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PubMed2006

[Effects of birth asphyxia or intrauterine distress on renal functions in newborns in the first week of life].

OBJECTIVE: To investigate the renal function in newborns with birth asphyxia or intrauterine distress in the first week of life. METHODS: Sixty full-term newborns born between June 2002 and February 2003 were assigned into three groups: Control group (healthy newborns), Intrauterine distress group (Apgar score > 7), and Birth asphyxia group without intrauterine distress (12 mild asphyxia and 8 severe asphyxia) (n=20 each). Urinary levels of alpha1-microglobulin (alpha1-MG), beta2-microglobulin (beta2-MG) and albumin (Alb) were detected by radioimmunoassay at 0-2, 3-4 and 6-7 days after birth. RESULTS: The urinary levels of alpha1-MG, beta2-MG and Alb in the Asphyxia group were significantly higher than those in the Control group at all time points (P < 0.05), peaking at 3-4 days after birth. Statistically significant differences were found between the severely and mildly asphyxiated newborns for the urinary levels of alpha1-MG, beta2-MG and Alb at all time points (P < 0.05). There were no significant differences in the urinary levels of alpha1-MG, beta2-MG and Alb between the Intrauterine distress and the Control groups at each time point. CONCLUSIONS: Birth asphyxia may lead to renal glomerular and tubular impairments and it is speculated that the most serious impairment occurs at the 3rd and 4th days of life. The severity of renal impairments is associated with the degree of asphyxia. The renal function of the newborn appears to be normal following intrauterine distress.

Albuminuria↗
PubMedDate not supplied

Prognosis in infants with birth asphyxia.

The risk of neurodevelopmental disability from birth asphyxia secondary to intrapartum complications and obstetric mismanagement is generally overestimated. Between 8-17% of all cerebral palsy is associated with adverse perinatal events suggestive of asphyxia. Less than 10% is probably due directly to birth asphyxia itself. Studies have shown that different methods of intrapartum assessment of fetal well-being (fetal heart rate monitoring, fetal scalp pH, presence of meconium) do not correlate well with each other or with neonatal parameters (acid-base status at birth, Apgar scores, seizures, neurological behaviour) and outcome measures (death, cerebral palsy, mental retardation). The prevalence rate of cerebral palsy in most communities of 2.0-2.5 per 1000 children is not falling in spite of increasing use of obstetric and neonatal interventions aimed at preventing or treating birth asphyxia. Prediction of neurodevelopmental outcome of birth asphyxia is difficult because of a limited ability to measure birth asphyxia quantitatively in the antenatal and neonatal period. The terminology used to describe the condition is often confusing. It has been recommended that substantial cerebral hypoxia can only be presumed when four criteria are met: the infant has an Apgar score < or = 3 at 10 minutes, metabolic acidosis at birth, hypotonia for several hours and seizures. For the paediatrician, a number of clinical observations and laboratory investigations have been suggested as helpful in the prediction of death or disability among term infants with birth asphyxia.

Asphyxia Neonatorum↗
PubMed1994

[Pathophysiological study of asphyxia and its applications to medico-legal diagnosis].

Asphyxia is commonly defined as "a hypoxic state in the body" which is caused by any one of a wide range of events, starting from an insufficiency of atmospheric oxygen to a failure in oxygen uptake by the cells. The present study outlines a physiopathological study of "mechanical asphyxia" various types of hypoxia caused by mechanical compression of the cervical and thoracic regions and its application to medicolegal diagnosis. We used an animal model in which an actual asphyctic condition was experimentally recreated. By elaborating the asphyctic mechanism through the physiological dynamics of the body fluids and tissues during the fatal process and the succeeding short time span, the study was intended to estimate the causes of death, time lapse after death before the examination, and the time of death in persons who were subjected to investigation, autopsy, or forensic examination. Our intention was also to establish medicolegal indices for the cause of death by examining patients who were resuscitated or expired before arrival (DOA). Our past superimental findings indicate that asphyxia is a state in which arterial blood gas anomalies (hypoxemia and hypercapnia) develop due to a disturbance in the respiratory mechanism, disrupting the maintenance of normal bodily functions by the organism. Among the clinical conditions of respiratory insufficiencies, asphyxia caused by external mechanical, factors (such as external application of pressure to the naso-oral, cervical, or thoracic region, insertion of a foreign body into the airway, and aspiration of fluids) corresponds to acute respiratory insufficiency due to hypercapnia type. In most of these cases with mechanical asphyxia, ventilatory insufficiency due to a lack of O2 in the inhaled air and insufficient removal of CO2 through expiration causes pulmonary alveolar hypoventilation and hyperemia associated with hypercapnia. Consequently, hypoxic hypoxia with systemic disturbances develops. The rapidity of development of the clinical events is correlated with the velocity of the rise in blood CO2 level and the development of acidemia from the early stage. The conditions culminate in non-compensatory (acute) respiratory acidosis. These abnormal physiological changes in turn produce symptoms such as congestion and cyanotic petechia. Asphyxia ensues if no resuscitation or other medical treatment is available during this stage (the so-called early asphctic stage). We believe that an understanding of these physiopathologic changes is useful in the diagnoses of asphyxia. It is also useful in the diagnosis of the above-cited process in cases of DOA and in patients who have received resuscitation or other medical treatment.

