Efficacy of prostaglandin E1 administered via pulmonary artery for treatment of pulmonary hypertension
10.3760/cma.j.issn.0254-1416.2013.01.023
- VernacularTitle:前列腺素E1肺动脉途径给药对肺动脉高压患者的降压效果
- Author:
Dangpei KOU
;
Zhun WANG
;
Wei BIAN
;
Jiange HAN
- Publication Type:Journal Article
- Keywords:
Alprostadil;
Pulmonary artery;
Hypertension,pulmonary
- From:
Chinese Journal of Anesthesiology
2013;(1):85-87
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the efficacy of prostaglandin E1 administered via the pulmonary artery for treatment of pulmonary hypertension in patients.Methods Thirty ASA Ⅱ or Ⅲ patients undergoing offpump coronary artery bypass grafting complicated with pulmonary hypertension,with pulmonary arterial systolic pressure (PASP) ＞ 40 mm Hg,were randomly divided into 2 groups (n =15 each):administration via the central vein group (group C) and administration via the pulmonary artery group (group P).Anesthesia was induced with midazolam,etomidate,cisatracurium and sufentanil.The patients were tracheal intubated and mechanically ventilated.Swan-Ganz catheter was placed via the right internal jugular vein for monitoring of hemodynamic parameters after induction of anesthesia.The central vein and pulmonary artery were cannulated for infusion of prostaglandin E1.Prostaglandin E1 was infused at a rate of 20-50 ng· kg-1 · min-1 starting from the end of skin incision until PASP was decreased to 20-30 mm Hg.Heart rate (HR),mean arterial pressure (MAP),central venous pressure (CVP),PASP,pulmonary capillary wedge pressure (PCWP) and cardiac index (CI) were recorded at 5 rain before administration (To) and 5 min after administration (T1).The pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR) were calculated.The amount of prostaglandin E1 consumed was recorded.Results Compared with group C,the amount of prostaglandin E1 consumed was significantly reduced,PASP and PVR were decreased at T1,while MAP and SVR were increased at T1 in group P(P ＜ 0.05).Conclusion Administration via the pulmonary artery can increase the potency of prostaglandin E1 for treatment of pulmonary hypertension and exerts no influence on the systemic hemodynamics.
