title: Cardiopulmonary effects of intravenous prostaglandin E1 during experimental one-lung ventilation.
abstract: BACKGROUND
  One-lung ventilation greatly improves operating conditions during thoracic surgery. Serious disadvantages of one-lung ventilation are hypoxaemia and increased pulmonary vascular resistance. Prostaglandins, like prostaglandin I2 (PGI2), are potent pulmonary vasodilators but may also influence venous admixture and systemic circulation. Since the lung is capable of extensive degradation of prostaglandin E1 (PGE1) but not of PGI2, PGE1 might affect systemic circulation to a lesser degree. Hence, we studied the effects of intravenous PGE1 on systemic and pulmonary circulation and on oxygenation during one-lung ventilation.
  
  
  METHODS
  Lateral thoracotomy and cross-clamping of the left main stem bronchus was performed in twelve anaesthetised and ventilated pigs. Animals were cannulated with arterial, central venous and fast response thermodilution pulmonary artery catheters for haemodynamic measurements. PGE1 was administered with infusion rates of 25, 50, and 100 ng x kg (-1) x min (-1) during one-lung ventilation.
  
  
  RESULTS
  All doses of PGE1 significantly decreased pulmonary vascular resistance and mean pulmonary artery pressure. However, a comparable significant reduction in systemic vascular resistance and mean arterial pressure was found. Arterial oxygen tension and venous admixture showed a slight but significant deterioration. Oxygen delivery remained unchanged or increased since the cardiac index increased.
  
  
  CONCLUSIONS
  During one-lung ventilation in the pig, infusion of PGE1 significantly decreased pulmonary vascular resistance and pulmonary artery pressure but failed to achieve selective pulmonary vasodilation.
authors.affiliation: Department of Anaesthesiology, Albert Schweitzer Hospital, Sturmbaume 8-10, 37154 Northeim, Germany. michael.bund@ask-northeim.de
authors.forename: M
authors.initials: M
authors.lastname: Bund
authors.forename: D
authors.initials: D
authors.lastname: Henzler
authors.forename: R
authors.initials: R
authors.lastname: Walz
authors.forename: R
authors.initials: R
authors.lastname: Rossaint
authors.forename: S
authors.initials: S
authors.lastname: Piepenbrock
mesh_terms: D000403:Airway Resistance / Q000187:drug effects*; D000527:Alprostadil / Q000008:administration & dosage* / Q000494:pharmacology*; D000818:Animals; D004305:Dose-Response Relationship, Drug; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D007262:Infusions, Intravenous; D008168:Lung / Q000098:blood supply / Q000378:metabolism; D023421:Models, Animal; D010101:Oxygen Consumption / Q000187:drug effects; D011651:Pulmonary Artery / Q000187:drug effects; D011652:Pulmonary Circulation / Q000187:drug effects*; D011667:Pulmonary Veins / Q000187:drug effects; D012123:Pulmonary Ventilation / Q000187:drug effects*; D011669:Pulmonary Wedge Pressure / Q000187:drug effects; D013318:Stroke Volume / Q000187:drug effects; D013552:Swine; D014655:Vascular Resistance / Q000187:drug effects*; D014661:Vasoconstriction / Q000187:drug effects; D014665:Vasodilator Agents / Q000008:administration & dosage* / Q000494:pharmacology*; D014692:Ventilation-Perfusion Ratio / Q000187:drug effects*; D016278:Ventricular Function, Right / Q000187:drug effects
chemical_list: D014665:Vasodilator Agents; D000527:Alprostadil