Objective: To compare foetal electrocardiogram (T/QRS ratio) and cardiotocography (CTG) during the second stage of labour with lactate and acid-base balance in cord artery blood al delivery. Design: Fortysix parturients delivered at the National University of Singapore were monitored during the second stage of labour with T/QRS ratios and CTG. At delivery blood from a segment of clamped cord was sampled for lactate and acid-base balance analyses. The Spearman Rank correlation, the Mann Whitney U-test and the Kruskal Wallis ANOVA were used when appropriate. Results: Maternal pushing time was significantly correlated to lactate (R=0.51; P=0.0003), pH (R=-0.38; P=0.009) and base deficit (R=0.33; P=0.026), but not to T/QRS ratio (R=0.002; P=0.99). No significant correlation between lactate and T/QRS ratios (R=0.06; P=0.70) or type of CTG pattern was found (P=0.10), though there were significant differences in pH (P=0.029) and T/QRS ratios (P=0.037) between groups with different FHR abnormalities. Conclusion: Lactate increases progressively with maternal pushing time. No significant correlation was found between lactate and the T/QRS ratio. Lack of correlation is likely to be due to poor sensitivity of foetal ECG at this level of foetal stress, though the influence from transplacentally transferred maternal lactate cannot be excluded. (C) 1998 Elsevier Science Ireland Ltd.

The interrelationships between lactate and pH, noradrenaline (NA), adrenaline (A) and dopamine (DA) were investigated in cord artery (CA) and vein (CV) blood at delivery. Sixty consecutive, spontaneous, vaginal deliveries with fetuses in cephalic presentation were assessed. Median gestational age at delivery was 40 weeks (range, 35–43). There were significant correlations between lactate and pH (P < 0.01), NA (P < 0.01), A (P < 0.05) and arterio-venous NA (P < 0.05) and DA differences (P < 0.01) in CA blood, while no variable correlated significantly to lactate in CV blood. The higher levels both of lactate and of catecholamines in CA blood are probably fetally derived. Dividing the material into high and low lactate subgroups (cut-off level, 75th percentile) showed a high lactate level to be associated with lower pH and higher catecholamine levels in CA blood, though the relationship was only statistically significant for pH. The levels both of catecholamines and of lactate were lower than those reported for cases of fetal distress, and reflect the lower level of fetal stress in the present series of normal deliveries. The low level of fetal stress and the differences in turnover rates between catecholamines and lactate might obscure their causal relationships, vis-á-vis fetal adaptation to extrauterine life during the course of parturition.

Fetal and neonatal glucose and lactate levels and acid-base balance after continuous maternal infusion of 5% dextrose at 180 mL/h (9 g/h) was compared with 0.9% saline solution in a prospective, randomized study from selected monitored labors. An infusion of 5% dextrose produced significantly increased glucose levels in maternal (p <0.01), cord artery (p <0.01), and cord vein (p <0.001) blood. An increased maternal insulin level was also present (p <0.05), but no differences in cord insulin levels were observed. beta-Hydroxybutyrate was lower in maternal (p <0.05) and cord vein (p <0.01), but not in cord artery blood, after maternal dextrose infusion. No significant changes occurred in blood lactate levels between the two groups in either mother, fetus, cord, or neonate. Acid-base balance in cord blood did not differ between the two groups. Maternal infusion of 5% dextrose at 180 mL/h (9 g/h), compared with saline solution, produces higher glucose levels in both mother and fetus, but increased insulin concentrations only in the mother. Dextrose infusion also lowers beta-hydroxybutyrate in maternal and cord vein blood. No differences were seen in lactate levels or cord acid-base balance. Both regimens seem safe according to risks for lactacidosis and neonatal hypoglycemia in the normoxemic, normal size fetus.

ABSTRACTObjective To determine fetal scalp blood lactate with a new test strip method in parturients with normal and abnormal cardiotocograms during labour and to describe the relation to maternal lactate, fetal scalp blood pH, cord artery lactate and acid‐base balance.Setting Labour wards at the University Hospitals of Huddinge and Lund and at the County Hospital of Östersund, Sweden.Materials and method Fetal scalp blood was sampled for lactate (n= 269) and pH (n= 285) determination in 177 parturients with abnormal intrapartum CTG. Lactate and pH were also analysed in a group of 64 women with normal pregnancies and with a reactive fetal heart rate tracing prior to sampling of fetal scalp blood. At fetal blood sampling lactate was also determined in maternal capillary blood, while at birth lactate and acid‐base balance in cord artery blood was performed in almost all cases.Main outcome measurements Medians and percentiles (lactate and acid‐base balance). Correlation between fetal scalp blood lactate (dependent) and scalp blood pH, cord artery blood lactate and acid‐base parameters and labour time prior to fetal blood sampling.Results In the group with abnormal cardiotocograms, fetal scalp and umbilical artery blood lactate and acid‐base parameters differed significantly from the same parameters in the normal group. The fetal‐maternal lactate gradient changed from negative in the normal group to positive in the fetal distress group. Multiple regression analysis, with scalp lactate as the dependent parameter, revealed a significant correlation with fetal scalp blood pH (P < 0.001) and umbilical artery lactate (P < 0.01).Conclusions Intrapartum scalp blood lactate was significantly correlated with pH and cord artery lactate. The results indicate that increased lactate levels in fetal blood sampling describes fetal lactacidosis. The new disposable test strip requiring only 5 μl of blood for lactate determination may be better than traditional methods for monitoring fetal wellbeing in labour.