Animals↗
PubMed1994

Sympathoadrenal reactions during asphyxia in hypoglycemia and hyperglycemia of cats.

In 26 cats anesthetized with alpha-chloralose and urethane, cardiovascular changes during asphyxia in hypoglycemia and hyperglycemia were studied. Systemic hypoglycemia (serum glucose decrease from 148 to 31 mg/100 ml) was produced by i.v. injection of insulin 20 U/kg, followed by continuous I.V. infusion of 10 U/kg/hr. Systemic hyperglycemia (serum glucose increase from 187 to 657 mg/100 ml) was produced by I.V. infusion of 25% glucose at a rate of 1.5 gm/kg/hr. During hypo- or hyperglycemia, resting mean systemic arterial pressure (MSAP) and heart rate did not change significantly. Brain transection at various levels, i.e., midcollicular decerebration, ponto-medullary or medulla-spinal transection progressively decreased the resting MSAP, but not the heart rate. The most apparent reduction was at the medulla-spinal junction. After induction of systemic hypo- or hyperglycemia, plasma catecholamine concentrations increased significantly. Further increase occurred during asphyxia. Increases of MSAP and plasma catecholamine concentrations during asphyxia were attenuated after midcollicular decerebration and decreased further after subsequent ponto-medullary and medulla-spinal transections. Increases in plasma catecholamines during asphyxia were greater in hypoglycemic than those in hyperglycemic state. The increase in plasma catecholamine persisted in hypoglycemic animals during asphyxia after midcollicular decerebration and ponto-medullary transections. As the terminal stage of asphyxia approached spasmodic contractions of urinary bladder occurred. Bladder contractions were abolished after intracerebroventricular (lateral) injection of insulin (0.25 unit/kg). In conclusion, asphyxia produced very marked cardiovascular and plasma catecholamine responses during hypo- or hyperglycemia and more so during the former condition. These reactions depend mainly on the neural mechanisms of medullary structures. Neural structures rostral to the midcollicular level are not essential.

Animals↗
PubMed1998

Effects of fetal asphyxia on brain cell structure and function: limits of tolerance.

The objective of this paper is to review the published information available on the effect of hypoxia on fetal cerebral integrity, and to attempt to define limits of fetal tolerance to asphyxia Data were obtained in experimental animals following imposed hypoxia or asphyxia. Studies were carried out in the fetus by physiologic, biochemical, histologic, and behavioral techniques. Human data were collected from newborns at birth and during subsequent development. It has been established that acute asphyxia of the fetus in utero may result in a spectrum of effects on the fetus, including death, or survival with permanent neurologic damage, or apparent complete recovery. The severity of damage depends on the degree and duration of asphyxia and a number of sensitizing factors, including prior metabolic and cardiovascular status of the fetus, differential sensitivity of the heart and brain to asphyxia, gestational age, plasticity, intermittency of asphyxial insults, and the pattern of intermittency. The fetus has a number of compensatory mechanisms that allow it to survive periods of oxygen limitation without permanent damage to the brain. The fetus can increase cerebral blood flow to increase oxygen delivery to the brain, and can decrease its metabolism by electrophysiological and behavioral state changes. Cerebral ischemia and reduced metabolism to < 50% of control is probably necessary for permanent brain damage to occur. In human pregnancy, factors consistent with intrapartum asphyxia lasting until delivery as a cause of fetal neurologic damage include absent fetal heart rate variability, umbilical cord arterial pH < 6.8, base access < -20 mEql-1, severe and prolonged newborn depression with Apgar score of < or = 3 at 10 min, seizure activity in the first day of life, and damage to the noncerebral organs and regions. However, these factors are neither independently nor collectively predictive of asphyxial brain damage. It is concluded that permanent neurologic damage or death can occur in the fetus due to single or repetitive episodes of hypoxia or asphyxia, but it is not yet possible to predict the occurrence or extent of such damage in an individual fetus.

