin-1 levels did not change during hypoxia and reoxygenation in controls. These levels correlated with increased pulmonary vascular resistance and lung injury. In contrast, endothelin-1 levels decreased in the Bosentan-treated animals during hypoxia and reoxygenation because of the release of receptor-bound endothelin-1 by Bosentan. ∗p < 0.05 Bosentan versus controls; ∗∗p < 0.005 Bosentan versus controls; ‡p < 0.005 time point versus baseline. The Annals of Thoracic Surgery 1999 68, 1714-1721DOI: (10.1016/S0003-4975(99)00988-1)

Fig 5 Arterial nitric oxide levels, measured as nitrite, decreased 50% in control animals during hypoxia and slowly returned to baseline by end-recovery. Animals treated with Bosentan maintained nitric oxide levels throughout hypoxia and reoxygenation. ∗p < 0.005 Bosentan versus controls; ‡p < 0.005 time point versus baseline. The Annals of Thoracic Surgery 1999 68, 1714-1721DOI: (10.1016/S0003-4975(99)00988-1)

Fig 6 Pulmonary myeloperoxidase activity increased after reoxygenation in controls but not in Bosentan-treated animals, despite higher baseline values in the Bosentan group. End-recovery myeloperoxidase activity was higher in the controls than in the Bosentan group, suggesting increased leukocyte activity in the control group. ∗p < 0.05 Bosentan versus controls; ‡p < 0.005 time point versus baseline. The Annals of Thoracic Surgery 1999 68, 1714-1721DOI: (10.1016/S0003-4975(99)00988-1)

Fig 7 Pulmonary tissue lipid peroxidase activity was higher than baseline and end-hypoxia levels after reoxygenation in control animals. In contrast, there was a trend for lipid peroxidase levels to decrease in the Bosentan group at end-hypoxia and end-recovery. At end-recovery lipid peroxidase levels were greater in controls than in Bosentan-treated animals. ∗p < 0.05 Bosentan versus controls; ‡p < 0.005 time point versus baseline. The Annals of Thoracic Surgery 1999 68, 1714-1721DOI: (10.1016/S0003-4975(99)00988-1)

Fig 8 Total lung water, determined by the wet:dry tissue ratio, was increased over baseline at end-recovery in control animals. The lung wet:dry ratio of the Bosentan-treated animals was lower than that in controls at end-recovery and did not differ from baseline. ∗p < 0.05 Bosentan versus controls; ‡p < 0.05 time point versus baseline. The Annals of Thoracic Surgery 1999 68, 1714-1721DOI: (10.1016/S0003-4975(99)00988-1)

Fig 9 Alveolar-arterial (A-a) gradient was increased above baseline at end-recovery in both groups. In addition, the A-a gradient of the Bosentan-treated animals was lower than control animals at end-recovery. ∗p < 0.05 Bosentan versus controls; ‡p < 0.005 time point versus baseline. The Annals of Thoracic Surgery 1999 68, 1714-1721DOI: (10.1016/S0003-4975(99)00988-1)

Fig 10 Inspiratory airway resistance increased during hypoxia in both treatment groups, although less dramatically in the animals treated with Bosentan. The airway resistance returned to baseline levels by end-recovery in the Bosentan-treated group but remained elevated in the controls. ∗p < 0.05 Bosentan versus controls; ‡p < 0.05 time point versus baseline. The Annals of Thoracic Surgery 1999 68, 1714-1721DOI: (10.1016/S0003-4975(99)00988-1)