Donor information considered important to donors, recipients and offspring: an Australian perspective.

Donor conception research supports open-identity donor programmes and disclosure to donor-conceived offspring. This study examines Australian donors', recipients' and donor-conceived offspring's views on the importance of different types of biographical information about the donor. Participants (125 recipients, 39 donors (known, identity-release and anonymous), 23 donor-conceived offspring) completed an online or paper self-administered anonymous questionnaire. Individuals rated the importance of 15 types of biographical information and subsequently chose the three they deemed most important. All groups included donor's health history and name as key variables to be available to donor-conceived offspring. Recipients viewed the donor's decision to donate as important, donors thought their feelings about being contacted were important and donor-conceived offspring expressed an interest in the donor's own family. Sperm donors were less inclined to view the provision of information as important compared with offspring. For recipients, the importance of information became apparent once they had disclosed to their children. This is the first study to gauge Australian stakeholders' attitudes to release of information in the donor conception process. The findings support the move to open-identity donation systems and emphasize the importance of considering the varying perspectives of all stakeholders by policy developers.

Myometrial expression of 11 beta-hydroxysteroid dehydrogenase type 2 in rat pregnancy.

The enzyme 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta-HSD2), which reduces glucocorticoid potency in target cells by metabolism of active glucocorticoids, is expressed in the non-pregnant rat uterus in an oestrogen-dependent manner. Because glucocorticoids appear to facilitate parturition in many species, expression of 11 beta-HSD2 in pregnant myometrium is likely to influence pregnancy maintenance and possibly the onset and progression of labour. The present study therefore examined myometrial 11 beta-HSD2 mRNA, protein and bioactivity across rat pregnancy, with emphasis on the peripartum period. A single 1.9 kb transcript of 11 beta-HSD2 mRNA was evident in myometrium at all stages, with maximal (P<0.05) levels observed at day 16 (term=day 23). Consistent with this pattern of mRNA expression, Western blot analysis showed the presence of a 40 kDa 11 beta-HSD2 protein at all stages, with the maximal immunoreactive signal also observed on day 16. The 11 beta-HSD2 signal was immunolocalized to myometrial smooth muscle cells and endometrial stromal cells. Bioactivity specific to 11 beta-HSD2 was detectable in myometrium at all stages, but in contrast to the patterns of 11 beta-HSD2 mRNA and protein, the V(max) decreased at the beginning of pregnancy and remained stable until term. The apparent K(m) of 11 beta-HSD2 for corticosterone increased from 47 +/- 11 nM in non-pregnant myometrium to 75 +/- 7 nM by day 10 of pregnancy, and remained high until returning to an intermediate level on the day of delivery (60 +/- 8 nM). Progesterone competitively inhibited 11 beta-HSD2 bioactivity (K(i)=1.75 muM) whereas 20 alpha-hydroxypregn-4-en-3-one, the other major progestin present during rat pregnancy, had no such effect. In conclusion, these data suggest that local levels of active glucocorticoid in the myometrium are determined by the net effects of myometrial 11 beta-HSD-1 and -2 expression across pregnancy. Because the previously reported increase in myometrial 11 beta-HSD-1 near term occurs with little change in myometrial 11 beta-HSD2 bioactivity, this is likely to facilitate parturition by increasing local concentrations of active glucocorticoid.

Apoptosis in rat placenta is zone-dependent and stimulated by glucocorticoids.

Apoptosis, or physiological cell death, is elevated in the placenta of human pregnancies complicated by fetal growth retardation, suggesting that placental apoptosis may be a key factor in the overall control of feto-placental growth. The present study used DNA internucleosomal fragmentation analysis to characterize apoptosis in the two morphologically and functionally distinct regions of the rat placenta, the basal and labyrinth zones, during the last week of pregnancy (Days 16, 22, and 23). In addition, because glucocorticoids are potent inhibitors of feto-placental growth and can stimulate apoptosis in other tissues, we examined whether dexamethasone treatment in vivo induces placental apoptosis. DNA fragmentation was clearly evident in both placental zones at each stage of pregnancy, with higher levels evident in the basal zone compared with the labyrinth zone on Days 22 and 23. TUNEL analysis, which identifies dying cells in situ, demonstrated positive staining of cells in the basal zone, particularly giant trophoblast cells. Dexamethasone treatment increased DNA fragmentation in the basal zone but not the labyrinth zone. Similarly, maternal treatment with carbenoxolone, which can enhance local concentrations of endogenous glucocorticoid by inhibition of 11 beta-hydroxysteroid dehydrogenase, also increased DNA fragmentation in the basal zone but not in the labyrinth zone. These effects of dexamethasone and carbenoxolone on placental apoptosis were associated with reduced placental and fetal weights. In conclusion, this study shows that apoptosis occurs in both zones of the rat placenta, particularly in the basal zone near term, and is elevated after increased glucocorticoid exposure in vivo. These data support the hypothesis that placental apoptosis is an important player in the regulation of feto-placental growth, and establish the rat as a useful model to study the endocrine control of placental apoptosis.

