[Pulse oximetry versus electrocardiogram for heart rate assessment during resuscitation of the preterm infant]. / Pulsioximetría frente al monitor de electrocardiograma para la determinación de la frecuencia cardíaca durante la reanimación del recién nacido pretérmino.

BACKGROUND: Heart rate (HR) assessment is essential during neonatal resuscitation, and it is usually done by auscultation or pulse oximetry (PO). The aim of the present study was to determine whether HR assessment with ECG is as fast and reliable as PO during preterm resuscitation. MATERIAL AND METHODS: Thirty-nine preterm (<32 weeks of gestational age and/or<1.500g of birth weight) newborn resuscitations were video-recorded. Simultaneous determinations of HR using ECG and PO were registered every 5s for the first 10min after birth. Time needed to place both devices and to obtain reliable readings, as well as total time of signal loss was registered. The proportion of reliable HR readings available at the beginning of different resuscitation manoeuvres was also determined. RESULTS: Time needed to connect the ECG was shorter compared with the PO (26.64±3.01 vs. 17.10±1.28 s, for PO and ECG, respectively, P<.05). Similarly, time to obtain reliable readings was shorter for the ECG (87.28±12.11 vs. 26.38±3.41 s, for PO and ECG, respectively, P<.05). Availability of reliable HR readings at initiation of different resuscitation manoeuvres was lower with the PO (PO vs. ECG for positive pressure ventilation: 10.52 vs. 57.89% P<.05; intubation: 33.33 vs. 91.66%, P<.05). PO displayed lower HR values during the first 6min after birth (P<.05, between 150 and 300s). CONCLUSIONS: Reliable HR is obtained later with the PO than with the ECG during preterm resuscitation. PO underestimates HR in the first minutes of resuscitation.

The cannabinoid WIN 55212-2 mitigates apoptosis and mitochondrial dysfunction after hypoxia ischemia.

Perinatal hypoxia-ischemia has significant mortality and morbidity due to there is still no specific treatment as a consequence of the complexities of hypoxic-ischemic pathophysiology. The aim of this work was to evaluate the effects of the cannabinoid agonist WIN 55212-2 on apoptotic cell death and mitochondrial dysfunction after perinatal asphyxia in fetal lambs. Animals were assigned to: one SHAM group and two hypoxic-ischemic groups that received a dose of 0.01 µg/kg WIN 55,212-2 (HI + WIN) or not (HI + VEH) after 60 min of partial occlusion of the umbilical cord, and sacrificed 3 h later. Different brain regions were separated for morphological studies, and the same territories were dissociated and analyzed by flow cytometry to quantify apoptosis, to determine mitochondrial integrity and transmembrane potential and to analyze intracellular calcium levels. Our results showed that WIN 55,212-2 reduced apoptotic cell death in all regions studied through the maintenance of mitochondrial integrity and functionality.

The neuroprotective effect of cannabidiol in an in vitro model of newborn hypoxic-ischemic brain damage in mice is mediated by CB(2) and adenosine receptors.

To investigate the mechanisms involved in cannabidiol (CBD)-induced neuroprotection in hypoxic-ischemic (HI) immature brain, forebrain slices from newborn mice underwent oxygen and glucose deprivation in the presence of vehicle, or CBD alone or with selective antagonists of cannabinoid CB(1) and CB(2), and adenosine A(1) and A(2) receptors. CBD reduced acute (LDH efflux to the incubation medium) and apoptotic (caspase-9 concentration in tissue) HI brain damage by reducing glutamate and IL-6 concentration, and TNFalpha, COX-2, and iNOS expression. CBD effects were reversed by the CB(2) antagonist AM630 and by the A(2A) antagonist SCH58261. The A(1A) antagonist DPCPX only counteracted the CBD reduction of glutamate release, while the CB(1) antagonist SR141716 did not modify any effect of CBD. In conclusion, CBD induces robust neuroprotection in immature brain, by acting on some of the major mechanisms underlying HI cell death; these effects are mediated by CB(2) and adenosine, mainly A(2A), receptors.

[Tracheal agenesis associated with laryngeal malformations as an unusual cause of airway failure]. / Agenesia traqueal asociada a malformaciones laríngeas como causa inusual de fracaso de la vía aérea.

Tracheal agenesis is an uncommon congenital malformation with an extremely high mortality rate. This malformation manifests after delivery as severe respiratory distress, cyanosis, lack of crying and impossibility of endotracheal respiratory support. This anomaly is usually associated with cardiovascular, respiratory and gastrointestinal malformations. Only a high index of suspicion and early surgical management will prevent death. An early diagnosis may also help the parents and the medical team to take appropriate decisions. Currently, there is no effective therapy that guarantees long-term survival.