Animals↗
PubMed1991

How much of neonatal encephalopathy is due to birth asphyxia?

In the literature on neonatal encephalopathy, the pervasive assumption is that once infants with major malformations or infections have been excluded, most of the remaining cases are due to birth asphyxia. Assessing the proportion of neonatal encephalopathy that is due to asphyxia during birth is difficult because of problems in defining asphyxia and neonatal encephalopathy and in recognizing the cause of neonatal neurologic illness. Available evidence indicates that neonatal neurologic signs are not strongly related to obstetric complications, signs of fetal distress, or biochemical markers usually considered to indicate perinatal asphyxia. Most studies that have sought positive evidence of independent markers of intrapartum asphyxia have found them to be absent in a large majority of neurologically symptomatic neonates. We conclude that the proportion of neonatal encephalopathy that is asphyxial in origin is not known but warrants examination, especially in view of the probable need in the near future to identify, on the basis of evidence available in the first hour or so of life, suitable candidates for clinical trials of powerful but risky treatments of birth asphyxia.

Asphyxia Neonatorum↗
PubMed2002

Detection of asphyxia using heart rate variability.

The long-term aims of this study are to find a parameter derived from the ECG that has a high sensitivity and specificity to asphyxia and, once we know or suspect that asphyxia occurred, to estimate how severe it was. We carried out a pilot study in which 24 adult Wistar rats were anaesthetised and subjected to controlled asphyxia for specified durations. We measured the pH, 'neurological score' and the ECG, extracting from this heart rate and heart rate variability (HRV). We have developed a technique capable of detecting asphyxia in less than 1 min, based on monitoring the ECG and estimating HRV by measuring the standard deviation of normal RR intervals (the RR interval is the time interval between two consecutive R-points of the QRS complex). In all cases the heart rate decreased and HRV increased, by an average of 46 +/- 33 ms in relation to the baseline, at the onset of asphyxia. The comparison of the base level of HRV after and before asphyxia shows promise for the estimation of the severity of the episode; however, the limitations of this study should be noted as they include the small size of the cohort and the methods of analysis.

Animals↗
PubMedDate not supplied

Effect of birth asphyxia on serum calcium levels in neonates.

Serum calcium and phosphorus levels were measured at birth, 6 hours, 24 hours, and on 5th day of life in 35 neonates with birth asphyxia (one-minute Apgar score of 6 or less), and in 37 neonates without asphyxia (one-minute Apgar score of 7 or more). Infants were divided into three groups: FT-AGA (n = 30, asphyxia = 15), FT-IUGR (n = 20, asphyxia = 10) and PT-AGA (n = 22, asphyxia = 10). Asphyxiated infants--FT-AGA as well as FT-IUGR--had significantly lower serum calcium levels than control infants during each of the time period studied. In PT-AGA infants with asphyxia, the serum calcium was significantly low only on 5th day of life. Lack of calcium intake, and hyperphosphatemia were identified as possible risk factors for low serum calcium in asphyxiated infants. No change in serum calcium levels was found in bicarbonate-treated asphyxiated infants in comparison to those who did not receive sodium bicarbonate. In view of the high incidence of low serum calcium in asphyxiated infants, serial monitoring of serum calcium levels is recommended in these infants.

Apgar Score↗
PubMed2002

Nicotinamide prevents the long-term effects of perinatal asphyxia on basal ganglia monoamine systems in the rat.

