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Effects of oxygen and nitric oxide inhalation in a porcine model of recurrent microembolism
Author(s) -
Weimann J.,
Zink W.,
Gebhard M. M.,
Gries A.,
Martin E.,
Motsch J.
Publication year - 2000
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1034/j.1399-6576.2000.440913.x
Subject(s) - medicine , inhalation , pulmonary hypertension , nitric oxide , pulmonary embolism , anesthesia , hemodynamics , vascular resistance , respiratory disease , pulmonary artery , cardiology , lung
Background: Inhalation of nitric oxide (iNO) has been proposed for the treatment of acute pulmonary embolism. The present study evaluates the effects of oxygen (O 2 ) and nitric oxide inhalation in a porcine model of sustained pulmonary hypertension induced by recurrent pulmonary microembolism. Methods: Twelve pigs were embolized under general anesthesia with 300‐μm microspheres intravenously three times over a period of seven weeks. Five pigs served as untreated controls. Hemodynamic and gas exchange responses to 100% oxygen and 40 ppm NO inhalation, and their combination (O 2 +iNO) were measured seven days after the last embolization. Results: Recurrent microembolism caused sustained pulmonary hypertension (pulmonary vascular resistance index; PVRI 408±57 dyn · s · cm −5 · m −2 ) as compared to the control group (PVRI 143±20 dyn · s · cm −5 · m −2 ; P <0.05). PVRI was significantly reduced by O 2 , iNO, and O 2 +iNO inhalation by 29±3, 28±4, and 32±3%, respectively. Conclusion: We conclude that both O 2 and iNO are selective pulmonary vasodilators in a porcine model of sustained pulmonary hypertension following recurrent pulmonary microembolism and, therefore, may be useful in the treatment not only in the acute phase of pulmonary embolism but also later in the time course of the disease.