Progressive right ventricular failure is not explained by myocardial ischemia in a pig model of right ventricular pressure overload
| Autor: | C. Sellin, Hilmar Doerge, Heiner Post, Friedrich A. Schoendube, Samuel Sossalla, Marlon Coulibaly, Jan D. Schmitto, Aron F Popov |
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| Rok vydání: | 2009 |
| Předmět: |
Male
Pulmonary and Respiratory Medicine medicine.medical_specialty Ventricular Dysfunction Right Sus scrofa Myocardial Ischemia Hemodynamics 030204 cardiovascular system & hematology 03 medical and health sciences Oxygen Consumption 0302 clinical medicine Troponin T Afterload Coronary Circulation Internal medicine medicine.artery Animals Medicine 030304 developmental biology Heart Failure Pressure overload 0303 health sciences business.industry General Medicine Hydrogen-Ion Concentration 3. Good health Disease Models Animal Right coronary artery Circulatory system Pulmonary artery Disease Progression Cardiology Aortic pressure Ventricular pressure Female Surgery Pulmonary Embolism Cardiology and Cardiovascular Medicine business |
| Zdroj: | European Journal of Cardio-Thoracic Surgery. 35:229-234 |
| ISSN: | 1010-7940 |
| Popis: | Background: Current concepts of acute pulmonary embolism suggest that right ventricular (RV) dilatation and failure are the consequence of pressureoverload-inducedRVhypoperfusionandischemia.Methods:Sixteenhuman-sizedhybridpigswereinstrumented forthemeasurementof RVand aortic pressure, aortic and right coronary artery blood flow (RCA BF), RVoxygen consumption (RV MVO2) and RV free wall segment length. The pulmonary artery was constricted (PAC) to increase RV peak pressure acutely 2.5-fold (from 27 2t o 64 3 mmHg, n = 9), and the constriction was maintained for 6 h. Results: At 10 min after PAC, a RV work index (RVWI, RV pressure-segment length loops) was increased 2.3fold, indicating an initial RV adaptation to increased afterload. At 1 h, 3 h and 6 h after PAC, however, RVWI decreased progressively towards control levels, while RCA BF and RV MVO2 continued to increase. The arterial-coronary venous pH difference did not increase throughout the protocol. Arterial troponin Tconcentration increased from 0.08 0.03 to 0.80 0.20 ng/ml at 6 h after PAC. None of the parameters changed in control animals (n = 7). Conclusion: We conclude that in our model RV failure during PAC develops in spite of increased coronary blood flow and MVO2. Thus, mechanisms different from ischemia may contribute to progressive RV failure after pulmonary embolism. # 2008 European Association for Cardio-Thoracic Surgery. Published by Elsevier B.V. All rights reserved. |
| Databáze: | OpenAIRE |
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