Asphyxia during birth can cause gross brain damage, but also subtle perturbations expressed as biochemical or motor deficits with late onset in life. Thus, it has been shown that brain dopamine levels can be increased or decreased depending upon the severity of the insult, and the region where the levels are determined. In this study, perinatal asphyxia was evoked by immersing pup-containing uterus horns removed by hysterectomy in a water bath at 37 degrees C for various periods of time from 0 to 20 min. After the insult, the pups were delivered, given to surrogate mothers, treated with nicotinamide, further observed and finally, 4 weeks later, killed for monoamine biochemistry of tissue samples taken from substantia nigra, neostriatum and nucleus accumbens. The main effect of perinatal asphyxia was a decrease in dopamine and metabolite levels in nucleus accumbens, and a paradoxical increase in the substantia nigra. Nicotinamide (100 mg/kg i.p., once a day for 3 days, beginning 24 h after the perinatal asphyctic insult) prevented the effect of asphyxia in nucleus accumbens. Furthermore, striatal dopamine levels were increased by nicotinamide in asphyctic animals. No apparent changes were observed in substantia nigra. A prominent unexpected effect of perinatal asphyxia alone was on the levels of the metabolite of 5-hydroxytryptamine, 5-hydroxyindoleacetic acid (5-HIAA), which were increased in substantia nigra and decreased in both neostriatum and accumbens. However, nicotinamide increased 5-HIAA levels in all regions, which appeared to be related to the extent of the asphyctic insult. These results suggest that nicotinamide is a useful treatment against the long-term consequences produced by perinatal asphyxia on brain monoamine systems, and that there is a therapeutic window following the insult, providing a therapeutic opportunity to protect the brain.

Animals↗
PubMed1994

Long-term effects of perinatal asphyxia on basal ganglia neurotransmitter systems studied with microdialysis in rat.

Asphyxia was induced in pups delivered by caesarean section on pregnant Sprague-Dawley rats. Rats within the last day of gestation were anaesthetised and hysterectomized. The uterus horns including the foetuses were placed in a water bath for various periods of time. Following asphyxia the uterus horns were opened. The pups were removed, stimulated to breathe, left to recover and given to surrogate mothers. Control and asphyctic pups were obtained from each mother. Rats surviving asphyctic periods longer than 20 min at 37 degrees C showed chronic deficits in the release of neurotransmitters monitored with microdialysis in the basal ganglia. The main change observed in 6-month-old male rats that underwent severe perinatal asphyxia was a marked decrease in striatal dopamine release, monitored under basal and D-amphetamine stimulated conditions, as compared with control (normal- or caesarean-delivered) rats. Striatal glutamate and aspartate levels were also decreased following asphyxia. In the substantia nigra, the main effect of asphyxia was a decrease of both gamma-aminobutyric acid (GABA) and aspartate levels. Thus, this study provides evidence that perinatal asphyxia leads to chronic deficits in neurotransmission in the basal ganglia.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2004

Effect of perinatal asphyxia on tyrosine hydroxylase and D2 and D1 dopamine receptor mRNA levels expressed during early postnatal development in rat brain.

This study was designed to investigate the postnatal developmental plasticity of the mesostriatal and mesolimbic dopamine systems that occurs following perinatal asphyxia. The time course and patterning of the changes in levels of tyrosine hydroxylase (TH), and D1 and D2 dopamine receptor (R) mRNA in the cell body region, substantia nigra and ventral tegmental area (SN/VTA), and projection fields, striatum and limbic regions at the age of 6 and 24 h, and 1 week after asphyxia were studied with a quantitative reverse transcription polymerase chain reaction method with appropriate internal cRNA standard. In Caesarean-delivered control rats (Sprague-Dawley), TH, D2R and D1R mRNA levels showed regional and temporal specificity in both absolute levels and developmental kinetics during the first week of life. TH mRNA levels were >10-fold higher in SN/VTA than in striatum and limbic regions. Compared to Caesarean delivered controls, severe asphyxia (15-20 min) induced an increase of TH and D2R mRNA in SN/VTA 6 h and 1 week after birth. In addition, asphyxia induced an increase of TH mRNA in the projection fields, striatum and limbic regions, at 1 week. Perinatal asphyxia did not appear to exert any effect on D1R mRNA levels. No differences in any of the parameters were observed between spontaneous- and Caesarean-delivered animals. The present results indicate that perinatal asphyxia triggers coordinated changes in the expression of TH, and dopamine receptor mRNA in SN/VTA, striatum and limbic regions. These changes may affect differently dopamine D2R and D1R expression along development, contributing to long-term neurocircuitry imbalances.

