Coumans A B C, Garnier Y, Supçun S, Jensen A, Hasaart T H M, Berger R
Department of Obstetrics and Gynecology, University of Maastricht, Maastricht, The Netherlands.
J Soc Gynecol Investig. 2003 Jul;10(5):275-82. doi: 10.1016/s1071-5576(03)00085-6.
The role of nitric oxide in control of fetal cardiovascular functions and of cerebral blood flow during normoxia and acute hypoxia is only partially known. We studied the effects of nitric oxide synthase inhibition on the distribution of cardiac output in preterm sheep using N(omega)-nitro-L-arginine methyl ester (L-NAME).
Thirteen fetal sheep were instrumented at a gestational age of 107 days. Three days later fetuses received L-NAME (n = 7) or vehicle infusion (n = 6). At 0 minutes, acute hypoxia was induced by occlusion of the maternal aorta for 2 minutes. Organ blood flows (microsphere method) and physiologic variables (fetal heart rate, mean arterial pressure [MAP], oxygen saturation, and pH) were measured at -75, -1, +2, +4, and +30 minutes.
L-NAME caused bradycardia and an increase in MAP. A significant decrease in cardiac output by 32% occurred in the control group during the control period, which was consequently reflected in organ blood flows. L-NAME injection reduced cardiac output by 64% during normoxia. Blood flow to the fetal body, placenta, and cerebrum decreased by 62%, 66%, and 55%, respectively. During acute hypoxia, L-NAME did not change the redistribution of cardiac output toward the central organs. In the L-NAME group MAP increased, and fetal heart rate was maintained; in contrast, in controls MAP initially decreased and then returned to control values while fetal heart rate decreased. After hypoxia L-NAME delayed the recovery of cardiac output and blunted the increase in blood flow to the brain and heart.
Although influenced by fetal stress after extensive instrumentation, the results of this study indicate that nitric oxide plays a role in fetal cardiovascular control during normoxia and acute hypoxia. Nitric oxide also mediates the increase in blood flow to the brain and heart immediately after hypoxia.
一氧化氮在常氧和急性缺氧期间对胎儿心血管功能及脑血流控制中的作用仅部分为人所知。我们使用N（ω）-硝基-L-精氨酸甲酯（L-NAME）研究了一氧化氮合酶抑制对早产绵羊心输出量分布的影响。
13只胎羊在妊娠107天时进行仪器植入。三天后，胎儿接受L-NAME（n = 7）或载体输注（n = 6）。在0分钟时，通过阻断母体主动脉2分钟诱导急性缺氧。在-75、-1、+2、+4和+30分钟时测量器官血流量（微球法）和生理变量（胎儿心率、平均动脉压[MAP]、氧饱和度和pH）。
L-NAME导致心动过缓和MAP升高。对照组在对照期内心输出量显著下降32%，这进而反映在器官血流量上。常氧期间注射L-NAME使心输出量减少64%。流向胎儿身体、胎盘和大脑的血流量分别减少62%、66%和55%。急性缺氧期间，L-NAME未改变心输出量向中心器官的重新分布。在L-NAME组中MAP升高，胎儿心率维持不变；相比之下，在对照组中MAP最初下降，然后恢复到对照值，而胎儿心率下降。缺氧后，L-NAME延迟了心输出量的恢复，并减弱了流向大脑和心脏的血流量增加。
尽管在广泛仪器植入后受胎儿应激影响，但本研究结果表明一氧化氮在常氧和急性缺氧期间对胎儿心血管控制中起作用。一氧化氮还介导缺氧后立即流向大脑和心脏的血流量增加。
