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C E Blanco

Publications and source records attributed to C E Blanco.

At least 19 recordsLinked to original sources
PubMed2006

Prenatal stress in the rat alters 5-HT1A receptor binding in the ventral hippocampus.

Exposure of a pregnant woman to physical and/or psychological stress might affect her offspring by promoting the development of various learning, behavioral and/or mood disorders in later life. The 5-HT1A and 5-HT2A receptors are prominently implicated in the modulation of anxiety and mood-related behaviors. Using a semi-quantitative radiolabel immunocytochemical analysis (immunobinding), we studied the effect of prenatal stress on binding of these two receptor subtypes in the hippocampus of 4-week-old male and female Fischer 344 rats. Levels of 5-HT1A immunobinding in the ventral hippocampus, which is primarily implicated in emotional processing, were significantly decreased in male offspring after prenatal stress. A trend towards a decrease was observed in the ventral hippocampus of females. In contrast, 5-HT1A immunobinding within the dorsal hippocampus, which is mainly related to learning and memory, was not affected by prenatal stress in offspring of either gender. Likewise, no significant differences between control and prenatally stressed rats were observed for levels of 5-HT2A immunobinding in either part of the hippocampus or gender. The observed reduction in hippocampal 5-HT1A receptor binding in male offspring after prenatal stress may have important consequences for adult anxiety- and depressive-like behavior.

Animals↗
PubMed2005

Prenatal stress and neonatal rat brain development.

Chronic or repeated stress during human fetal brain development has been associated with various learning, behavioral, and/or mood disorders, including depression in later life. The mechanisms accounting for these effects of prenatal stress are not fully understood. The aim of this study was to investigate the effects of prenatal stress on early postnatal brain development, a disturbance of which may contribute to this increased vulnerability to psychopathology. We studied the effects of prenatal stress on fetal growth, stress-induced corticosterone secretion, brain cell proliferation, caspase-3-like activity and brain-derived neurotrophic factor protein content in newborn Fischer 344 rats. In addition to a slight reduction in birth weight, prenatal stress was associated with elevated corticosterone levels (33.8%) after 1 h of maternal deprivation on postnatal day 1, whereas by postnatal day 8 this pattern was reversed (-46.5%). Further, prenatal stress resulted in an approximately 50% decrease in brain cell proliferation just after birth in both genders with a concomitant increase in caspase-3-like activity within the hippocampus at postnatal day 1 (36.1%) and at postnatal day 5 (females only; 20.1%). Finally, brain-derived neurotrophic factor protein content was reduced in both the olfactory bulbs (-24.6%) and hippocampus (-28.2%) of prenatally stressed male offspring at postnatal days 1 and 5, respectively. These detrimental central changes observed may partly explain the increased susceptibility of prenatally stressed subjects to mood disorders including depression in later life.

Animals↗
PubMed2005

Prenatal restraint stress and long-term affective consequences.

Chronic or repeated stress during critical periods of human fetal brain development has been associated with various learning, behavioral and/or mood disorders in later life. In this investigation, pregnant Fischer 344 rats was individually restrained three times a day for 45 min during the last week of gestation in transparent plastic cylinders while at the same time being exposed to bright light. Control pregnant females were left undisturbed in their home cages. Anxiety and depressive-like behavior was measured in the offspring at an age of 6 months using the open field test, the home cage emergence test and the forced swim test. Prenatally stressed rats spent more time in the corners and less time along the walls of an open field, while no difference in total distance moved was observed. In addition, prenatally stressed rats took more time to leave their home cage in the home cage emergence test. On the other hand, no differences in immobility were observed in the forced swim test. Moreover, prenatally stressed rats showed lower stress-induced plasma corticosterone levels compared with control rats. Prenatal stress (PS) had no effect on the number of 5-bromo-2-deoxyuridine-positive cells - used as a measure for cell proliferation - in the dentate gyrus of these rats. These data further support the idea that PS may perturb normal anxiety-related development. However, the present data also suggest that an adaptive or protective effect of PS should not be ignored. Genetic factors are likely to play a role in this respect.

Adaptation, Physiological↗
PubMed2004

Neonatal electrocortical brain activity and cerebral tissue oxygenation during non-acidotic, normocarbic and normotensive graded hypoxemia.

