Pourcyrous M, Bada H S, Yang W, Parfenova H, Wong S P, Korones S B, Leffler C W
Laboratory for Research in Neonatal Physiology, Department of Pediatrics, The University of Tennessee, Memphis, USA.
J Pediatr. 1999 Jan;134(1):90-6. doi: 10.1016/s0022-3476(99)70377-x.
In piglets prolonged asphyxia resulted in decreased cerebrospinal fluid (CSF) 3;,5;-cyclic adenosine monophosphate (cAMP) during recovery; this was associated with reduced pial arteriolar responses to stimuli that use cAMP as a second messenger. We hypothesized that asphyxia in human neonates results in decreased CSF cAMP and that low CSF cAMP is associated with abnormal outcome.
We studied 27 infants with evidence of hypoxic-ischemic insult; 19 were term (group 1) and 8 were preterm (group 2). The normal values of CSF cAMP were determined from 75 infants with no asphyxia; 44 were term (group 3) and 31 were preterm (group 4). CSF cAMP was measured by using radioimmunoassay procedures.
CSF cAMP levels in infants with asphyxia (groups 1 and 2) were 12 +/- 9. 5 and 7.9 +/- 7.1 pmol/mL, respectively, significantly lower than those of groups 3 and 4 (control infants), that is, 21.1 +/- 8.7 and 27.1 +/- 9.2 pmol/mL, respectively (P <.0001). Among infants with asphyxia, 3 died and 10 had abnormal neurologic outcome. Univariate analysis showed that abnormal outcomes were significantly related to CSF cAMP levels, phenobarbital use, and multi-organ failure. However, only CSF cAMP was retained in the model by stepwise logistic regression. CSF cAMP of 10.0 pmol/mL discriminated between those with normal and those with abnormal neurologic outcome. Low CSF cAMP concentration was associated with abnormal long-term outcome, estimated odds ratio of 12.4 (95% CI, 2.1-109.3; P <.006), and sensitivity, specificity, and positive and negative predictive values of 85%, 69%, 73%, and 80%, respectively.
CSF cAMP concentrations were decreased in infants with asphyxia. Low CSF cAMP levels were associated with poor neurologic outcome.
仔猪长时间窒息导致复苏期间脑脊液（CSF）3′,5′-环磷酸腺苷（cAMP）水平降低；这与软脑膜小动脉对以cAMP作为第二信使的刺激反应减弱有关。我们推测人类新生儿窒息会导致脑脊液cAMP水平降低，且脑脊液cAMP水平低与异常预后相关。
我们研究了27例有缺氧缺血性损伤证据的婴儿；19例为足月儿（第1组），8例为早产儿（第2组）。从75例无窒息的婴儿中确定脑脊液cAMP的正常值；44例为足月儿（第3组），31例为早产儿（第4组）。采用放射免疫分析方法测量脑脊液cAMP。
窒息婴儿（第1组和第2组）的脑脊液cAMP水平分别为12±9.5和7.9±7.1 pmol/mL，显著低于第3组和第4组（对照婴儿），即分别为21.1±8.7和27.1±9.2 pmol/mL（P<.0001）。在窒息婴儿中，3例死亡，10例有异常神经学预后。单因素分析显示，异常预后与脑脊液cAMP水平、苯巴比妥使用和多器官功能衰竭显著相关。然而，逐步逻辑回归分析中只有脑脊液cAMP被保留在模型中。脑脊液cAMP为10.0 pmol/mL可区分神经学预后正常和异常的婴儿。脑脊液cAMP浓度低与异常长期预后相关，估计比值比为12.4（95%CI，2.1 - 109.3；P<.006），敏感性、特异性、阳性和阴性预测值分别为85%、69%、73%和80%。
窒息婴儿的脑脊液cAMP浓度降低。脑脊液cAMP水平低与不良神经学预后相关。