Full induction of rat myometrial 11beta-hydroxysteroid dehydrogenase type 1 in late pregnancy is dependent on intrauterine occupancy.

The 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD-1) enzyme catalyses the conversion of the biologically inert glucocorticoid 11-dehydrocorticosterone to active corticosterone (11-oxoreductase activity) in vivo, and it is dramatically up-regulated in uterine myometrium in the days leading up to parturition. 11beta-HSD-1 is likely to enhance local concentrations of glucocorticoid within the myometrium and thus facilitate uterine contractility, but the stimulus for the increase in myometrial 11beta-HSD-1 is unknown. The objective of the present study was to test whether the induction of myometrial 11beta-HSD-1 is dependent on uterine occupancy or systemic hormonal signals of late pregnancy. This involved use of a unilateral pregnancy (ULP) model in which the gravid and nongravid uterine horns are both exposed to the normal systemic hormonal milieu of pregnancy. Western blot analysis showed that the 11beta-HSD-1 signal was only partially induced in the nongravid horn of ULP rats on Day 22 of pregnancy (term: Day 23). Moreover, artificial distension of this nongravid horn had no effect on myometrial 11beta-HSD-1 immunoreactivity or bioactivity at either Day 16 or Day 22 of pregnancy. Removal of fetuses and placentas on Day 18 reduced myometrial 11beta-HSD-1 bioactivity 4 days later, and this effect was not overcome by artificial maintenance of uterine distension. In contrast, after fetectomy at Day 18 (i.e., removal of the fetus but not placenta), myometrial 11beta-HSD-1 bioactivity was largely maintained on Day 22, indicative of placental support for myometrial 11beta-HSD-1 over this period. In conclusion, our data show that full induction of myometrial 11beta-HSD-1 expression and associated 11-oxoreductase bioactivity late in rat pregnancy is dependent upon intrauterine occupancy. Although the hormonal milieu of late pregnancy appears to stimulate myometrial 11beta-HSD-1 marginally, full induction clearly requires an additional stimulus. Manipulations involving fetectomy and artificial uterine distension indicate that the placenta provides at least part of this stimulus, but uterine stretch does not appear to play a role.

Dual function of 11beta-hydroxysteroid dehydrogenase in placenta: modulating placental glucocorticoid passage and local steroid action.

Target cell metabolism of glucocorticoids is now recognized as an important modulator of ligand access to the glucocorticoid receptor (GR). This metabolism occurs via two distinct 11beta-hydroxysteroid dehydrogenase (11beta-HSD) enzymes (types 1 and 2) that catalyze interconversion of active glucocorticoids (cortisol and corticosterone) and their inactive 11-keto products (cortisone and 11-dehydrocorticosterone, respectively). The focus of this review is on the biology of the 11beta-HSD enzymes in the placenta, where they also regulate passage of maternal glucocorticoids to the fetus. The presence of this metabolic barrier at the maternal-fetal interface is potentially crucial to fetal growth and development, since maternal glucocorticoid levels are elevated in pregnancy and since excess glucocorticoid exposure in fetal life has detrimental effects on prenatal growth and increases susceptibility to disease in subsequent adult life. In primates, transplacental glucocorticoid passage also appears to play an important role in the induction of an autonomous fetal hypothalamic-pituitary-adrenal axis near term. Placental 11beta-HSD is also likely to modulate glucocorticoid actions within the placenta, per se, by regulating their access to placental GR. Moreover, because some progesterone effects are exerted via the GR, placental 11beta-HSD may regulate progesterone-glucocorticoid competition for access to this receptor and thereby affect the biological actions of both steroids in the placenta.

