Acute pulmonary embolism decreases adenosine plasma levels in anesthetized pigs

Adenosine plays a role in pulmonary arterial (PA) resistance due to its vasodilator properties. However, the behavior of adenosine plasma levels (APLs) during pulmonary embolism remains unknown. We investigated the effects of gradual pulmonary embolism on right ventricular (RV) contractility and PA coupling and on APLs in an piglet experimental model of RV failure. PA distal resistance by pressure-flow relationships and pulmonary vascular impedance were measured. RV contractility was determined by the end-systolic pressure-volume relationship (Ees), PA effective elastance by the end-diastolic to end-systolic relationship (Ea), and RV-PA coupling efficiency by the Ees/Ea ratio. APLs were measured before and during gradual pulmonary embolization. PA embolism increased PA resistance and elastance, increased Ea from 1.08 ± 0.15 to 5.62 ± 0.32 mmHg/mL, decreased Ees from 1.82 ± 0.10 to 1.20 ± 0.23 mmHg/mL, and decreased Ees/Ea from 1.69 ± 0.15 to 0.21 ± 0.07. APLs decreased from 2.7 ± 0.26 to 1.3 ± 0.12 μM in the systemic bed and from 4.03 ± 0.63 to 2.51 ± 0.58 μM in the pulmonary bed during embolism procedure. Pulmonary embolism worsens PA hemodynamics and RV-PA coupling. APLs were reduced, both in the systemic and in the pulmonary bed, leading then to pulmonary vasoconstriction.