[Group therapy for the treatment of obesity in children and adolescents]. / Terapia de grupo para el tratamiento de la obesidad infantil.

THERAPY: Although obesity is one of the leading health problems in developed countries, effective treatment is lacking. The aim of the present study was to determine whether group therapy is more efficient in inducing weigh loss than individual therapy in the pediatric age group. EXPERIMENTAL DESIGN: Fifty obese patients, 15 preadolescents and 33 adolescents (12 boys and 23 girls) were studied. In all patients, dietary intake was modified to reduce calorie intake. Initially all patients were followed-up individually every 3 months (individual therapy) until the beginning of group therapy when the patients were seen monthly in groups of 10-15 patients with their parents (preadolescents) or alone (adolescents). In the group sessions, talks were given about diet and exercise. In each session, the patient who had shown the greatest improvement in habits and weight loss received a prize. The patients were followed-up for 2 years, with individual therapy in the first year and group therapy in the second. Differences in body mass index (BMI) z-score before the beginning of therapy and during therapy were analyzed using Student's paired T test. RESULTS: With individual therapy, no changes in BMI z-score were observed throughout the study. In contrast, with group therapy, BMI z-score decreased in all the groups studied. During the 1-year follow-up with individual therapy, 60 % of the patients gained more than 5 kg. With group therapy, only 10 % of patients gained more than 5 kg. CONCLUSIONS: In obese children and adolescents, group therapy was more efficient than individual therapy in inducing weight loss.

[The cannabinoid system and its importance in the perinatal period]. / El sistema cannabinoide y su importancia en el período perinatal.

The cannabinoid system has been recently described, including the endogenous ligands, mainly arachidonic acid derivatives, and their specific receptors. Endocannabinoids are involved in the modulation of synaptic transmission, through which they exert their psychoactive, motor and antinociceptive effects, among others; they also exert extraneural effects, mainly immunomodulation and vasodilation. Recent data suggest that the cannabinoid system might play an important role in human ontogeny and could participate in the implantation and early development of the embryo, in fetal brain development, and in the beginning of breast feeding after birth. In addition, the vasodilatory effect of cannabinoids, together with inhibition of the release of excitotoxic amino acids and cytokines, as well as modulation of oxidative stress and the toxic production of nitric oxide, justify the growing evidence pointing to a possible neuroprotective effect of cannabinoids in perinatal asphyxia.

Neuroprotective effect of L-arginine in a newborn rat model of acute severe asphyxia.

The left common carotid artery was ligated in anaesthetized 7-day-old Wistar rats (P7), prior to asphyxia by inhaling 100% nitrogen for 9 min. Pups recovered from asphyxia received i.p. saline (n = 16), or L-Arg 300 mg/kg (n = 14). Pups undergoing sham operation remained as controls (n = 12). At day 14, the amount of surviving or degenerating neurons was quantified under optical microscopy by Nissl technique or by Fluoro-Jade B (FJB) in CA1 area of hippocampus and in parietal cortex. In these areas, asphyxia reduced the neuronal density by 23.6 and 30%, and increased the proportion of degenerating neurons two and four times, respectively. L-Arg administration to asphyxiated pups reduced the neuronal loss and the proportion of degenerating neurons by 50% (p < 0.05). We conclude that L-Arg administration after acute severe asphyxia in newborn rats is neuroprotective, reducing early and delayed neuronal loss.

[Presence of genu valgum in obese children: cause or effect?]. / Presencia de genu valgum en obesos: causa o efecto.

BACKGROUND: Changes in body configuration that may affect the physical activity may play a role in the caloric consumption and led to the development of obesity. OBJECTIVES: To determine the presence of genu valgum, an alteration that may decrease physical activity and caloric expenditure, in overweight children. METHODS: Thirty-five overweight children without any endocrinological alterations that could lead to obesity were studied. Twenty-nine non-overweight children of a similar age were studied as a control group. In all children weight, height, and body mass index (BMI) were studied, and intermalleolar distance was used to measure the degree of genu valgum. The differences between groups were studied using ANOVA and the correlation between variables was determined using Pearson's correlation. RESULTS: BMI was higher in overweight children than in the control group. Intermalleolar distance was greater in overweight children than in the non-overweight group (11.0 0.6 vs 2.90 0.43; p < 0.001). A positive correlation between the intermalleolar distance and the BMI was observed in the overweight group (p < 0.009). Fifty percent of the overweight children showed an intermalleolar distance of more than 10 cm, a value considered abnormal. CONCLUSIONS: The incidence of genu valgum is much higher in overweight children than in non-overweight children of the same age. This alteration may lead to decreased physical activity and lead to obesity.