Analysis of Variance↗
PubMed2005

Effects of perinatal asphyxia on cell proliferation and neuronal phenotype evaluated with organotypic hippocampal cultures.

The present report summarizes studies combining an in vivo and in vitro approach, where asphyxia is induced in vivo at delivery time of Wistar rats, and the long term effects on hippocampus neurocircuitry are investigated in vitro with organotypic cultures plated at postnatal day seven. The cultures preserved hippocampus layering and regional subdivisions shown in vivo, and only few dying cells were observed when assayed with a viability test at day in vitro 27. When properly fixed, cultures from asphyxia-exposed animals showed a decreased amount of microtubule-associated protein-2 immunocytochemically positive cells (approximately 30%), as compared with that from controls. The decrease in microtubule-associated protein-2 immunocytochemistry was particularly prominent in Ammon's horn 1 and dentate gyrus regions (approximately 40%). 5-Bromo-2'deoxyuridine labeling revealed a two-fold increase in cellular proliferation in cultures from asphyxia-exposed, compared with that from control animals. Furthermore, confocal microscopy and quantification using the optical disector technique demonstrated that in cultures from asphyxia-exposed animals approximately 30% of 5-bromo-2'deoxyuridine-positive cells were also positive to microtubule-associated protein-2, a marker for neuronal phenotype. That proportion was approximately 20% in cultures from control animals. Glial fibrillary acidic protein-immunocytochemistry and Fast Red nuclear staining revealed that the core of the hippocampus culture was surrounded by a well-developed network of glial fibrillary acidic protein-positive cells and glial fibrillary acidic protein-processes providing an apparent protective shield around the hippocampus. That shield was less developed in cultures from asphyxia-exposed animals. The increased mitotic activity observed in this study suggests a compensatory mechanism for the long-term impairment induced by perinatal asphyxia, although it is not clear yet if that mechanism leads to neurogenesis, astrogliogenesis, or to further apoptosis.

Animals↗
PubMed2001

Relative risk of birth asphyxia in babies of booked women who deliver in unorthodox health facilities in Calabar, Nigeria.

Babies of booked women who delivered in unorthodox health facilities in Calabar, Nigeria were studied. The aims were to determine the relative risk of birth asphyxia in these babies and to find out the management of birth asphyxia in these unorthodox delivery centres. The incidence (14.3%) of birth asphyxia in the study population was significantly higher than the incidence (4.8%) in babies of booked women who delivered in the University of Calabar Teaching Hospital (P < 0.001) with a relative risk of 3.0 (95% C.I.=1.74-5.19). Apart from prolonged labour, the predisposing factors to birth asphyxia in both the study group and control did not show any significant difference (P > 0.05). The treatment of birth asphyxia in unorthodox delivery centres consisted mainly of prayers (43.8%) and immersion of the asphyxiated baby in cold water (25%). A birth asphyxia case fatality rate of 20.8% was recorded in these unorthodox delivery facilities but no death in the control population. Appropriately directed antenatal health education on the benefit of delivering under supervision of trained personnel is strongly advocated.

Asphyxia Neonatorum↗
PubMed1999

Prognostic significance of cerebrospinal fluid cyclic adenosine monophosphate in neonatal asphyxia.