Gamma-Glutamyltransferase (GGT), formerly called gamma-glutamyltranspeptidase, is predominantly a membrane-bound enzyme. The estimation of enzyme activity in serum is useful in monitoring hepatobiliary complaints. The electrophoresis with surfactant (Triton X-100) developed by the authors demonstrates five distinct bands of enzyme activity in the serum from patients with hepatitis. These bands are called isoenzyme GGT1 to 5 from anode to cathode, respectively. Four isoenzymes GGT2 to 5, except GGT1 are demonstrated in normal adult serum. The affinity electrophoresis is more variable to identify the hepatoma associated isoenzyme, namely HA-GGT. Concanavalin A used in the method has no affinity with HA-GGT and this isoenzyme is separated from GGT2. The diagnostic sensitivity and specificity for the measurement of HA-GGT were 58% and 83%, respectively.

A sensitive and specific method was developed for measuring medium-chain dicarboxylic acids (adipic and suberic acid) in urine. These acids were extracted from urine with diethyl ether and converted into fluorescent derivatives with 9-anthryldiazomethane, which can be separated by high-performance liquid chromatography. The reproducibility was high and the recovery from urine was above 90%. Urinary concentrations of adipic acid in streptozotocin-induced diabetic rats were significantly higher than those in control rats. In diabetic patients, both adipic acid and suberic acid tended to be high, but not significantly. This method should be useful for measuring dicarboxylic acids in urine.

It is known that the metabolism of some drugs is altered in diabetic patients and in rats with experimental diabetes induced by chemical agents, such as streptozocin. The induction and/or suppression of hepatic cytochrome P450 isozymes seen in diabetes seem to contribute to this alteration. Both metabolic and hormonal disturbances following insulin deficiency in diabetic rats are responsible for these changes. Marked changes in hepatic P450 isozymes in diabetic rats include increases in the isozymes induced by ketones and lipids, including fatty acids, and decreases in the isozymes regulated by growth hormone and testosterone. Suppressed secretion of thyroid hormones also participates in the mechanism causing these changes. Analysis of cytochrome P450 isozymes in diabetic rats is helpful in elucidating the impaired metabolism of some endogenous substrates catalyzed by the cytochrome P450, such as steroid hormones and fatty acids, in diabetes. The results of these analyses also provide insight into the prescription of drugs for diabetic patients.

A new test strip method was used to determine the lactate concentration in fetal scalp blood during normal labor. Sixty-six fetal scalp blood samples were collected at cervical dilatations between 4 cm and 10 cm. The mean lactate value was 1.7 +/- 0.8 mmol/l simultaneously (IS.D.) and the mean pH sampled simultaneously was 7.36 +/- 0.04 (IS.D.). The corresponding values for base deficit was 2.1 (+/- 1.9) and for pCO2 5.8 (+/- 0.8). No difference was seen in lactate concentrations or pH values in early compared to late first stage of labor. The mean lactate concentration in the umbilical artery immediately after delivery was 3.7 mmol/l +/- 1.2 (IS.D.). The method was easy to handle and gave the result within 60 seconds.

We have developed a method for the quantitative analysis of Lewis antigens on human red blood cells (RBC) using immunofluorescence labeling and flow cytometry. Initially, Lewis a and Lewis b (Le(a) and Le(b)) antigens were labeled with monoclonal anti-Le(a) or anti-Le(b) antibodies followed by labeling with the fluorescein isothiocynate (FITC)-conjugated second antibody. This method was not sensitive enough to identify the Lewis antigens on RBC, although the FITC method is very commonly used for antigens on white blood cells. Next, we selected the enhanced labeling technique using the avidin-biotin procedure. Biotinylated anti-mouse IgM was used for the second label and the reaction with R-phycoerythrin (RPE)-conjugated streptavidin followed to produce the fluorescence. The method was found to be effective for our objectives. From the results analyzed by the enhanced labeling technique, differences were not found in either the levels of the antigen-positive percentage and the peak mean channel of Le(a) antigens on RBC in the groups of blood type O and A (in ABO system). On the other hand, both the levels of Leb antigens on RBC were higher in the groups of blood type O than in those of blood type A. We found both Le(a) and Le(b) antigens on RBC from a few blood type O subjects. We conclude that enhanced labeling and flow cytometry constitute a useful technique for the determination of Lewis antigens on RBC and that this method enables the precise quantification of such antigens.