[Congenital adrenal hyperplasia: an association with increased fetal nuchal translucency]. / Hiperplasia suprarrenal congénita: asociación con translucencia nucal fetal aumentada.

A neonate with increased nuchal translucency and congenital adrenal hyperplasia is described. The possible interferences in hormone assays when values are much higher than the average assay range are also discussed.

Nitric oxide-dependent and -independent mechanisms in the relaxation elicited by acetylcholine in fetal rat aorta.

The aim of the present study was to analyze the mechanisms involved in the relaxation induced by 1 microM acetylcholine (ACh) in aortic segments from fetal rats at term precontracted with 3 microM prostaglandin F2alpha (PGF2alpha) and incubated with 1 microM indomethacin. The endothelium-dependent relaxation caused by ACh was reduced by the nitric oxide (NO) synthase inhibitor NG-monomethyl-L-arginine (L-NMMA, 0.1 mM), such an effect was reversed by 0.1 mM L-arginine (L-Arg). After precontraction of segments with 50 mM KCl the relaxant response to ACh was smaller than that after precontraction with PGF2alpha; this reduction was increased by L-NMMA, whereas L-NMMA plus L-Arg potentiated the relaxation. Thiopentone sodium (0. 1 mM), ouabain (10 microM), tetraethylammonium (TEA, 0.5 mM) and apamin (1 microM), inhibitors of cytochrome P450 monooxygenases, Na+ pump, Ca2+-activated (KCa) and small-conductance (SKCa) K+ channels, respectively, reduced the relaxation to ACh, which was unaffected by charybdotoxin (0.1 microM) and glibenclamide (1 microM), inhibitors of large-conductance BKCa and ATP-sensitive K+ channels. The L-NMMA/indomethacin-resistant relaxation to ACh was markedly reduced by thiopentone sodium, and similarly decreased by either ouabain or TEA. The endothelium-independent relaxation induced by exogenous NO (10 microM) in segments precontracted with PGF2alpha was unaltered by ouabain, glibenclamide, TEA and after precontraction with 50 mM KCl, and potentiated by L-NMMA. The potentiation of NO responses by L-NMMA was also observed in segments precontracted with KCl. These results suggest that ACh relaxes the fetal rat aorta by endothelial release of both NO and endothelium-derived hyperpolarizing factor (EDHF), a metabolite derived from cytochrome P450 monooxygenases, that hyperpolarizes smooth muscle cells by activation of KCa, essentially SKCa channels, and Na+ pump. It seems that when the effect of EDHF is abolished, the formation of NO could be increased.

The L-arginine inhibition of rat middle cerebral artery contractile responses is mediated by inducible nitric oxide synthase.

1. The effect of L-arginine (L-Arg), the nitric oxide synthase (NOS) substrate, on the responses to prostaglandin F2alpha (PGF2alpha, 10 microM) and K+ (120 mM) in rat middle cerebral artery (MCA) segments was analysed. 2. PGF2alpha induced a stable contraction of 0.35+/-0.06 mN mm(-1); the subsequent addition of bradykinin (BK, 1 microM) produced a relaxation of 42+/-9% of the PGF2alpha-induced tone. K+ induced a response consisting of a rapid basal tone increase (1.42+/-0.16 mN mm(-1)) followed by a decrease to a stable phase (1.24+/-0.15 mN mm(-1)). 3. L-Arg (0.1 mM), but not D-Arg, decreased the basal tone and reduced the contraction to PGF2alpha in segments with and without endothelium. The contractile response to K+ was also reduced and not maintained in the presence of L-Arg. 4. The inhibitory effect of L-Arg on the PGF2alpha- and K+-induced contractions was completely reversed by the NOS inhibitor, NG-monomethyl-L-arginine (L-NMMA, 0.1 mM). 5. Pre-incubation of segments with dexamethasone (1 microM), to inhibit inducible NOS (iNOS), or with the antibiotic polymyxin B (10 microg ml(-1)) reduced the L-Arg inhibition, whereas it was increased by lipopolysaccharide (LPS, 100 ng ml(-1)), an inductor of iNOS. L-NMMA antagonized the effects of dexamethasone and LPS. 6. The present results suggest that L-Arg inhibition of the PGF2alpha- and K+-induced contractions in rat MCA is the result of NO synthesis by iNOS stimulation.

