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Biventricular cardiac dysfunction after acute massive pulmonary embolism in the rat
D M Sullivan1, J A Watts, J A Kline
1Division of Research, Department of Emergency Medicine, Carolinas Medical Center, Charlotte, North Carolina 28232-2861, USA.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|April 12, 2001
Summary
Acute massive pulmonary embolism (AMPE) causes intrinsic biventricular dysfunction in rat hearts, independent of arterial hypotension. This study reveals direct cardiac impairment following AMPE.
Area of Science:
- Cardiology
- Physiology
- Pathophysiology
Background:
- Cardiac dysfunction is observed in vivo following acute massive pulmonary embolism (AMPE).
- The direct impact of AMPE on intrinsic ventricular function requires further investigation.
Purpose of the Study:
- To determine if acute massive pulmonary embolism induces intrinsic ventricular dysfunction in isolated rat hearts.
- To differentiate AMPE-induced cardiac dysfunction from that caused by arterial hypotension.
Main Methods:
- Acute massive pulmonary embolism (AMPE) was induced in rats via thrombus infusion.
- Isolated hearts were perfused in isovolumetric mode to measure simultaneous right ventricular (RV) and left ventricular (LV) pressures.
- Comparison groups included hypotensive controls and sham-operated rats.
Main Results:
- AMPE induced significant systolic contractile dysfunction in both RV and LV ex vivo.
- AMPE hearts exhibited hypoxemia, acidemia, and elevated lactate levels.
- Coronary flow and ventricular compliance remained unaltered; soluble tumor necrosis factor-alpha decreased in both ventricles.
Conclusions:
- Acute massive pulmonary embolism leads to intrinsic biventricular dysfunction.
- Arterial hypotension is not the primary driver of this observed cardiac dysfunction.