Immunolocalization of 11beta-hydroxysteroid dehydrogenase types 1 and 2 in rat uterus: variation across the estrous cycle and regulation by estrogen and progesterone.

Glucocorticoid hormone action in several target tissues is dependent not only on the expression of the glucocorticoid receptor, but also on that of the 11beta-hydroxysteroid dehydrogenase (11betaHSD) enzymes, 11betaHSD-1 and -2. In the uterus, glucocorticoids can exert inhibitory effects on a range of important functions, particularly in relation to the effects of estrogen. Therefore, the present study examined immunolocalization of the two 11betaHSD enzymes in the rat uterus at each stage of the estrous cycle and after ovariectomy with or without estrogen/progesterone replacement. In cycling rats 11betaHSD-1 was localized to luminal and glandular epithelial cells and to eosinophils in both the endometrial stroma and myometrium. In contrast, 11betaHSD-2 immunostaining was localized to endometrial stromal cells and myometrial cells, with no staining evident in epithelial cells or eosinophils. Immunostaining for both enzymes was cycle dependent, being maximal at proestrus and minimal at diestrus. Western blot analysis of whole uterus at proestrus showed the presence of 34- and 40-kDa immunoreactive species for 11betaHSD-1 and -2, respectively. These immunoreactive signals were almost abolished by ovariectomy, but this effect was reversed for both enzymes by estrogen replacement with or without progesterone. These effects of ovariectomy and steroid replacement were confirmed by immunocytochemical analysis, with the exception that progesterone appeared to enhance the stimulatory effects of estrogen on 11betaHSD-2 specifically within the endometrial stroma. In conclusion, these results establish the presence of both 11betaHSD-1 and -2 in the nonpregnant rat uterus and show distinct distributions for the two enzymes and cyclic variation related to positive regulation by ovarian steroids. The physiological implications of these patterns of 11betaHSD expression will ultimately depend on the reaction direction for each enzyme, but 11betaHSD-2 is likely to limit disruptive effects of glucocorticoids on the endometrial stroma, and 11betaHSD-1 may then serve to selectively reactivate glucocorticoids in epithelial cells.

The activity of a combination of penicillin and novobiocin against bovine mastitis pathogens: development of a disk diffusion test.

The combination of penicillin and novobiocin is currently available for the treatment of bovine mastitis, but methods are not available for susceptibility testing of the combination by veterinary diagnostic laboratories. The minimum inhibitory concentration (MIC) and disk diffusion data were determined for penicillin, novobiocin, and a combination of the two in a 1:2 ratio for 225 staphylococcal, streptococcal, and Gram-negative isolates from bovine intramammary infections. Based on the drug concentrations in milk following infusion, linear regression analysis, and error rate bounding, the interpretive zone diameters selected were < or = 16 mm for resistant isolates and > or 17 mm for susceptible isolates with a disk containing 10 U of penicillin and 30 micrograms of novobiocin. Additionally, MIC breakpoints of < or = 2 micrograms/ml of penicillin and 4 micrograms/ml of novobiocin were selected to categorize isolates as susceptible and > or = 4 micrograms/ml of penicillin and 8 micrograms/ml of novobiocin were selected to categorize isolates as resistant. The MIC and disk diffusion results, as well as studies to monitor bacterial killing by antimicrobial agents over time, indicated that the combination of penicillin and novobiocin in a 1:2 ratio was more active than were the individual drugs. Kinetics of the kill curves with the penicillin and novobiocin combination (1:2 ratio) showed that the combination was bactericidal for Staphylococcus aureus and Staphylococcus xylosus.

Induction of myometrial 11beta-hydroxysteroid dehydrogenase type 1 messenger ribonucleic acid and protein expression late in rat pregnancy.

