Effects of U-46619 on Pulmonary Hemodynamics Before and After Administration of BM-573, a Novel Thromboxane A2 Inhibitor

Lambermont, Bernard; Kolh, Philippe; Dogné, Jean‐Michel; Ghuysen, Alexandre; Tchana‐Sato, Vincent; Morimont, Philippe; Benoit, P; Gérard, Paul; Masereel, Bernard; Limet, Raymond; D’Orio, Vincenzo

doi:10.1076/apab.111.3.217.23459

Cited by 8 publications

(6 citation statements)

References 15 publications

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“…For the pulmonary circulation, our results evidenced significant correlation between both methods, as well as between E a ‫ء‬ (PV) and RT/T, despite dramatic changes in pulmonary vascular compliance. Our laboratory previously showed a concordant evolution between E max /E a and stroke work in pulmonary embolism or septic shock (6,13,15). This could be explained by higher basal pulmonary vascular compliance compared with the values obtained on the systemic circuit.…”

Section: Discussionmentioning

confidence: 93%

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Effective arterial elastance as an index of pulmonary vascular load

Morimont¹,

Lambermont²,

Ghuysen³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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Morimont P, Lambermont B, Ghuysen A, Gerard P, Kolh P, Lancellotti P, Tchana-Sato V, Desaive T, D'Orio V. Effective arterial elastance as an index of pulmonary vascular load. Am J Physiol Heart Circ Physiol 294: H2736-H2742, 2008. First published April 18, 2008 doi:10.1152/ajpheart.00796.2007.-The aim of this study was to test whether the simple ratio of right ventricular (RV) endsystolic pressure (Pes) to stroke volume (SV), known as the effective arterial elastance (E a), provides a valid assessment of pulmonary arterial load in case of pulmonary embolism-or endotoxin-induced pulmonary hypertension. Ventricular pressure-volume (PV) data (obtained with conductance catheters) and invasive pulmonary arterial pressure and flow waveforms were simultaneously recorded in two groups of six pure Pietran pigs, submitted either to pulmonary embolism (group A) or endotoxic shock (group B). Measurements were obtained at baseline and each 30 min after injection of autologous blood clots (0.3 g/kg) in the superior vena cava in group A and after endotoxin infusion in group B. Two methods of calculation of pulmonary arterial load were compared. On one hand, Ea provided by using three-element windkessel model (WK) of the pulmonary arterial system [Ea(WK)] was referred to as standard computation. On the other hand, similar to the systemic circulation, Ea was assessed as the ratio of RV Pes to SV [Ea(PV) ϭ Pes/SV]. In both groups, although the correlation between Ea(PV) and Ea(WK) was excellent over a broad range of altered conditions, Ea(PV) systematically overestimated Ea(WK). This offset disappeared when left atrial pressure (Pla) was incorporated into Ea [Ea ‫ء‬ (PV) ϭ (Pes Ϫ Pla)/SV]. Thus Ea ‫ء‬ (PV), defined as the ratio of RV Pes minus Pla to SV, provides a convenient, useful, and simple method to assess the pulmonary arterial load and its impact on the RV function.hemodynamics; pulmonary hypertension; right ventricle; ventriculoarterial coupling IN CURRENT CLINICAL practice, pulmonary arterial load [or right ventricular (RV) afterload] is usually expressed as the mean pulmonary vascular resistance, computed as the ratio of the pressure drop through the pulmonary circulation [difference between mean pulmonary arterial pressure (PAP mean ) and left atrial pressure (Pla)] to the mean pulmonary blood flow [cardiac output (CO)]. Such an evaluation ignores the pulsatile nature of both pressure and flow. Although oscillatory components of the pulmonary arterial load are low, and mean resistance may be a valuable index of the pulmonary vascular load, the pulsatile nature of the load may be prominent in numerous pathological situations. Wave reflections play an important role and should be taken into account in pulmonary hypertension resulting from several pathological conditions, like pulmonary embolism and septic shock (1,2,5,14). In this way, the pulmonary arterial impedance spectrum, which is defined in the frequency domain, provides a more precise and complete description of the pulmonary vascular load (12, 17). However, be...

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Section: Discussionmentioning

confidence: 93%

“…Our laboratory previously showed that, in heart failure due to pulmonary embolism and sepsis, the decreased value of E max /E a was related to an impaired use of energy by the failing heart (6,13,15). In combination with E max , E a (PV) appears to be a simple way to characterize ventriculo-arterial interaction (18,26,27).…”

Section: Discussionmentioning

confidence: 99%

Effective arterial elastance as an index of pulmonary vascular load

Morimont¹,

Lambermont²,

Ghuysen³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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“…Under normal operating conditions, the right ventricle operates at a maximum efficiency and a submaximal stroke work ( /( > 1), while uncoupling occurs when / < 1 (Fourie et al, 1992, Lambermont et al, 2003a.…”

Section: Discussionmentioning

confidence: 99%

Assessment of ventricular-arterial coupling with a model-based sensor

Desaive

Lambermont

Ghuysen

et al. 2010

UKACC International Conference on CONTROL 2010

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Estimation of ventricular contractility is clinically important in diagnosing cardiac dysfunction in the critically ill. However, experimental assessment of indexes of ventricular contractility, such as the end-systolic pressure-volume relationship requires a highly invasive maneuver. This research describes the use of a previously validated cardiovascular system (CVS) model and identification process to evaluate the right-ventricle contractility as well as the right ventricular arterial coupling in septic shock. The results show good agreement with the gold-standard experimental assessment (conductance catheter method), and offer the potential to develop a model-based sensor to monitor the coupling in clinical realtime.

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“…This novel TXA 2 receptor antagonist and synthase inhibitor has a powerful antiplatelet potency and was shown to relax the rat aorta artery precontracted with U-46619, a stable TXA 2 agonist [21][22][23]. In the pig, our team demonstrated that BM-573 revealed a protective effect against pulmonary hypertension induced by U-46619 [24]. Besides, we also reported the preventive effect of BM-573 in the early phase of endotoxin induced pulmonary hypertension [25], and during embolic induced pulmonary vasoconstriction [26].…”

Section: Introductionmentioning

confidence: 99%