OBJECTIVE: In piglets prolonged asphyxia resulted in decreased cerebrospinal fluid (CSF) 3;,5;-cyclic adenosine monophosphate (cAMP) during recovery; this was associated with reduced pial arteriolar responses to stimuli that use cAMP as a second messenger. We hypothesized that asphyxia in human neonates results in decreased CSF cAMP and that low CSF cAMP is associated with abnormal outcome. DESIGN: We studied 27 infants with evidence of hypoxic-ischemic insult; 19 were term (group 1) and 8 were preterm (group 2). The normal values of CSF cAMP were determined from 75 infants with no asphyxia; 44 were term (group 3) and 31 were preterm (group 4). CSF cAMP was measured by using radioimmunoassay procedures. RESULTS: CSF cAMP levels in infants with asphyxia (groups 1 and 2) were 12 +/- 9. 5 and 7.9 +/- 7.1 pmol/mL, respectively, significantly lower than those of groups 3 and 4 (control infants), that is, 21.1 +/- 8.7 and 27.1 +/- 9.2 pmol/mL, respectively (P <.0001). Among infants with asphyxia, 3 died and 10 had abnormal neurologic outcome. Univariate analysis showed that abnormal outcomes were significantly related to CSF cAMP levels, phenobarbital use, and multi-organ failure. However, only CSF cAMP was retained in the model by stepwise logistic regression. CSF cAMP of 10.0 pmol/mL discriminated between those with normal and those with abnormal neurologic outcome. Low CSF cAMP concentration was associated with abnormal long-term outcome, estimated odds ratio of 12.4 (95% CI, 2.1-109.3; P <.006), and sensitivity, specificity, and positive and negative predictive values of 85%, 69%, 73%, and 80%, respectively. CONCLUSION: CSF cAMP concentrations were decreased in infants with asphyxia. Low CSF cAMP levels were associated with poor neurologic outcome.

Apgar Score↗
PubMed1997

Short- and long-term effects of perinatal asphyxia on monoamine, amino acid and glycolysis product levels measured in the basal ganglia of the rat.

The effects of perinatal asphyxia on levels of dopamine (DA) and its metabolites, amino acids and glycolysis products, measured in tissue samples from substantia nigra (SN), striatum, ventral tegmental area (VTA), and nucleus accumbens (Acb), were studied 80 min to 8 days after birth with high performance liquid chromatography (HPLC). Furthermore, extracellular levels of DA, amino acids and glycolysis products were measured with in vivo microdialysis in the striatum 40-140 min and 4 weeks after birth. Asphyxia was induced by immersing foetus-containing uterus horns, removed from ready-to-deliver Sprague-Dawley rats, in a water bath at 37 degrees C for various time periods (0-22 min). Spontaneous- and caesarean-delivered pups were used as controls. Perinatal asphyxia led to a decrease in the rate of survival, depending upon the length of the insult. In parallel, lactate (LACT) levels were increased with the length of the insult in all examined brain regions, monitored ex vivo or in vivo immediately after birth. DA, glutamate (GLU) and aspartate (ASP) levels were also increased, mainly in tissue samples taken from the mesencephalon. Only minor changes were observed in tissue samples taken from the telencephalon. However, in experiments with in vivo microdialysis, DA and GLU levels were increased following 20-21 and 21-22 min of perinatal asphyxia, but the effect of K+ depolarisation on extracellular DA and ASP levels was strongly diminished. DA and metabolites increased with development in SN and striatum, with no clear differences between control and asphyctic rats. However, 8 days after birth, it was found that DA levels were increased, alternatively decreased in mesencephalic and telencephalic regions following 20-21 and 21-22 min of perinatal asphyxia, periods associated with 60% and 90% of perinatal mortality, respectively. Furthermore, in microdialysis experiments performed 4 weeks after birth, extracellular DA and its metabolites levels were also increased, alternatively decreased in rats exposed to a 20-21 and 21-22 min perinatal asphyctic insult. In this last group, GLU and ASP levels were also decreased. Furthermore, the effect of K+ depolarisation on DA and ASP levels was strongly decreased in both asphyctic groups. Thus, perinatal asphyxia produces short- and long-term consequences in general metabolism, and induces region-specific changes in several neurotransmitter systems, mainly affecting meso-telencephalic DA systems.

Acute Disease↗
PubMed2000

Perinatal asphyxia induces region-specific long-term changes in mRNA levels of tyrosine hydroxylase and dopamine D(1) and D(2) receptors in rat brain.

