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. 2025 Sep 8;14(17):6342.
doi: 10.3390/jcm14176342.

Extracorporeal Life Support in a Porcine Model of Septic Endotoxemia with Acute Pulmonary Hypertension: An Experimental Study

Stany Sandrio  1 , Joerg Krebs  1 , Tobias Spanier  1 , Grietje Beck  1 , Manfred Thiel  1 , Peter Tobias Graf  1
Affiliations

Extracorporeal Life Support in a Porcine Model of Septic Endotoxemia with Acute Pulmonary Hypertension: An Experimental Study

Stany Sandrio et al. J Clin Med. .

Abstract

Background: This study evaluated the effects of veno-arterial (V-A) and veno-venoarterial (V-VA) ECMO in a porcine model of septic endotoxemia-induced acute pulmonary arterial hypertension (PAH). Our hypotheses were as follows: (1) V-VA ECMO lowers pulmonary vascular resistance (PVR) by delivering oxygenated blood to the pulmonary circulation, and (2) both V-A and V-VA ECMO improve perfusion to vital organs while simultaneously unloading the right ventricle (RV). Methods: Acute PAH was induced with Salmonella abortus equi lipopolysaccharide (LPS) in 34 pigs. Animals were randomized to either a control group without ECMO or to two groups receiving V-A or V-VA ECMO. Results: All animals developed PAH after one hour of LPS infusion: mean pulmonary artery pressure (PAP) increased significantly from 26 (24-30) mmHg to 40 (34-46) mmHg (p < 0.0001), and PVR increased from 314 (221-390) to 787 (549-1073) (p < 0.0001). Neither V-A nor V-VA ECMO significantly reduced PVR compared to controls. RV end-diastolic area increased in the control group [6.1 (4.3-8.6) cm vs. 8.5 (7.8-9.7) cm, p = 0.2], but not in the V-A [4.7 (3.3-7.6) cm] and V-VA [4.3 (2.5-8.3) cm] ECMO groups. Blood flow in the cranial mesenteric artery and celiac trunk did not differ significantly with or without ECMO. Conclusions: Elevating pulmonary artery oxygen tension through V-A or V-VA ECMO did not reduce PVR or PAP. However, both ECMO configurations effectively unloaded the RV and maintained perfusion to abdominal organs.

Keywords: lipopolysaccharide; pulmonary hypertension; right ventricle; sepsis; veno-arterial extracorporeal membrane oxygenation; veno-venoarterial extracorporeal membrane oxygenation.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
Experimental timeline. Hemodynamic measurements, echocardiography, and blood sampling were conducted at baseline, after one hour of continuous LPS infusion (pre-ECMO), and after a further two hours of LPS infusion with or without ECMO support (final). ECMO: extracorporeal membrane oxygenation; LPS: lipopolysaccharide; V-A: veno-arterial; V-VA veno-venoarterial.
Figure 2
Figure 2
Mean pulmonary artery pressure (PAP) measured at baseline, after one hour of continuous LPS infusion (pre-ECMO), and at the final evaluation in the V-VA ECMO group (dark gray), the V-A ECMO group (light gray), and the control group without ECMO support (white).
Figure 3
Figure 3
Pulmonary vascular resistance (PVR) calculated at baseline, after one hour of continuous LPS infusion (pre-ECMO), and at the final evaluation in the V-VA ECMO group (dark gray), the V-A ECMO group (light gray), and the control group without ECMO support (white).
Figure 4
Figure 4
Pulmonary artery oxygen tension (PpaO2) measured at baseline, after one hour of continuous LPS infusion (pre-ECMO), and at the final evaluation in the V-VA ECMO group (dark gray), the V-A ECMO group (light gray), and the control group without ECMO support (white).
See this image and copyright information in PMC

References

    1. Kovacs G., Bartolome S., Denton C.P., Gatzoulis M.A., Gu S., Khanna D., Badesch D., Montani D. Definition, classification and diagnosis of pulmonary hypertension. Eur. Respir. J. 2024;64:2401324. doi: 10.1183/13993003.01324-2024. - DOI - PMC - PubMed
    1. Spapen H., Vincken W. Pulmonary Arterial Hypertension in Sepsis and the Adult Respiratory Distress Syndrome. Acta Clin. Belg. 1992;47:30–41. doi: 10.1080/17843286.1992.11718207. - DOI - PubMed
    1. Pischke S.E., Hestenes S., Johansen H.T., Fure H., Bugge J.F., Espinoza A., Skulstad H., Edvardsen T., Fosse E., Mollnes T.E., et al. Sepsis causes right ventricular myocardial inflammation independent of pulmonary hypertension in a porcine sepsis model. PLoS ONE. 2019;14:e0218624. doi: 10.1371/journal.pone.0218624. - DOI - PMC - PubMed
    1. Vallabhajosyula S., Shankar A., Vojjini R., Cheungpasitporn W., Sundaragiri P.R., DuBrock H.M., Sekiguchi H., Frantz R.P., Cajigas H.R., Kane G.C., et al. Impact of Right Ventricular Dysfunction on Short-term and Long-term Mortality in Sepsis: A Meta-analysis of 1373 Patients. Chest. 2021;159:2254–2263. doi: 10.1016/j.chest.2020.12.016. - DOI - PMC - PubMed
    1. Dessap A.M., Boissier F., Charron C., Bégot E., Repessé X., Legras A., Brun-Buisson C., Vignon P., Vieillard-Baron A. Acute cor pulmonale during protective ventilation for acute respiratory distress syndrome: Prevalence, predictors, and clinical impact. Intensive Care Med. 2016;42:862–870. doi: 10.1007/s00134-015-4141-2. - DOI - PubMed

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