Abstract
BackgroundThe effects of low concentration of sevoflurane on right ventricular (RV) function and intracellular calcium in the setting of pulmonary arterial hypertension (PAH) have not been investigated clearly. We aim to study these effects and associated signaling pathways in rats with PAH.MethodsHemodynamics were assessed with or without sevoflurane inhalation in established PAH rats. We analysis the classic RV function parameters and RV-PA coupling efficiency using steady-state PV loop recordings. The protein levels of SERCA2, PLB and p-PLB expression was analyzed by western blot to assess their relevance in PAH.ResultsRats with PAH presented with RV hypertrophy and increased pulmonary arterial pressure. The values of Ea, R/L ratio, ESP, SW, PRSW, +dP/dtmax and the slope of the dP/dtmax-EDV relationship increased significantly in PAH rats (P<0.05). Sevoflurane induced a concentration-dependent decrease of systemic and pulmonary blood pressure, HR, RV contractility, and increased the R/L ratio in both groups. Sevoflurane reduced the expression of SERCA2 and increased the expression of PLB in both groups. Interestingly, sevoflurane only reduced the p-PLB/PLB ratio in PAH rats, not in normal rats.ConclusionsRats with chronic, stable pulmonary hypertension tolerate low concentrations of sevoflurane inhalation as well as normal rats do. It may be related to the modulation of the SERCA2-PLB signaling pathway.
Highlights
Pulmonary arterial hypertension (PAH) is characterized by chronically increased intravascular pressure and resistance, which results in right ventricular (RV) hypertrophy, dilatation, right heart failure, and death[1,2,3]
Rats with PAH presented with RV hypertrophy and increased pulmonary arterial pressure
It may be related to the modulation of the SERCA2PLB signaling pathway
Summary
Pulmonary arterial hypertension (PAH) is characterized by chronically increased intravascular pressure and resistance, which results in right ventricular (RV) hypertrophy, dilatation, right heart failure, and death[1,2,3]. PAH is a major risk factor for mortality in patients undergoing surgery. In non-cardiac surgery, PAH is associated with worse perioperative outcomes. In-hospital mortality of severe PAH patients is up to 10%. [6, 7] The choice of anesthetic agent is crucial in the perioperative management of patients with PAH. Fentanyl, neuromuscular blocking agents with minimal hemodynamic effects and a small dose of propofol has been recommended for induction of anesthesia in pediatric PAH patients[8, 9]. Little is known about the effects of sevoflurane on RV function in patients with PAH. The effects of low concentration of sevoflurane on right ventricular (RV) function and intracellular calcium in the setting of pulmonary arterial hypertension (PAH) have not been investigated clearly. We aim to study these effects and associated signaling pathways in rats with PAH
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