OBJECTIVE: Neonates are commonly exposed to isolated hypoxemic episodes. In order to identify the risk of this, we correlated cerebral oxygen delivery and electrocortical brain activity during isolated graded and repetitive hypoxemia in 1-week-old piglets. METHODS: Six halothane-anesthetized piglets were subjected to two episodes of graded hypoxemia of 45 min duration. The fractional concentration of inspired oxygen (FiO(2)) was stepwise decreased at 15 min intervals from 0.21 to 0.15, 0.10 and 0.05. A second identical hypoxemic event was induced after 1 h of normoxemia (FiO(2) 0.21). Mean arterial pressure (MAP) and pH were maintained at baseline values during the whole experiment. We measured near infrared spectroscopy parameters (cerebral oxidized cytochrome aa(3) (Cytaa3), total hemoglobin (tHb: oxy- +deoxyhemoglobin)) corresponding to cerebral blood volume (CBV), carotid blood flow (Q(car)), intra-arterial oxygen saturation (SaO(2)), and mean maximal EEG amplitude and relative spectral power. RESULTS: Delta (delta) power increased significantly and the EEG amplitude dropped below 10 and 5 microV at the end of the first and the second hypoxemic period (PaO(2) 2.68+/-1.08 (P<0.05) and 2.87+/-0.58 kPa, respectively). Both EEG variables normalized during recovery (FiO(2) 0.21). Q(car), CBV and Cytaa3 were not changed. CONCLUSION: Acute isolated hypoxemia has to be sustained to induce neuronal hypofunction in normotensive animals. Hypoxic hypoxemia led to acute changes in neuronal activity, whereas cellular oxygenation remained unaffected.

Animals↗
PubMed2003

Chronic moderate hypoxia during in ovo development alters arterial reactivity in chickens.

We previously observed arterial sympathetic hyperinnervation and endothelial dysfunction in the chicken embryo after exposure to chronic hypoxia. We now investigate whether changes in arterial properties could also be observed at 14-15 weeks of life. Eggs of White Leghorn chicken were incubated under normoxic or moderately hypoxic (15% O2 from days 6-19 of a 21-day incubation) conditions. Experiments were performed at 14-15 weeks of life under standard conditions (Hm: males exposed to hypoxia; Hf: females exposed to hypoxia; Nm: males exposed to normoxia; Nf: females exposed to normoxia). Body weight at hatching and at 14-15 weeks was not affected by in ovo exposure to hypoxia. Mean arterial pressure and heart rate were not significantly altered by chronic in ovo hypoxia. However, isolated femoral arteries were more sensitive to electrical stimulation (frequency in Hz of half-maximal contraction, Hm: 1.62+/-0.33, Hf: 1.92+/-0.88, Nm: 2.49+/-0.49, Nf: 2.83+/-0.31) and pharmacological stimulation of peri-arterial sympathetic nerves (contraction in N/m in response to tyramine: Hm: 5.27+/-0.85, Hf: 4.10+/-0.9, Nm: 2.26+/-0.67, Nf: 3.65+/-0.51, p=0.07) after in ovo hypoxia. In side branches of the femoral artery, the effect of NO synthase blockade with L-NAME on contraction (in N/m) in response to high K+ (Hm: 0.35+/-0.91, Hf: 1.29+/-0.36, Nm: 2.88+/-0.19, Nf: 2.79+/-0.58) and on the sensitivity to acetylcholine (DeltapD2, H: 0.32+/-0.11, N: 0.62+/-0.05) was reduced after in ovo hypoxia. The present study shows that exposure to chronic moderate hypoxia during development affects the contractile and relaxing arterial responses of 14- to 15-week-old chickens. Although hypoxia did not lead to changes in blood pressure at this age, the observed effects on arterial sympathetic and endothelial function may represent early signs of future cardiovascular abnormalities.

Animals↗
PubMed2003

Impact of perinatal asphyxia on the GABAergic and locomotor system.

