Acute Pulmonary Embolism Decreases Adenosine Plasma Levels in Anesthetized Pigs

François Kerbaul,Serge Brimioulle,Frédéric Collart,Régis Guieu,Vlad Gariboldi,Pierre Fesler,Choukri Mekkaoui,Yves Jammes,Jean Ruf,Youlet By

doi:10.5402/2011/750301

Abstract

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.

Highlights

It is generally assumed that acute pulmonary embolisminduced pulmonary hypertension results from the interaction of main factors such as mechanical obstruction of pulmonary vessels associated with pulmonary arterial (PA) constriction [1]
Adenosine (ADO), a purine nucleoside released by vascular endothelium and myocytes, may be implicated in the control of healthy and pathologic pulmonary circulation [7, 8]
Mean pulmonary arterial pressure Psa (Ppa)/Q plots were linear with correlation coefficients from 0.96 to 1

Summary

Introduction

It is generally assumed that acute pulmonary embolisminduced pulmonary hypertension results from the interaction of main factors such as mechanical obstruction of pulmonary vessels associated with PA constriction [1] In this setting, RV outflow impedance is suddenly increased [2], RV ejection fraction is impaired, and the RV is enlarged [3]. Acute pulmonary embolism-induced pulmonary hypertension was shown to persistently deteriorate RV contractility by increasing RV afterload, thereby providing a rationale for inotropic support [4] Other factors such as PA constriction attributable to neurogenic reflex and hypoxia and release of vasoconstrictors by activated platelets, leukocytes, and endothelial and lung cells could be involved [1].

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Discussion

Conclusion