Myometrial function in pregnancy is regulated by a range of hormonal stimuli, including glucocorticoids, particularly in the period leading up to parturition. Glucocorticoid hormone action is dependent not only on expression of glucocorticoid receptor (GR) within target cells, but also on local expression of the enzyme 11beta-hydroxysteroid dehydrogenase (11betaHSD). Therefore, this study examined changes in myometrial 11betaHSD bioactivity and expression (messenger RNA and protein) of the 11betaHSD-1 isoform and whether 11betaHSD-1 and GR are colocalized to myometrial cells. Myometrial 11-oxoreductase activity (conversion of [3H]11-dehydrocorticosterone to [3H]corticosterone) was only just detectable (<6%) at the postestrus stage of the cycle and on days 5 and 10 of pregnancy, but then increased markedly by day 16 (45 +/- 2%). This activity increased further to maximal levels on day 22 of pregnancy (55 +/- 3%) and remained high on day 23 (term; 34 +/- 3%) before decreasing by 24 h postpartum (9 +/- 2%). High 11beta-dehydrogenase activity was evident before (87 +/- 1%) and during the first half (day 5,91 +/- 1%; day 10, 88 +/- 2%) of pregnancy, was lower on days 16 (55 +/- 2%), 22 (39 +/- 3%), and 23 (58 +/- 1%), then returned to prepregnancy levels 24 h postpartum (86 +/- 1%). The marked induction of 11-oxoreductase activity late in pregnancy was strongly and positively correlated with both 11betaHSD-1 messenger RNA expression (by Northern analysis) and protein (by Western analysis; r = 0.96 and 0.98, respectively; P < 0.001). Moreover, 11betaHSD-1 and GR immunoreactivity were colocalized to the smooth muscle cells of the myometrium and the uterine epithelium late in pregnancy. Collectively, these data demonstrate that a marked induction of 11betaHSD-1 expression occurs in the rat myometrium near term, and this is associated with increased 11-oxoreductase bioactivity. As GR is coexpressed in the myometrium, we suggest that the induction 11betaHSD-1 serves to enhance local glucocorticoid actions and thus facilitate parturition.

Zonal distribution of 11 beta-hydroxysteroid dehydrogenase types 1 and 2 messenger ribonucleic acid expression in the rat placenta and decidua during late pregnancy.

Glucocorticoid action in several target tissues is dependent on expression of 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD), and in the placenta 11 beta-HSD is thought to regulate transfer of active glucocorticoid to the fetus. This study compared expression of the two recognized 11 beta-HSD enzymes, types 1 and 2, in the rat placenta and decidua on Days 16 and 22 of gestation (term = Day 23). According to S1 nuclease protection analysis, although mRNA for 11 beta-HSD-1 was only just detectable in the labyrinth zone on Day 16, by Day 22 this expression had increased almost 20-fold. There was also an increase (approximately 2-fold) in 11 beta-HSD-1 mRNA in the basal zone between Days 16 and 22. In Day 16 decidua, 11 beta-HSD-1 mRNA was also highly expressed, but insufficient tissue was available for analysis on Day 22. Western blot analysis showed that immunoreactive 11 beta-HSD-1 (molecular mass 34 kDa) was present in those tissues with the highest 11 beta-HSD-1 mRNA expression (Day 16 decidua and Day 22 labyrinth zone). With respect to mRNA for 11 beta-HSD-2, high expression was observed in the decidua and labyrinth zone at Day 16, but in the latter this expression then declined 90% by Day 22. In contrast, expression of mRNA for 11 beta-HSD-2 increased more than 3-fold in the basal zone over the same period. Consistent with coexpression of the two 11 beta-HSD enzymes, both 11-oxoreductase and 11 beta-dehydrogenase bioactivity were clearly evident in all tissues, and each varied with stage of gestation. Specifically, 11 beta-dehydrogenase activity in the basal zone increased from 38 +/- 2% (mean +/- SEM) on Day 16 to 56 +/- 2% on Day 22, while 11-oxoreductase activity fell from 55 +/- 3% to 43 +/- 2% over the same period. In contrast, 11 beta-dehydrogenase activity in the labyrinth zone fell with advancing pregnancy (Day 16: 63 +/- 2%; Day 22: 48 +/- 2%). Both 11-oxoreductase (58 +/- 3%) and 11 beta-dehydrogenase (38 +/- 4%) activities were also evident in decidua at Day 16. In conclusion, this study shows that expression of 11 beta-HSD-1 and -2 is zone-specific in the placenta and maternal decidua. Moreover, opposite changes in the expression of the two enzymes occur in the basal and labyrinth zones of the placenta over the last days of pregnancy, indicative of distinct regulatory mechanisms and functional significance for the enzymes in the two placental zones.

Interpretive criteria for antimicrobial susceptibility testing of ceftiofur against bacteria associated with swine respiratory disease.