To study the effects of neonatal asphyxia on gene expression of the dopaminergic systems, we determined quantitatively the mRNA levels of tyrosine hydroxylase, dopamine transporter, dopamine D(1) and D(2) receptors in substantia nigra/ventral tegmental area, striatum and limbic area. The mRNA levels were determined at one and 4 weeks after asphyxia by a quantitative reverse transcription polymerase chain reaction method. Spontaneously and Caesarean section born rats showed similar mRNA levels with the exception of an increase of tyrosine hydroxylase mRNA levels in the limbic area of 4-week-old animals. Five min of asphyxia did not change the mRNA levels in any region compared to that in the spontaneously born rats. Fifteen and twenty min of asphyxia induced region-specific alterations in mRNA levels. In SN/VTA an increase of tyrosine hydroxylase mRNA levels in the 1-week-old rats and in striatum an increase of D(1) and D(2) dopamine receptor mRNA levels in the 4-week-old rats were observed. Fifteen min of asphyxia induced a selective increase of D(1) and D(2) dopamine receptor mRNA levels in the limbic area of 4-week-old rats. These observations indicate that neonatal asphyxia triggers a cascade of gene expressions for tyrosine hydroxylase and D(1) and D(2) dopamine receptors. In 1-week-old rats, the gene expression of tyrosine hydroxylase increased in the cell body region substantia nigra/ventral tegmental area. This change may increase the D(1) and D(2) dopamine receptor expression in the target regions striatum and limbic area during further development.

Aging↗
PubMed1999

Nitric oxide and nitric oxide synthase in the early phase of perinatal asphyxia of the rat.

The role of nitric oxide, a compound involved in neurotransmission and regulation of cerebral blood flow, in cerebral ischemia is still not fully elucidated yet. Although well studied in adult systems of cerebral ischemia/hypoxia, information on nitric oxide in perinatal asphyxia is limited and, in particular, no direct evidence for its generation has been provided. We therefore decided to study nitric oxide generation in brain of asphyctic rat pups by biophysical and biochemical methods. We used a simple, non-invasive rat model resembling the clinical situation in perinatal asphyxia: rat pups delivered by Caesarean section were placed into a water bath at 37 degrees C still in patent membranes for various asphyctic periods (up to 20 min). Brain pH, cerebral blood flow, neuronal nitrix oxide synthase messenger RNA (by northern and dot blot analysis), immunoreactive protein (by western blot analysis) and nitric oxide synthase activity were determined; generation of nitric oxide was evaluated directly by electron paramagnetic resonance spectroscopy. Neuronal nitric oxide synthase messenger RNA activity and nitric oxide generation were unaffected, whereas neuronal nitric oxide synthase-immunoreactive protein of 150,000 mol. wt was decreased and of 136,000 mol. wt was increased with the length of the asphyctic period. This is the first report on direct evidence for the generation of nitric oxide in perinatal asphyxia and we demonstrate that nitric oxide production remains unaffected even by 20 min of asphyxia, at a time-point when cerebral blood flow was increased four-fold and severe acidosis was present. However, it was found that levels of immunoreactive neuronal nitric oxide synthase of 136,000 mol. wt were increased paralleling the length of asphyxia. Levels of the 150,000 mol. wt immunoreactive neuronal nitric oxide synthase protein decreased, suggesting a different regulation pattern. Thus, the present biochemical and biophysical results form the basis for further investigations on nitric oxide in perinatal asphyxia.

Animals↗
PubMed2001

Is the appearance of macrophages in pulmonary tissue related to time of asphyxia?

In order to connect the appearance of macrophages and giant cells in pulmonary tissue with the time of asphyxia the authors analyzed 50 asphyxiated human lungs paying their attention on the number of alveolar and interstitial macrophages and giant cells. They compared histological specimens of 25 asphixiated humans lungs following a slow asphyxia (30 min or more) with 25 histological specimens of asphyxiated human lungs following a rapid asphyxia (10-15 min). Alveolar and interstitial macrophages and giant cells per section, were considered and numbered. Controls were done on histological examination of traumatized lungs. In the pulmonary alveoli following on acute asphyxia there were 27.7+/-4.4 macrophages per section. Subjects dead after a slow asphyxiation showed 68.2+/-7.1 alveolar macrophages per section (p<0.001). Interstitial macrophages were also frequently present. No differences are detectable in the number of polynuclear giant cells between rapidly and slowly asphyxiated human lungs. The number of alveolar and interstitial macrophages per section can be considered as a further histological evidence of a slow asphyxia and can differentiate a slow asphyxia from an acute one.

Asphyxia↗