Ogoh Shigehiko, Moralez Gilbert, Washio Takuro, Sarma Satyam, Hieda Michinari, Romero Steven A, Cramer Matthew N, Shibasaki Manabu, Crandall Craig G
Department of Biomedical Engineering, Toyo University, Kawagoe-shi, Saitama, Japan;
Institute for Exercise and Environmental Medicine, University of Texas Southwestern Medical Center, Dallas, Texas; and.
Am J Physiol Heart Circ Physiol. 2017 Dec 1;313(6):H1155-H1161. doi: 10.1152/ajpheart.00287.2017. Epub 2017 Sep 15.
The effect of acute increases in cardiac contractility on cerebral blood flow (CBF) remains unknown. We hypothesized that the external carotid artery (ECA) downstream vasculature modifies the direct influence of acute increases in heart rate and cardiac function on CBF regulation. Twelve healthy subjects received two infusions of dobutamine [first a low dose (5 μg·kg·min) and then a high dose (15 μg·kg·min)] for 12 min each. Cardiac output, blood flow through the internal carotid artery (ICA) and ECA, and echocardiographic measurements were performed during dobutamine infusions. Despite increases in cardiac contractility, cardiac output, and arterial pressure with dobutamine, ICA blood flow and conductance slightly decreased from resting baseline during both low- and high-dose infusions. In contrast, ECA blood flow and conductance increased appreciably during both low- and high-dose infusions. Greater ECA vascular conductance and corresponding increases in blood flow may protect overperfusion of intracranial cerebral arteries during enhanced cardiac contractility and associated increases in cardiac output and perfusion pressure. Importantly, these findings suggest that the acute increase of blood perfusion attributable to dobutamine administration does not cause cerebral overperfusion or an associated risk of cerebral vascular damage. A dobutamine-induced increase in cardiac contractility did not increase internal carotid artery blood flow despite an increase in cardiac output and arterial blood pressure. In contrast, external carotid artery blood flow and conductance increased. This external cerebral blood flow response may assist with protecting from overperfusion of intracranial blood flow.
心脏收缩力急性增加对脑血流量（CBF）的影响尚不清楚。我们推测，颈外动脉（ECA）下游血管系统会改变心率和心脏功能急性增加对CBF调节的直接影响。12名健康受试者接受了两次多巴酚丁胺输注（首先是低剂量（5μg·kg·min），然后是高剂量（15μg·kg·min）），每次输注12分钟。在多巴酚丁胺输注期间进行心输出量、通过颈内动脉（ICA）和ECA的血流量以及超声心动图测量。尽管多巴酚丁胺使心脏收缩力、心输出量和动脉压增加，但在低剂量和高剂量输注期间，ICA血流量和传导率均较静息基线略有下降。相比之下，在低剂量和高剂量输注期间，ECA血流量和传导率均显著增加。在心脏收缩力增强以及心输出量和灌注压相应增加期间，更大的ECA血管传导率和相应的血流量增加可能会保护颅内脑动脉免于过度灌注。重要的是，这些发现表明，多巴酚丁胺给药引起的血液灌注急性增加不会导致脑过度灌注或脑血管损伤的相关风险。尽管心输出量和动脉血压增加，但多巴酚丁胺引起的心脏收缩力增加并未增加颈内动脉血流量。相比之下，颈外动脉血流量和传导率增加。这种脑外血流反应可能有助于防止颅内血流过度灌注。