Hepatic microsomal cytochrome P450s. which are involved in the metabolism of drugs, hormones. prostaglandins and fatty acids. change when animals develop diabetes. We studied changes in cytochrome P450 isozymes in both hepatic and renal microsomes of rats with diabetes caused by streptozocin, and compared the results with changes in catalytic activities in the microsomes. In hepatic microsomes of diabetic rats, the amount of cytochrome P450 2E1. an acetone-inducible isozyme. was two and a half times that of control rats, and that of P450 4A2, a major renal isozyme, was three times that in the controls. The amounts of cytochrome P450s 2A1, 2C6, 2C7, 3A2 and 4A3 increased in hepatic microsomes of diabetic rats. and P450 2C11 decreased. Treatment with insulin restored these to the levels in the controls. The catalytic activities of aniline hydroxylation, 7-ethoxycoumarin O-dealkylation, testosterone 2beta, 6beta, 7alpha. and 16beta-hydroxylation, and omega-, (omega - 1)-hydroxylation of lauric acid were high in the hepatic microsomes of diabetic rats, and testosterone 2alpha and 16alpha-hydroxylation activities were low. In renal microsomes of diabetic rats, cytochrome P450s 2E1, 4A2 and K-4 were induced, and omega- and (omega - 1)-hydroxylation activities were high. These changes were reversed by insulin treatment. The induction and suppression of cytochrome P450 isozymes in diabetic rats were consistent with the changes in the catalytic activities. In both hepatic and renal microsomes, P450s 2E1 and 4A2 were induced, altered metabolism of ketones and fatty acids in diabetes may contribute to these changes.

Effects of thyroid hormone treatment on renal P450 expression in the diabetic rats were investigated. Diabetes produced by streptozotocin induced CYP4A2 and P450 K-2 (similar form with CYP2C23) but not P450 K-4 (similar form with CYP4A8) and induced lauric acid hydroxylation activity. The serum thyroid hormone level was decreased with diabetes. Treatment of diabetic rats with thyroid hormone (T3) as well as with insulin reversed the increase in the levels of CYP4A2 and P450 K-2. Thyroidectomy also induced CYP4A2 and P450 K-2 in the rat kidney. The increase was reversed by treatment of thyroidectomized rats with T3. These findings suggest that expression of CYP4A2 and P450 K-2 in rat kidney is suppressively regulated by thyroid hormone and the decrease in thyroid hormone level in the diabetic state affects the levels of CYP4A2 and P450 K-2.

We have developed an assay system for measuring lactate in whole blood, consisting of a single-use strip of an enzyme-coated electrode and a small meter. The electrode strip is made of three plastic films: a cover sheet, a spacer, and an insulation layer printed with electrodes that are coated with lactate oxidase (EC 1.1.3.x) and ferricyanide as an electron mediator. The meter measures the magnitude of the anodic current of the reduced mediator by the enzymatic reaction and displays the lactate concentration 60 s after a blood sample (5 microL) is applied. The calibration curve was linear up to 20 mmol/L, and the between-run CVs at three concentrations were 1.7-8.4%. Lactate concentrations determined by this method (y) in blood samples from healthy individuals before and after exercise agreed with the results obtained by the conventional enzymatic method (x): y = 0.97x - 0.3, Sy/x = 0.7. This assay provides a rapid and convenient test for measuring blood lactate concentrations.

ABSTRACTObjective To compare the measurement of lactate in fetal scalp and umbilical artery blood by a new dry reagent strip method with a commercially available enzymatic method using plasma (Monotest).Design Comparative study.Subjects Fetal scalp blood samples were obtained during labour from 24 fetuses and umbilical artery blood samples were obtained at birth in a further 51 deliveries.Results The concentration of lactate in scalp and umbilical artery blood measured by the reagent strip method correlated well (r= 0.94, P<0.001 and 0.95, P<0.001 respectively) with the enzymatic plasma method. The paper strip method tended to give lower readings than the enzymatic method when the fetal haematocrit was ≥50%.Conclusions The new dry reagent strip method which takes only 1 min to carry out and requires only 20 μl of blood seems to be handy and reliable. This system provides a convenient and rapid test for measuring fetal blood lactate.