Objective To determine the effect of labour on free oxygen radical activity in the fetus, as reflected Design Prospective, observational study. SettingMethods by lipid peroxide levels in umbilical cord arterial blood.Department of Obstetrics and Gynaecology, The Chinese University of Hong Kong.Umbilical cord arterial and venous blood samples were collected from singleton term infants delivered by elective caesarean section. Base excess, PO,, pC0, and pH were measured in both samples and compared to identify double venous samples. Cord arterial acid-base balance and concentrations of organic hydroperoxides and malondialdehyde were compared with those obtained from normal vaginal deliveries. ResultsCord arterial blood samples, obtained from cases of uncomplicated labour followed by spontaneous vaginal delivery, had significantly higher lipid peroxide concentrations than those delivered following elective caesarean section. Ths was most marked for malondialdehyde with a median value increased by 105%, whilst organic hydroperoxide was increased by only 27%. Of the acid-base parameters, base excess was increased by 78%, with only minimal changes in pH, $0, and PO,. These differences remained highly significant after including other pregnancy characteristics in multivariate analysis. ConclusionThe findings indicate that high levels of free oxygen radical activity in the fetus are a function of the labour process, as are changes in acid-base balance.

1 The modulatory effects of L-glutamate and its structural analogues, and of y-aminobutyric acid (GABA), on sympathetic co-transmission were studied in the rat isolated vas deferens exposed to electrical field stimulation (EFS). 2 Application of exogenous L-glutamate caused a concentration-dependent (1 /M -3 mM) inhibition of the rapid twitch component of the biphasic EFS contraction. However, L-glutamate (1 MM-3 mM) had a minimal effect on the phasic contraction induced by exogenous adenosine 5'-triphosphate (ATP, 150 MM) and noradrenaline (50 Mm). Unlike L-glutamate, D-glutamate had no effect on the EFS contraction. 3 The L-glutamate-induced inhibition of the EFS contractions was significantly attenuated by the glutamate decarboxylase (GAD) inhibitor 3-mercapto-propionic acid (150 Mm) and was abolished in the presence of the GABA transaminase (GABA-T) inhibitor, 2-aminoethyl hydrogen sulphate (500 gM).4 The L-glutamate-induced inhibition of the electrically evoked contraction was not affected by the adenosine Al-receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX)(30 nM), reactive blue 2 (30 Mm) or the GABAA receptor antagonist bicuculline (50 gM). However, the GABAB receptor antagonist 2-hydroxysaclofen (50 uM) significantly inhibited the L-glutamate effect. 5 Similar to L-glutamate, GABA also caused a concentration-dependent (0.1 -100 Mm) inhibition of the EFS contractions. This GABA-induced inhibition was not affected by either the GABAA receptor antagonist bicuculline (50 gM) or reactive blue 2 (30 gM). However, a significant attenuation of the GABA-mediated effect was recorded with the GABAB receptor antagonist 2-hydroxysaclofen (50 gM).Contractions of the vas deferens induced by exogenous ATP and noradrenaline were not affected by GABA (0.1-100 gM).6 The L-glutamate analogues, N-methyl-D-aspartate (NMDA) (1 MM-I mM) and quisqualate (Quis 0.1 Mm -0.3 mM) had no effect, whilst kainate (Kain, 1 MM-I mM) caused an inhibition of the EFSinduced contractions. Effects of Kain could be abolished by the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dioxine (CNQX, 10 gM). NMDA, Quis and Kain had no effect on the exogenous ATP-or noradrenaline-induced contractions. 7 It is concluded that the excitatory amino acid L-glutamate modulates the electrically evoked vas deferens contraction through conversion to the inhibitory amino acid GABA by a specific GABA transaminase. The GABA formed may then act on GABAB receptors and cause inhibition of the contraction through a presynaptic mechanism.

Cholesterol and cholesteryl ester concentrations and cholesteryl ester fatty acid substituents have been measured during the first 10 weeks of life in tissues of normal and dystrophic mice. In normal Swiss and 129ReJ(+/?) mice the concentrations of both cholesterol and cholesteryl esters remain essentially constant in liver, increase in brain and fall sharply in both thigh (mixed fiber type muscles) and chest muscles (predominantly slow oxidative muscles) over this period. In all cases the concentration of free cholesterol exceeds that of esterified cholesterol. In dystrophic mice, similar patterns are found in brain and liver. In both thigh and chest muscles, however, the developmental pattern is significantly different. After an initial decrease the concentrations of cholesterol and cholesteryl esters increase rapidly with the largest increase occurring in the concentration of cholesteryl esters which by 10 weeks of age exceeds the concentration of cholesterol in chest muscle. During the same period the pattern of esterified fatty acids changes gradually in dystrophic tissues towards an increasing ratio of unsaturated/saturated fatty acids. By 10 weeks of age this ratio is significantly higher in dystrophic tissues than normal in all tissues tested.