Abstract
BackgroundHypotensive neonates who have been treated with dopamine have poorer neurodevelopmental outcome than those who have not been treated with dopamine. We speculate that dopamine stimulates adrenoceptors on cerebral arteries causing cerebral vasoconstriction. This vasoconstriction might lead to a rightward shift of the cerebral autoregulatory curve; consequently, infants treated with dopamine would have a higher risk of low cerebral blood flow at a blood pressure that is otherwise considered “safe”.MethodsIn anaesthetized piglets, perfusion of the brain, monitored with laser-doppler flowmetry, and cerebral venous saturation was measured at different levels of hypotension. Each piglet was studied in two phases: a phase with stepwise decreases in MAP and a phase with stepwise increases in MAP. We randomized the order of the two phases, whether dopamine was given in the first or second phase, and the infusion rate of dopamine (10, 25, or 40 μg/kg/min). In/deflation of a balloon catheter, placed in vena cava, induced different levels of hypotension. At each level of hypotension, fluctuations in MAP were induced by in/deflations of a balloon catheter in descending aorta.ResultsDuring measurements, PaCO2 and arterial saturation were stable. MAP levels ranged between 14 and 82 mmHg. Cerebral autoregulation (CA) capacity was calculated as the ratio between %-change in cerebrovascular resistance and %-change in MAP induced by the in/deflation of the arterial balloon. A breakpoint in CA capacity was identified at a MAP of 38±18 mmHg without dopamine and at 44±18, 31±14, and 24±14 mmHg with dopamine infusion rates of 10, 25, and 40 μg/kg/min (p = 0.057). Neither the index of steady-state cerebral perfusion nor cerebral venous saturation were affected by dopamine infusion.ConclusionDopamine infusion tended to improve CA capacity at low blood pressures while an index of steady-state cerebral blood flow and cerebral venous saturation were unaffected by dopamine infusion. Thus, dopamine does not appear to impair CA in newborn piglets.
Highlights
Hypotension in newborn infants is associated with higher incidence of mortality and cerebral injury[1,2,3,4,5]
Cerebral autoregulation (CA) capacity was calculated as the ratio between %-change in cerebrovascular resistance and %-change in mean arterial blood pressure (MAP) induced by the in/deflation of the arterial balloon
A breakpoint in CA capacity was identified at a MAP of 38±18 mmHg without dopamine and at 44±18, 31±14, and 24±14 mmHg with dopamine
Summary
Hypotension in newborn infants is associated with higher incidence of mortality and cerebral injury[1,2,3,4,5]. Cerebral injuries caused by hypotension are heterogeneous with both peri- and intraventricular haemorrhage as well as ischemic cerebral lesions[1,2,3,5]; predominantly the white matter being the most vulnerable area to hypotensive periods[6] These cerebral injuries result in poorer long-term neurodevelopmental outcome[4,7]. Dopamine raises mean arterial blood pressure (MAP) effectively[8,9] and is the most commonly used vasopressor in newborn infants[10] It stimulates both dopaminergic and adrenergic receptors on the arterial smooth muscle cells, and has a concentration-dependent biphasic response: vasodilation at low concentrations, caused by stimulation of dopaminergic receptor, and vasoconstriction at higher concentrations due to adrenergic stimulation[11]. This vasoconstriction might lead to a rightward shift of the cerebral autoregulatory curve; infants treated with dopamine would have a higher risk of low cerebral blood flow at a blood pressure that is otherwise considered “safe”
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