Background: Levosimendan was hypothesized to attenuate hypoxic pulmonary vasoconstriction (HPV).
Methods: Fourteen anaesthetized pigs (30.9 ± 1.0 kg) were studied in normoxia (FiO₂∼0.21) and hypoxia (FiO₂∼0.10), before and 10-90 minutes after infusion of placebo (n = 7) or levosimendan (n = 7).
Results: Compared with normoxia, hypoxia baseline at FiO₂∼0.10 (n = 14) increased pulmonary vascular resistance (PVR) by 1.9 ± 0.4 Wood Units (WU) (P < 0.001), mean pulmonary artery pressure (MPAP) by 14.3 ± 0.9 mm Hg (P < 0.001), mean right atrial pressure (MRAP) by 2.1 ± 0.4 mm Hg (P < 0.001), pulmonary capillary wedge pressure (PCWP) by 1.5 ± 0.3 mm Hg (P < 0.001), cardiac output (CO) by 1.3 ± 0.2 L/minute (P < 0.001) and heart rate (HR) by 19.9 ± 5.5 beats·per minute (P < 0.001). Systemic vascular resistance (SVR) decreased by 7.2 ± 1.0 WU (P < 0.001), MAP and stroke volume (SV) remained unaltered (P = ns). Compared with hypoxia baseline, levosimendan decreased MPAP and PVR (P < 0.05), by approximately 9% and 19%, respectively, plateauing between 10 and 90 minutes. SV increased (P < 0.05) by approximately 22%, plateauing after 60 minutes. MRAP, PCWP, HR, CO, MAP, SVR, and blood-O₂ consumption remained unaltered (P = ns). Compared with hypoxia baseline, with placebo, MPAP remained stable (P = ns), PVR increased (P < 0.05) and CO decreased (P < 0.05) by approximately 20% and 11% after 60-90 and 30-90 minutes, respectively. SV decreased (P < 0.05) by approximately 8%, plateauing after 60-90 minutes. PCWP and MRAP decreased (P < 0.05) by approximately 12%, plateauing after 10-60 and 10-90 minutes, respectively. MPAP, HR, MAP, SVR, and blood-O₂ consumption remained unchanged (P = ns), except at 60 minutes where MAP decreased (P < 0.05) by approximately 4%.
Conclusions: Levosimendan attenuated HPV and the cardiodepressive effect of sustained hypoxia.