No abstract

Vilanova JM, Figueras J, Roselló J, Gómez G, Gelpí E, Jiménez R. Arachidonic acid metabolites in CSF in hypoxic-ischaemic encephalopathy of newborn infants. Acta Paediatr 1998; 87: 588-92. Stockholm. ISSN 0803-5253The aim of this study was to evaluate the cerebral synthesis of eicosanoids in the asphyctic newborn and to investigate the relation between the prostanoid profiles in cerebrospinal fluid (CSF) and the appearance and severity of hypoxic-ischaemic encephalopathy (HIE). Levels of 6-keto-PGF 1-a , TXB 2 , PGE 2 and PGF 2-a in CSF were measured in 40 full term newborns during the first day of life. Thirty of these newborns had birth asphyxia and were divided into three groups: 10 without HIE, 12 with mild HIE and 8 with moderate-severe HIE. They were compared to a control group of 10 non-hypoxic newborns. Determinations of the metabolites in CSF were performed by RIA and expressed as pg/ml (mean Ϯ SD). The CSF TXB 2 (thromboxane A 2 metabolite) in asphyxiated newborns was always higher than in the control group (28.12 Ϯ 10.6), and related to the severity of HIE ( p ¼ 0:005): without HIE (50.84 Ϯ 16.4; p ¼ 0:02), mild HIE (80.65 Ϯ 12.64; p Ͻ 0:01) and moderate-severe HIE (178.14 Ϯ 20.5; p Ͻ 0:01). The CSF 6-keto-PGF 1-a (prostacyclin metabolite) in asphyxiated newborns was always higher than in the control group (80.55 Ϯ 12.56), but indirectly related to the severity of HIE: without HIE (240.95 Ϯ 28.12; p Ͻ 0:01), mild HIE (183.65 Ϯ 30.1; p Ͻ 0:01) and moderate-severe HIE (140.55 Ϯ 25.12; p Ͻ 0:01). In the moderatesevere HIE group, the increase in TXB 2 was higher than the rise in 6-keto-PGF 1-a . ٖ Eicosanoids, hypoxicischaemic encephalopathy, newborn, perinatal asphyxia, prostaglandins, prostanoids J Figueras-Aloy,

Roldán A, Figueras-Aloy J, Deulofeu R, Jiménez R. Glycine and other neurotransmitter amino acids in cerebrospinal fluid in perinatal asphyxia and neonatal hypoxic-ischaemic encephalopathy. Acta Paediatr 1999; 88: 1137-41. Stockholm. ISSN 0803-5253The aim of this study was to evaluate the concentrations of neurotransmitter amino acids in the cerebrospinal fluid (CSF) of asphyctic newborns, and to establish whether these concentrations are related to the degree of hypoxic-ischaemic encephalopathy (HIE). Levels of glutamate, aspartate, glycine and taurine in CSF were measured in 48 full-term newborns during the first 2 d of life. Thirty-nine of these newborns had birth asphyxia and were divided into three groups: 11 without HIE, 19 with mild HIE and 9 with moderate HIE. None suffered from severe HIE. They were compared with a control group of 9 non-hypoxic newborns. Determinations of the amino acids in CSF were made by chromatography and expressed as mmol/l (mean AE SD). CSF glycine value was related to erythrocyte count, and CSF taurine value was related to its plasmatic level. Levels of CSF glycine were related to the severity of HIE (p = 0.020): control (12.08 AE 4.

Vasopressin in cerebrospinal fluid has been measured in 27 fullterm newborns with hypoxic-ischemic encephalopathy. These newborns were divided into three groups according to the degree of neurological involvement, and they have been compared with a control group of 10 newborns. Determinations of vasopressin in cerebrospinal fluid and plasma were done by RIA. The cerebrospinal fluid vasopressin in asphyxiated newborns was higher than in the control group (p < 0.001); the mean concentration in the group of newborns classified as moderate or severe hypoxic-ischemic encephalopathy was higher than in the control group (18.7 pg/ml vs 4.66 pg/ml), and also higher than in the group classified as mild (14.2 pg/ml). Cerebrospinal fluid vasopressin values have a direct relationship to the plasmatic values at 12 hours of life (r = 0.76; p < 0.001). We concluded that vasopressin values in cerebrospinal fluid at 12 hours increase according to the clinical severity of the neonatal hypoxic-ischemic encephalopathy and that they have a strong relationship with plasmatic vasopressin.

Two groups of 30 term newborns (normal and anoxic) were analyzed to study the influence of anoxia in the heart rate. The experiment consisted in a polygraphic EEG register before, during and after an acoustic stimulus. In basal conditions of active sleep, the heart rate in the asphyctic newborn was higher than in the normal group. The acoustic stimulation caused a transitional tachycardia. The variability of the heart rate was smaller in the asphyctic group. The basal heart rate varied in relation to the grade of Hypoxic-Ischemic Encephalopathy (HIE) and there was also a difference in the capacity of response to acoustic stimulation between the moderate HIE group and the normal group.