Eriksen Vibeke Ramsgaard, Rasmussen Martin Bo, Hahn Gitte Holst, Greisen Gorm
Department of Neonatology, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark.
University of Copenhagen, Faculty of Health and Medical Sciences, Copenhagen, Denmark.
PLoS One. 2017 Jan 31;12(1):e0170738. doi: 10.1371/journal.pone.0170738. eCollection 2017.
Hypotensive 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".
In 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.
During 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.
Dopamine 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.
接受多巴胺治疗的低血压新生儿的神经发育结局比未接受多巴胺治疗的新生儿更差。我们推测多巴胺刺激脑动脉上的肾上腺素能受体,导致脑血管收缩。这种血管收缩可能导致脑自动调节曲线向右移动;因此,接受多巴胺治疗的婴儿在原本被认为“安全”的血压水平下发生低脑血流量的风险更高。
在麻醉的仔猪中,用激光多普勒血流仪监测脑灌注,并在不同低血压水平下测量脑静脉饱和度。每只仔猪分两个阶段进行研究:一个阶段是平均动脉压(MAP)逐步降低,另一个阶段是MAP逐步升高。我们随机安排两个阶段的顺序、多巴胺是在第一阶段还是第二阶段给予以及多巴胺的输注速率(10、25或40μg/kg/min)。放置在下腔静脉的球囊导管的充/放气诱导不同程度的低血压。在每个低血压水平,通过降主动脉球囊导管的充/放气诱导MAP波动。
测量期间,动脉血二氧化碳分压(PaCO2)和动脉血氧饱和度稳定。MAP水平在14至82mmHg之间。脑自动调节(CA)能力通过脑血管阻力变化百分比与动脉球囊充/放气诱导的MAP变化百分比之间的比值计算。在未使用多巴胺时,CA能力的断点出现在MAP为38±18mmHg处;在多巴胺输注速率为10、25和40μg/kg/min时,断点分别出现在44±18、31±14和24±14mmHg处(p = 0.057)。稳态脑灌注指数和脑静脉饱和度均不受多巴胺输注的影响。
多巴胺输注在低血压时倾向于改善CA能力,而稳态脑血流量指数和脑静脉饱和度不受多巴胺输注的影响。因此,多巴胺似乎不会损害新生仔猪的CA。