Perinatal asphyxia can cause neuronal loss and depletion of neurotransmitters within the striatum. The striatum plays an important role in motor control, sensorimotor integration and learning. In the present study we investigated whether perinatal asphyxia leads to motor deficits related to striatal damage, and in particular to the loss of GABAergic neurons. Perinatal asphyxia was induced in time-pregnant Wistar rats on the day of delivery by placing the uterus horns, containing the pups, in a 37 degrees C water bath for 20 min. Three motor performance tasks (open field, grip test and walking pattern) were performed at 3 and 6 weeks of age. Antibodies against calbindin and parvalbumin were used to stain GABAergic striatal projection neurons and interneurons, respectively. The motor tests revealed subtle effects of perinatal asphyxia, i.e. small decrease in motor activity. Analysis of the walking pattern revealed an increase in stride width at 6 weeks of age after perinatal asphyxia. Furthermore, a substantial loss of calbindin-immunoreactive (-22%) and parvalbumin-immunoreactive (-43%) cells was found in the striatum following perinatal asphyxia at two months of age. GABA(A) receptor autoradiography revealed no changes in GABA binding activity within the striatum, globus pallidus or substantia nigra. We conclude that perinatal asphyxia resulted in a loss of GABAergic projection neurons and interneurons in the striatum without alteration of GABA(A) receptor affinity. Despite a considerable loss of striatal neurons, only minor deficits in motor performance were found after perinatal asphyxia.

Animals↗
PubMed2003

Long-chain polyunsaturated fatty acids at birth and cognitive function at 7 y of age.

OBJECTIVE: During the central nervous system (CNS) growth spurt, rapid accretion of long chain polyunsaturated fatty acids (LCPUFA) takes place. This particularly concerns docosahexaenoic acid (DHA, 22:6n-3) and arachidonic acid (AA, 20:4n-6), which are thought to play important roles in CNS development and function. The aim of this study was to investigate the relationship between cognitive performance at 7 y of age and LCPUFA levels in umbilical venous plasma phospholipids, representing the prenatal fatty acid availability, and in plasma phospholipids sampled at 7 y. DESIGN: As part of a follow-up study, the cognitive performance of 306 children, born at term, was assessed at 7 y of age with the Kaufman Assessment Battery for Children. Backward stepwise regression analysis was used to study the relationship between the outcomes and LCPUFA status. Social class, maternal intelligence and parenting skills were included as covariables, among others. RESULTS: Results show no significant association with either DHA or AA at birth and the cognitive performance at 7 y of age. The LCPUFA levels at 7 y were not associated with these outcomes either. Consistent with the literature, significant relationships were found between cognitive outcome measures and maternal education, maternal intelligence and the child's birthweight. CONCLUSIONS: In conclusion, our results do not provide evidence for a positive association between cognitive performance at 7 y and LCPUFA status at birth or at 7 y of age.

Arachidonic Acid↗
PubMed2002

Developmental apoptosis in the spinal cord white matter in neonatal rats.

We investigated developmental apoptosis in the white matter of the cervical spinal cord at postnatal days 2, 5, and 8. Apoptotic cells were labeled using TUNEL and caspase-3 immunostaining. Apoptotic cells were diffusely distributed throughout the white matter of the spinal cord. The total amount of apoptotic cells in the cervical spinal cord white matter was related to postnatal age, with the lowest at P2 (mean 7.9, SD 5.6) and the highest at P8 (mean 109, SD 21.4). Using double immunostaining for ED-1 and O4, apoptotic cells were identified as microglia and oligodendrocytes.

Aging↗
PubMed2002

Apoptosis in the rat spinal cord during postnatal development; the effect of perinatal asphyxia on programmed cell death.

The aim of our study was to investigate the effect of perinatal asphyxia on developmental apoptosis in the cervical and lumbar spinal cord in the neonatal rat. Perinatal asphyxia was induced by keeping pups at term in utero in a water bath at 37 degrees C for 20 min, followed by resuscitation. Effects of this treatment on developmental apoptosis were studied on postnatal days 2, 5 and 8 using terminal deoxynucleotidyl transferase (TdT)-dUTP-biotin nick end labelling (TUNEL) and caspase-3 staining. TUNEL positive cells were identified using double immunostaining. On postnatal day 2 an increase of 215% in TUNEL positive cells was detected (P=0.005) in laminae IV-VII of the lumbar spinal cord of rats which underwent perinatal asphyxia compared to controls. An increase of 55% compared to controls (P=0.03) was seen in laminae I-III of the lumbar spinal cord at postnatal day 8. TUNEL positive cells could be partly identified as microglia cells (ED1 positive) and oligodendrocytes (O4 positive). The effect of perinatal asphyxia on programmed cell death in the neonatal rat spinal cord was mainly observed in the intermediate zone and dorsal horn of the lumbar spinal cord. We conclude that perinatal asphyxia has a pronounced effect on the survival of cells in a specific region of the spinal cord and thus may have a profound effect on the development of motor networks.

