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Myocardial work load is a major determinant of norepinephrine-induced left ventricular dysfunction
F J Bosso1, F D Allman, C F Pilati
1Department of Physiology, Northeastern Ohio Universities College of Medicine, Rootstown 44272.
The American Journal of Physiology
|February 1, 1994
Summary
Norepinephrine (NE) can cause left ventricular (LV) dysfunction. This dysfunction is worsened by increased myocardial energy demand, but NE can also independently cause modest LV dysfunction.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
Background:
- Norepinephrine (NE) is a key hormone and neurotransmitter.
- Left ventricular (LV) dysfunction can arise from various stressors.
- The role of myocardial energy demand in NE-induced LV dysfunction requires clarification.
Purpose of the Study:
- To investigate the role of increased myocardial energy demand in norepinephrine (NE)-induced left ventricular (LV) dysfunction.
- To differentiate between direct NE effects and those mediated by energy demand.
Main Methods:
- Rabbits were treated with NE, inducing varying levels of myocardial energy demand (arterial pressure-heart rate product).
- LV function was assessed in vivo and in isolated hearts exposed to NE under controlled energy demand.
- Dose-dependent effects of NE on LV function were evaluated.
Main Results:
- Elevated myocardial energy demand during NE treatment markedly diminished in vitro LV function.
- LV function remained largely unaffected when myocardial energy demand was kept at control levels during NE treatment.
- Isolated hearts exposed to NE showed modest, dose-dependent LV dysfunction, independent of energy demand.
Conclusions:
- Norepinephrine (NE) can induce left ventricular (LV) dysfunction independently of increased myocardial energy demand.
- Elevated myocardial energy demand exacerbates NE-induced LV dysfunction.
- Myocardial energy demand is a critical factor modulating the severity of NE cardiotoxicity.