Abstract

Objective To investigate the mechanism and significance of low concentration nitric oxide (NO) inhalation in the treatment of pulmonary thromboembelism in swine. Method The pulmonary thromboem-bolism(PTE) model was made in 15 healthy infantile swines which were subsequently assigned to either control group (n = 8) or NO group (n = 7). Swines of the control group were not treated with any medicine, while 10 ppm of NO was administered by continuous inhalation for 2 hours to swines of NO group. Volume of physiological dead space (VDphy), volume of alveolar dead space (VDalv), intrapulmonary shunt (Qs/Qt), mean pulmonary arterial pressure (PAP), systolic blood pressure (SBP), heart rate (HR), cardiac output (CO), arterial blood pH (pH), arterial partial pressure of carbon dioxide (PaCO2) and arterial partial pressure of oxygen (PaO2) were measured 30 min before and 0 min, 30 min, 60 min, 120 min and 180 min after establishment of VIE. Results The post-FIE VDphy, VDalv, Qs/Qt and PAP in both groups increased markedly after PTE compared with the cor-responding pre-PTE measurements (P 0.05). Both post-PTE PAP and VDalv in NO group were markedly lower(P <0.05 and P <0.01) and beth PaCO2 and PaO2 were much higher than those of the control group (P <0.05). No signi-fieant difference were found in other measurements between two groups. Conclusions Pulmonary arterial pressure may be lowered, alveoli dead space may be reduced and PaCO2 increased by low concentration NO inhalation for the treatment of PIE without decline in haemodynamic status. Key words: Pulmonary thromboembolism; Nitric oxide; Dead space; Shunt; Gas exchange; Pulmonary ar-terial pressure; Model; Arterial partial pressure of oxygen;

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