Department of Physiology, University of Auckland, Auckland, New Zealand.
Department of Pediatrics and Center for Perinatal Biology, Division of Neonatology, Loma Linda University School of Medicine, Loma Linda, CA, USA.
Reprod Sci. 2014 Dec;21(12):1483-91. doi: 10.1177/1933719114530187. Epub 2014 Apr 16.
In this study, we tested the hypothesis that cerebral hypoperfusion after asphyxia and induced hypothermia is associated with reduced circulating nitrite levels as an index of nitric oxide synthase (NOS) activity. The preterm fetal sheep at 0.7 gestation (103-104 days, term = 147 days) received 25-minute umbilical cord occlusion, followed by mild whole-body cooling from 30 minutes to 72 hours after occlusion. Occlusion and induced hypothermia were independently associated with reduced carotid vascular conductance (CaVC) from 2 to 72 hours, and with transiently suppressed plasma nitrite levels at 6 hours. There was a significant within-subjects correlation (r(2) = 0.33, P = .002) between CaVC and plasma nitrite values in the first 24 hours after occlusion but not after sham occlusion. These findings suggest that in preterm fetal sheep, changes in NOS activity are an important mediator of changes in carotid vascular tone in the early recovery phase after asphyxia and may help mediate some of the vascular effects of induced hypothermia.
在这项研究中，我们检验了这样一个假设，即在窒息和诱导性低温后大脑灌注不足与循环亚硝酸盐水平降低有关，亚硝酸盐水平降低作为一氧化氮合酶（NOS）活性的指标。妊娠 0.7 期（103-104 天，足月= 147 天）的早产胎儿羊接受 25 分钟脐带结扎，然后在结扎后 30 分钟至 72 小时进行全身轻度降温。结扎和诱导性低温与 2 至 72 小时的颈动脉血管传导性（CaVC）降低以及 6 小时时血浆亚硝酸盐水平的短暂抑制有关。在结扎后 24 小时内，CaVC 和血浆亚硝酸盐值之间存在显著的受试者内相关性（r²= 0.33，P =.002），但在假结扎后则没有。这些发现表明，在早产胎儿羊中，NOS 活性的变化是窒息后早期恢复阶段颈动脉血管张力变化的重要介导物，可能有助于介导诱导性低温的一些血管效应。
