Effects of thoracic epidural anesthesia and adrenoceptor blockade on the cardiovascular response to dopamine in the dog

The cardiovascular effects of dopamine are different before and during thoracic epidural anesthesia (TEA). To evaluate underlying adrenoceptor-mediated mechanisms, dopamine effects were investigated in nine chloralose-anesthetized dogs. The circulatory response to dopamine (0–40 μg · kg-1 · min-1) was studied before and during TEA, and during TEA after introducing the α1-antagonist prazosin (0.3 mg · kg-1), the α2-antagonist rauwolscine (0.3 mg · kg-1), and the β1-antagonist metoprolol (0.5 mg · kg-1). TEA decreased mean arterial pressure (MAP) by 29%, cardiac output (CO) by 36%, heart rate (HR) by 27%, and the maximum rate of change of left ventricular pressure (LVdP/dt) by 52%. Systemic vascular resistance, pulmonary vascular resistance and mean pulmonary artery pressure (MPAP) remained unaltered by TEA. Dopamine-induced increases in MAP and HR were augmented by TEA. Both MAP and LVdP/dt increased above pre-TEA levels at 10 μg · kg-1 · min-1. Prazosin attenuated the increases in MAP and MPAP by dopamine. Adding rauwolscine almost abolished the dopamine response in MAP and MPAP. Metoprolol almost eliminated the dopamine effects on CO and LVdP/dt. Only minor alterations in cardiac filling pressures were observed during the study. Plasma norepinephrine (NE) concentration was lower during than before TEA at corresponding dopamine infusion rates. NE was reduced by the β1-blockade. During TEA, the plasma dopamine levels were generally higher, and they were further increased by adding β1-blockade. In conclusion, myocardial contractility and arterial pressure were restored to pre-TEA values by dopamine at 5–10 μg · kg-1 · min-1. The circulatory response to dopamine during TEA is mainly mediated by α1-, α2- and β1-adrenoceptor activation, and may be influenced by altered plasma catecholamine levels.