Animals↗
PubMed2002

Effects of pharmacologic androgen treatment duration on glucocorticoid receptor alpha immunoreactivity of lumbosacral motor neurons in the male rat.

It has previously been suggested that anabolic-androgenic steroids may affect neuromuscular function through their potential action as glucocorticoid receptor antagonists. Alternatively, androgens may regulate the sensitivity of neuromuscular systems to glucocorticoids by modulating GR levels. The purpose of this study was to determine the effects of chronic pharmacologic testosterone treatment of gonadally intact male rats on glucocorticoid receptor alpha immunoreactivity (GRalpha-IR) of motor neurons in the lumbosacral spinal cord. Circulating testosterone levels were chronically increased by subcutaneous Silastic capsules containing crystalline testosterone propionate (TP) for 7, 14, and 28 days. Age-matched sham-operated gonadally intact males served as controls. Relative cytoplasmic and nuclear GRalpha-IR of motor neurons located in the lateral motor column of spinal cord segments L(3) and L(4) (L(Lat); innervating rat hindlimb muscles) and the spinal nucleus of the bulbocavernosus (SNB; innervating the external anal sphincter, bulbocavernosus and levator ani muscles) was measured densitometrically. TP treatment duration had a significant impact on the mean GRalpha levels of both cellular compartments regardless of motor column (two-way ANOVA, P<0.001). The mean nuclear GRalpha-IR of lumbar motor neurons was significantly reduced after 7 days (OD: 0.239+/-0.013 S.E.M.; P<0.016) and 14 days (OD: 0.196+/-0.013; P<0.001) from the GRalpha-IR levels observed among the control group (OD: 0.296+/-0.012) by 20 and 40%, respectively. Interestingly, nuclear GRalpha-IR levels were similar to control levels after 28 days of TP treatment (OD: 0.307+/-0.010). Treatment-dependent changes in cytoplasmic GRalpha-IR paralleled the observed changes in nuclear GRalpha-IR. These data suggest that pharmacologic testosterone treatment effects on motor neuron gene expression may be mediated by testosterone-induced temporal fluctuations of GRalpha-dependent gene regulation.

Androgens↗
PubMed2002

Intracranial pressure and cerebral blood flow velocity in preterm infants with posthaemorrhagic ventricular dilatation.

AIM: To determine the volume of cerebrospinal fluid (CSF) that should be tapped in preterm infants with posthaemorrhagic ventricular dilatation as guided by intracranial pressure (ICP) and cerebral blood flow velocity (CBFV). METHODS: The total number of measurements was 106 in 22 infants. Birth weights ranged from 630 to 2050 g, gestational age from 24.5 to 30.3 weeks, and age at insertion from 12 to 67 days. A subcutaneous ventricular catheter reservoir for repetitive CSF drainage was placed when the diameter of a ventricle was > 4 mm above the 97th centile. A volume of 5 ml/kg body weight was removed twice daily. ICP and CBFV were determined before and after CSF tapping. RESULTS: If the ICP after tapping exceeded 7 cm H(2)O, tapping did not result in a significant improvement in CBFV. If the ICP before tapping was less than 6 cm H(2)O, tapping also had no effect on CBFV. Longitudinal studies in individual infants showed a slight correlation between ICP and CBFV. CONCLUSION: Volume of repetitive CSF drainage in preterm infants with posthaemorrhagic ventricular dilatation guided by ICP and CBFV may be a useful technique. An ICP of about 6 cm H(2)O is the cut off point for CSF drainage.

Blood Flow Velocity↗
PubMed2002

Sympathetic control of the cardiovascular response to acute hypoxemia in the chick embryo.