Ceftiofur, an extended-spectrum cephalosporin, is active against a variety of animal pathogens, including organisms associated with swine respiratory disease. However, minimum inhibitory concentration (MIC) breakpoint and disk diffusion interpretive criteria have not been established for swine pathogens. Susceptibility tests were performed by broth microdilution MIC and disk diffusion methods on 246 bacterial species that cause swine respiratory disease. Ceftiofur was active against Salmonella sp., Pasteurella multocida, Actinobacillus pleuropneumoniae, Streptococcus suis, and Escherichia coli but was not active against Bordetella bronchiseptica measured by MIC. Based on pharmacokinetic studies of ceftiofur in swine after a single intramuscular injection of 3 or 5 mg/kg body weight of ceftiofur and on the MIC and disk diffusion data, we recommend MIC breakpoints and disk diffusion distances, respectively, of < or = 2 micrograms/ml and > or = 21 mm for susceptible, 4 micrograms/ml and 18-20 mm for intermediate, and > or = 8 micrograms/ml and > or = 17 mm for resistant classification for swine pathogens. When these breakpoints were applied to data from a previous study using bovine pathogens, only 1 minor interpretive error occurred.

High-performance liquid chromatographic assay for the quantitation of L-arginine in human plasma.

L-Arginine is metabolized to nitric oxide by nitric oxide synthase, and abnormalities in nitric oxide production have been implicated in the pathogenesis of some diseases involving the vasculature. Thus, there has been interest in the effects of pharmacologic doses of L-arginine in patients with cardiovascular and renal diseases. To study the disposition of exogenous doses, an HPLC method was developed to analyze plasma samples for L-arginine. The assay involves precolumn derivatization of arginine with naphthalenedicarboxaldehyde and cyanide followed by HPLC with UV detection. Only a simple deproteinization of the plasma samples was required. The derivatized arginine was stable (less than 5% degradation in 20 h), facilitating batch sample processing and analysis in an autosampler. Calibration curves were generated in Ringer's lactate solution instead of plasma to correct for endogenous plasma L-arginine. Recovery in plasma, compared to Ringer's solution (n = 4), was 103%. Mean intraday assay precision (n = 6), expressed as coefficient of variation, was 3.4%. Interassay precision (n = 6) was 7%. The assay was applied for the quantitation of L-arginine in plasma samples from a normal subject who had been given a single oral (10 g) and a single intravenous dose (30 g) of exogenous L-arginine.

11 beta-Hydroxysteroid dehydrogenase in the rat placenta: developmental changes and the effects of altered glucocorticoid exposure.

The enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) catalyses the interconversion of corticosterone, the major glucocorticoid of the rat, and the biologically-inactive 11-dehydrocorticosterone. In the placenta, 11 beta-HSD is thought to regulate glucocorticoid transport between maternal and fetal compartments, and may also affect the local action of glucocorticoids. The present study assessed whether 11 beta-dehydrogenase (corticosterone to 11-dehydrocorticosterone) and 11-oxoreductase (11-dehydrocorticosterone to corticosterone) activities are both present in rat placenta, and whether these activities change with advancing pregnancy. Enzyme activity was estimated on days 16, 19 and 22 of pregnancy (term = day 23) in placental fragments incubated for 6 h with either [3H]corticosterone or [3H]11-dehydrocorticosterone. The percentage conversion of these substrates to [3H]11-dehydrocorticosterone and [3H]corticosterone, respectively, were determined at the end of the incubation. Both 11-oxoreductase and 11 beta-dehydrogenase activities were clearly evident in placental tissue fragments, and while 11-oxoreductase activity declined with advancing pregnancy (P < 0.01), 11 beta-dehydrogenase activity increased (P < 0.01). Thus, 11-oxoreductase exceeded (P < 0.05) 11 beta-dehydrogenase at day 16, but thereafter activities were similar. These changes do not appear to be glucocorticoid-induced, since pretreatment of rats with either metyrapone or dexamethasone acetate from day 15 of pregnancy did not affect placental 11 beta-HSD on day 22.(ABSTRACT TRUNCATED AT 250 WORDS)

Release of bioactive ACTH by perifused human placenta at early and late gestation.