Endothelial factors and autoregulation during pressure changes in isolated newborn piglet cerebral arteries.

To analyze newborn cerebrovascular autoregulation, middle cerebral arteries from 3-4-d-old piglets were cannulated, and diameter changes after transmural pressure variation were measured. After an equilibration period at 30 mm Hg, pressure was modified from 10 to 70 mm Hg in 20-mm Hg steps. Segments with endothelium showed vasodilation during pressure decrease and vasoconstriction during pressure increase. In each case the maximum response was about 5% that of the resting diameter. Segments without endothelium responded passively to pressure change. Vasodilation during pressure decrease was reduced by the preferential calcium-activated potassium (KCa) channel blocker, tetraethylammonium (1 mM), and was absent with the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methylester (L-NAME, 10 microM). The NO synthase substrate, L-arginine (10 microM), counteracted the dilation blockade caused by L-NAME. The cyclooxygenase inhibitor indomethacin (10 microM) and the endothelin A receptor antagonist BQ-123 (10O microM) eliminated the pressure increase-induced vasoconstriction. The ATP-sensitive potassium channel blocker, glibenclamide (1 microM), and the endothelin B receptor antagonist, BQ-788 (10 nM), did not modify the autoregulatory response. None of these drugs modified the passive changes produced by pressure variations in segments without endothelium. These results suggest that: 1) piglet middle cerebral artery autoregulation is endothelium-dependent; 2) NO and KCa channels are involved in vasodilation during transmural pressure decrease, and 3) endothelin-1, through endothelin A receptors, and prostanoids mediate vasoconstriction during pressure increase.

Impairment of acetylcholine relaxations by malondialdehyde, a marker of lipid peroxidation.

The effect of malondialdehyde (MDA), a lipid peroxidation marker, on the relaxations evoked by acetylcholine (ACh) was analyzed in tail arteries of Sprague-Dawley rats, which have MDA plasma levels of 0.43 +/- 0.10 microM. MDA (0.5-30 microM) produced an inhibition of ACh relaxations that persisted after repeated washing periods, and was independent of the incubation time. MDA did not modify the vasodilator responses to either exogenous nitric oxide (NO) or sodium nitroprusside, a NO donor. L-Arginine (the NO synthase substrate) did not prevent the impairment of relaxations to ACh caused by MDA. The association of N omega-nitro-L-arginine methyl ester (a NO synthase inhibitor) and MDA produced an additive inhibition of the ACh-induced relaxations. Superoxide dismutase (a superoxide anion scavenger) completely reversed the inhibitory effect of MDA. These results suggest: (1) MDA is not only a marker of lipid peroxidation but also an agent that can impair endothelium-dependent relaxations; (2) this impairment does not seem to be due to an interference with guanylate cyclase activation by NO or with NO synthase pathway; (3) the effect of MDA appears to be mediated by superoxide anion, and (4) MDA could propagate lipid peroxidation chain reactions in endothelial membranes, that could alter the function of muscarinic receptors.

Role of nitric oxide on the endothelium-dependent vasodilation in newborn piglet cerebral arteries.

1. The present study was undertaken to determine whether endothelial nitric oxide (NO) is involved in the endothelium-dependent vasodilation elicited by bradykinin (BK) in rings of newborn (1-7-day-old) piglet cerebral arteries precontracted with KCl (25 mM). 2. In these rings, BK (10(-10)-10(-6) M) induced concentration-dependent relaxation. The preincubation with the precursor of NO synthesis, L-arginine (10(-4) M), reduced KCl-induced contraction and increased the BK relaxation. However, preincubation with the NO synthase inhibitor, NG-nitro-L-arginine-methyl ester (L-NAME; 3 x 10(-5) M), increased KCl contraction and basal tone, and inhibited BK relaxation. 3. These results suggest that the endothelium of these arteries possesses the ability to produce NO, either basal or stimulated by agents like BK.

[Prediction of complications in children of hypertensive mothers]. / Predicción de complicaciones en el hijo de madre hipertensa.

The hypertensive disorders of pregnancy are a frequent cause of neonatal morbidity and mortality. 259 newborns of hypertensive women were study to establish the relationship between some maternal findings and the subsequent neonatal complications. The severity, early onset of hypertension, proteinuria and the gestation of 32 week or less, are related with special risk of small-for-date, anoxia, seizures and neutropenia. Preeclampsia was related with foetus more compromised. Also hyperuricemia, thrombocytopenia and cesarean section were light predictors of neonatal trouble. These findings can orientate the neonatologist to select the newborns prone to complications, watching them closely to start the treatment, if necessary, as soon as possible.