In response to an acute hypoxemic insult, the mammalian fetus shows a redistribution of the cardiac output in favor of the heart and brain. Peripheral vasoconstriction contributes to this response and is partly mediated by the release of catecholamines. Two mechanisms of catecholamine release in the fetus are reported: 1) neurogenic sympathetic stimulation and 2) a nonneurogenic mechanism via a direct effect of hypoxemia on chromaffin tissues. In the present study, the effects of sympathetic blockade on plasma catecholamine release and cardiac output distribution in response to acute hypoxemia were studied in the chick embryo at different stages of incubation. Only at the end of the incubation period, sympathetic blockade markedly attenuated the increase in plasma catecholamine concentrations and resulted in a greater fraction of the cardiac output distributed to the carcass. However, these effects did not prevent a significant increase in cardiac output to the brain and heart during acute hypoxemia. These data imply that in the chick embryo the contribution of neurogenic mechanisms to the catecholaminergic response to acute hypoxemia becomes greater by the end of the incubation period.

Acute Disease↗
PubMed2002

Direct effects of acute hypoxia on the reactivity of peripheral arteries of the chicken embryo.

In the chicken embryo, acute hypoxemia results in cardiovascular responses, including an increased peripheral resistance. We investigated whether local direct effects of decreased oxygen tension might participate in the arterial response to hypoxemia in the chicken embryo. Femoral arteries of chicken embryos were isolated at 0.9 of incubation time, and the effects of acute hypoxia on contraction and relaxation were determined in vitro. While hypoxia reduced contraction induced by high K(+) to a small extent (-21.8 +/- 5.7%), contractile responses to exogenous norepinephrine (NE) were markedly reduced (-51.1 +/- 3.2%) in 80% of the arterial segments. This effect of hypoxia was not altered by removal of the endothelium, inhibition of NO synthase or cyclooxygenase, or by depolarization plus Ca(2+) channel blockade. When arteries were simultaneously exposed to NE and ACh, hypoxia resulted in contraction (+49.8 +/- 9.3%). Also, relaxing responses to ACh were abolished during acute hypoxia, while the vessels became more sensitive to the relaxing effect of the NO donor sodium nitroprusside (pD(2): 5.81 +/- 0.21 vs. 5.31 +/- 0.27). Thus, in chicken embryo femoral arteries, acute hypoxia blunts agonist-induced contraction of the smooth muscle and inhibits stimulated endothelium-derived relaxation factor release. The consequences of this for in vivo fetal hemodynamics during acute hypoxemia depend on the balance between vasomotor influences of circulating catecholamines and those of the endothelium.

Acute Disease↗
PubMed2001

Electrocortical brain activity, cerebral haemodynamics and oxygenation during progressive hypotension in newborn piglets.

OBJECTIVES: To investigate the relationships between systemic and cerebral haemodynamics and oxygenation, and electroencephalogram (EEG) amplitude and frequency analysis studied by the cerebral function analyzing monitor (CFAM) during progressive hypovolemic hypotension. METHODS: Six piglets of 1 week of age, weighing 1.9-3.4 kg were mechanically ventilated under 1-1.5% halothane anaesthesia. After 1 h stabilization, blood was withdrawn in aliquots of 10 ml/kg over 15 min up to a total of 40-60 ml/kg. Arterial oxygenation was maintained at normal levels. Thereafter, the total blood volume previously withdrawn, was reinfused. Changes in near infrared spectroscopy (NIRS) parameters [cerebral oxidized cytochrome aa3 (Cytaa3), cerebral blood volume (CBV) or total haemoglobin (tHb: oxy- + deoxyhaemoglobin)], carotid blood flow (Q(car)), maximal EEG amplitude and EEG frequency percentages were analyzed continuously. RESULTS: The EEG amplitude remained stable until the mean arterial blood pressure (MAP), Q(car) and tHb dropped below 30 mmHg (41% of baseline), 20 ml/min (33% of baseline) and 82% of baseline, respectively. Delta (delta) wave frequency percentage of the CFAM increased significantly at MAP below 30 mm Hg. EEG amplitude remained depressed after blood reinfusion and haemodynamic recovery. Cytaa3 changes were not statistically significant, reflecting sufficient neuronal oxygenation. CONCLUSION: Our results show that electrocortical function is affected only by profound systemic hypotension. This occurred at a higher level of cerebral oxygen delivery than the level associated with neuronal hypoxia and secondary cell damage.

Animals↗
PubMed2001

Endoscopic quadricepsplasty: A new surgical technique.