This study assessed whether bioactive ACTH is released by the human placenta during perifusion in vitro at early and late gestation. Human placental villous fragments from early (8-12 weeks) and late (38-40 weeks) gestation were perifused at a constant rate for 6.5 h. To assess ACTH-like bioactivity released by this tissue, the perifusion effluent was redirected through adjacent chambers containing freshly dispersed adrenocortical cells obtained from adult rats. Baseline secretion of corticosterone by these adrenocortical cells averaged 95 +/- 26 (S.E.M.) fmol/min, and this increased at least fivefold (P < 0.01, two-way ANOVA) in response to placental effluent at early and late gestation. The magnitude of this increase, expressed as a percentage of the maximal response to a subsequent stimulus with ACTH(1-24), was similar for placentas obtained at early (41 +/- 12% of maximal response) and late (42 +/- 17%) gestation. Immunoreactive (I)-ACTH was readily detectable in placental effluent from all preparations (5.5 +/- 2.3 fmol/min per g tissue), and there was no apparent difference with stage of gestation. To determine whether all of the ACTH-like bioactivity released by the placenta was attributable to I-ACTH, a second series of placental/adrenal perfusions was conducted. In these, I-ACTH was selectively removed from placental effluent by immunoneutralization, and the residual bioactivity measured. Immunoneutralization involved preincubation of placental effluent with ACTH antiserum (1:100), and preincubation with normal rabbit serum (NRS) served as a control.(ABSTRACT TRUNCATED AT 250 WORDS)

Development of a sensor for non-invasive intracranial pressure measurement in the newborn.

A new system has been developed for the non-invasive monitoring of intracranial pressure (ICP) across the anterior fontanelle in the newborn. The system comprises a very small pneumatic sensor linked via two vinyl tubes to an instrument where the ICP value is displayed. The sensor is simply bonded to the anterior fontanelle, using industrial collodion normally used for attaching EEG electrodes. The sensor body is injection moulded in semi-flexible polyurethane with a very thin, compliant membrane bonded to its front surface. Using these manufacturing techniques the sensors are made to be disposable thus minimizing the risk of cross infection. ICP characteristics can now be recorded continuously in a wide range of neonates and the evaluation of currently used therapeutic treatments for lowering elevated ICP can be carried out safely and accurately.

Continuous non-invasive beat-by-beat blood pressure (B.P.) measurement in the newborn.

Intermittent measurement of blood pressure (BP) is frequently performed in newborn babies under intensive care using an inflatable cuff encircling either the arm or leg. This paper describes work aimed at achieving continuous beat-by-beat measurement of the arterial pressure waveform by means of a finger cuff, the pressure of which is controlled by a feedback arrangement utilising a photoplethysmograph. Preliminary results are encouraging, but improvements to cuff design are still needed.

Continuous, noninvasive measurement of fetal oxygen and carbon dioxide levels in labor by use of mass spectrometry.

Clinical evaluation of the continuous, simultaneous measurement of fetal scalp surface oxygen and carbon dioxide partial pressures by mass spectrometry was undertaken for 52 labors. The mass spectrometer (MM8-80, V.G. Gas Analysis, Winsford, England) was easy to operate and had good long-term stability. The mean drifts for both oxygen and carbon dioxide over the study periods were less than 2 mm Hg. The mean (+/- SD) cervical dilatation at the time of transducer application was 6.1 (+/- 1.9) cm and the mean (+/- SD) duration of the studies was 169 (+/- 122) minutes; 10.5% of the transducer applications were unsuccessful. Falls in fetal scalp surface oxygen levels and rises in carbon dioxide levels were more frequent with late than with variable and with variable than with early fetal heart rate decelerations and with increasing severity and frequency of decelerations. Fetal scalp surface pressure changes also occurred with fetal heart rate variability changes, including some related to behavioral state changes. There was not a constant reciprocal relationship between oxygen and carbon dioxide changes, and fetal heart rate patterns were not related to actual blood gas levels. Fetal scalp surface measurements were related to both fetal blood sample and umbilical artery results. Trends in both oxygen and carbon dioxide levels during the course of labor were compared and related to other fetal variables, and most of the time the scalp surface measurements were an accurate guide to systemic blood gas levels. Maternal oxygen administration resulted in significant increase in fetal scalp surface oxygen levels, and on two of eight occasions it also led to decreases in fetal carbon dioxide levels. Scalp surface gas measurement by means of mass spectrometry is a powerful new method of intrapartum fetal monitoring, which should increase the precision of fetal surveillance as well as allow the accurate assessment of both established and new methods for optimizing labor and delivery.