We present a new surgical subperiosteal endoscopic technique for the release of fibrosis of the quadriceps to the femur caused by gunshot injuries, postsurgical scarring, and fractures, that was developed at the Arthroscopy Group at Hospital Hermanos Ameijeiras in Havana, Cuba. The technique used is a proximal endoscopic subperiosteal extension of the usual arthroscopic intra-articular release of adhesions, using periosteal elevators and arthroscopic scissors placed through medial and lateral superior knee portals to release adhesions and bands of scar tissue beneath the quadriceps mechanism. The technique was used in a prospective case series of 26 male patients aged 19 to 22 years between February 1997 and March 1998 who presented with clinically and ultrasonically documented extra-articular fibrosis resulting in ankylosis of the knee in extension. Only patients who had reached a plateau in their aggressive physiotherapy program with no further progression in knee flexion for 3 months were selected. Those with joint instability, motion-limiting articular surface pathology, and muscle or neurologic injury were excluded. All patients had obtained satisfactory results at 2-year follow-up. The extra-articular release gained at final follow-up was between 30 degrees and 90 degrees of flexion in addition to that obtained at the completion of the standard intra-articular release. Complications included 1 case of deep vein thrombosis, 2 cases of scrotal edema, 5 cases of hemarthrosis, and 2 cases of reflex sympathetic dystrophy. We have found this technique useful in obtaining additional flexion and improved function in a difficult class of patients with ankylosis caused by extra-articular fibrosis of the quadriceps to the femur, allowing immediate aggressive rehabilitation and presenting a useful outpatient alternative with fewer and less severe complications than described with the classic open Thompson's quadricepsplasty.

Adult↗
PubMed2001

Minimally invasive selective osteotomy of the knee: A new surgical technique.

We present a simple surgical technique created by the authors to address degenerative chondral lesions of the knee and its application in a limited prospective case series. The technique assumes the concept of beneficial epiphyseal changes caused by disruption of the subchondral bone in improving symptoms, as with drilling, microfracture, periarticular osteotomy, and other invasive procedures. Minimally invasive selective osteotomy (MISO) is an expansion of the arthroscopic treatment of the knee, specifically targeting symptomatic lesions with minimal additional trauma and cost, while avoiding disruption of the articular surface of the subchondral bone. The technique involves a mimimal access approach with selective saw cuts placed with a 1-cm oscillating blade parallel to the joint surface 1 to 1.5 cm deep to identified lesions. The technique does not address malalignment but can address lesions not addressed by classic osteotomies and, as such, may be combined with other corrective alignment procedures as necessary. We present the results of MISO of the knee in a case series of 62 outpatients carried out at the Orthopaedic Division of the Clinical and Surgical Hermanos Ameijeiras Hospital in Havana, Cuba. At 2-year follow-up, there was improvement of symptoms without significant complications.

Adult↗
PubMed2001

Endoscopic treatment of calcaneal spur syndrome: A comprehensive technique.

We describe a comprehensive approach to the endoscopic treatment of calcaneal spur syndrome developed by the Arthroscopic Group of the Orthopedic Service of Hospital Hermanos Ameijeiras in Havana, Cuba. The surgical technique involves treatment of the heel spur and plantar fasciitis commonly found in calcaneal spur syndrome, but it also addresses adjacent calcaneal periostitis and allows decompression of the nerve to the abductor digiti quinti. Medial endoscopy and lateral instrumentation are used in a sequential approach with exposure and debridement of the posterior roof of the calcaneal arch, followed by removal of the calcaneal spur, lateral to medial release of the medial 75% of the plantar fascia, and if necessary, debridement of the calcaneal tuberosity periosteum. This technique was used in a prospective case series from June 1997 to May 1998 to treat a select group of 38 feet in 30 patients who reported unacceptable levels of pain despite 5 months of conservative treatment, which included an aggressive 8-week physical therapy program prescribed by the treating physician. Good to excellent results were obtained at 3 months postoperatively in all patients with regard to pain relief and return to normal activity, although 5 patients required a short course of physical therapy to resolve symptoms brought on by sports, trauma, or impact loading before 1-year follow-up, at which time all patients reported good to excellent results. Complications included 3 superficial wound infections cured by oral antibiotics and 2 transient lateral paresthesias that resolved with rest and nonsteroidal inflammatory medications. The described technique may provide a useful method for treating refractory heel spur syndrome and warrants further study.

Adult↗