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PubMed2004

Fetal heart rate variability and brain stem injury after asphyxia in preterm fetal sheep.

This study was undertaken to determine the mechanisms mediating changes in fetal heart rate variability (FHRV) during and after exposure to asphyxia in the premature fetus. Preterm fetal sheep at 0.6 of gestation (91 +/- 1 days, term is 147 days) were exposed to either sham occlusion (n = 10) or to complete umbilical cord occlusion for either 20 (n = 7) or 30 min (n = 10). Cord occlusion led to a transient increase in FHRV with abrupt body movements that resolved after 5 min. In the 30 min group there was a marked increase in FHRV in the final 10 min of occlusion related to abnormal atrial activity. After reperfusion, FHRV in both study groups was initially suppressed and progressively increased to baseline levels over the first 4 h of recovery. In the 20 min group this improvement was associated with return of normal EEG activity and movements. In contrast, in the 30 min group the EEG was abnormal with epileptiform activity superimposed on a suppressed background, which was associated with abnormal fetal movements. As the epileptiform activity resolved, FHRV fell and became suppressed for the remainder of the study. Histological assessment after 72 h demonstrated severe brain stem injury in the 30 min group but not in the 20 min group. In conclusion, during early recovery from asphyxia, epileptiform activity and associated abnormal fetal movements related to evolving neural injury can cause a confounding transient increase in FHRV, which mimics the normal pattern of recovery. However, chronic suppression of FHRV was a strong predictor of severe brain stem injury.

Animals↗
PubMed1989

Effect of beta-adrenergic blockade on lung liquid secretion during fetal asphyxia.

The hypothesis tested in this study was that beta-adrenergic stimulation is responsible for the inhibition of fetal lung liquid production during moderate fetal asphyxia. In chronically catheterized fetal sheep, net lung liquid production rates were measured over three consecutive periods: a control period, a period of reduced uterine blood flow (RUBF) or epinephrine infusion, and periods of RUBF or epinephrine infusion in the presence of the beta-adrenergic receptor antagonist propranolol. The net production rate of fetal lung liquid was decreased from a mean control value of 7.7 +/- 1.0 to 1.5 +/- 0.4 ml/h (P less than 0.001) by RUBF; the administration of propranolol had no further effect on these liquid production rates (1.1 +/- 0.5 ml/h). In other experiments epinephrine infusion reduced the net production rate of fetal lung liquid from a mean control value of 7.2 +/- 1.4 to 1.7 +/- 1.8 ml/h (P less than 0.025); the addition of propranolol reversed this inhibition (secretion rate 6.1 +/- 1.4 ml/h, P less than 0.005). We conclude that the inhibition of fetal lung liquid production induced by moderate fetal asphyxia does not solely result from catecholamine stimulation of pulmonary beta-receptors.

Animals↗
PubMed1982

Augmentation of ventilatory response to asphyxia by prochlorperazine in humans.

The effect of the dopamine-receptor blocking agent prochlorperazine on the ventilatory response to hypercapnic hypoxia was studied in six healthy adults. Repeated episodes of transient hypoxia were induced at the mixed venous PCO2 level by a nonrebreathing technique in five males and one female before and after an intravenous bolus injection of prochlorperazine mesylate (12.5 mg = 10 mg base). The ventilatory response to CO2 was also studied before and after drug administration. Prochlorperazine produced a modest (15%) increase in resting ventilation (P less than 0.05) but a marked increase in the ventilatory response to asphyxia such that the group mean response was double the control value [2.0 +/- 0.7 vs. 4.2 +/- 1.5 l . min-1 . % arterial O2 saturation (%SaO2); P less than 0.001]. Two-thirds of this change in ventilatory response was due to an increase in frequency response to hypoxia (0.34 +/- 0.20 vs. 0.81 +/- 0.52 breaths . min-1 . %SaO2; P less than 0.001). The position of the ventilatory response line, as judged by the computed ventilation at 95% SaO2, was increased by prochlorperazine (22.2 +/- 9.6 vs. 35.9 +/- 10.9 l . min-1; P less than 0.01) due to an increase in both tidal volume (P less than 0.05) and frequency of breathing (P less than 0.0125). The ventilatory response to CO2 was unchanged by drug injection. In separate experiments prochlorperazine was shown to 1) increase the ventilatory response to steady-state eucapnic hypoxia (P less than 0.01) demonstrating that the drug effect was not dependent on either the presence of hypercapnia or rapidly changing states of arterial oxygenation; and 2) reverse the depressant effect of intravenously infused dopamine hydrochloride (5 micrograms . kg-1 . min-1) on the ventilatory response to transient asphyxia (P less than 0.01). We conclude that prochlorperazine augments hypoxic responsiveness in humans. The mechanism may be blockade of dopaminergic receptors that modulate carotid body discharge.

Adult↗
PubMed1998

A case of auto-erotic asphyxia in a long-term psychiatric setting.

The syndrome of auto-erotic asphyxia (AEA) involves the deliberate induction of cerebral hypoxia to produce or enhance sexual excitement. This sexual practice is normally only discovered when death results from the act because these individuals rarely seek professional advice. The practice of AEA in the living case presented here was initially misinterpreted as parasuicidal behaviour. This type of sexual behaviour should always be considered a differential for parasuicidal activity involving asphyxia. Aetiology, treatment and the need for health professionals to be aware of this syndrome are discussed.

Adult↗
PubMed2002

Expression of transcription factors in the brain of rats with perinatal asphyxia.

No information is available on transcription factors (TF), the main regulators of gene expression, in perinatal asphyxia (PA), and as pathomechanisms in PA are different, data on TFs from ischemia or hypoxia cannot be simply extrapolated to PA, and no studies have been reported to show an expressional pattern or the concerted action of TFs. We, therefore, used a gene-hunting technique, subtractive hybridization, to show sequences different in brains of normoxic and perinatally asphyxiated (10 and 20 min of asphyxia) rats. These subtracted sequences were identified by gene bank and assigned to individual genes. At 10 min of PA the TFs NFI/CAAT-binding protein, NF-kappa-B p65, N-myc, basic helix loop helix protein D82868, and c-myc intron binding protein were upregulated. At 20 min of PA the TFs SOX4 and neuronal death factor were upregulated, whereas the TFs c-maf, PEBP major transcription factor, brn-2, homeodomain protein Af004431, and zinc finger transcriptional factor M65008 were downregulated. The biological meaning of our findings is the demonstration of a pathophysiological pattern of TFs including POU, zinc finger, homeodomain, and basic helix-loop helix motifs in PA, proposing pathomechanisms for brain damage from PA, explaining transcriptional changes in general (as, e.g., NF-kappa-B p65, etc.) or in specific terms (as, e.g., neuronal death factor).

Animals↗
PubMed1986

Circulatory changes in fetuses with imminent asphyxia.

Blood flow was measured in 11 term fetuses who were later delivered by means of emergency caesarean section because of cardiotocographic changes indicating imminent asphyxia. Blood flow was recorded in the fetal descending aorta and in the intraabdominal part of the umbilical vein by combined real-time and 2-MHz pulsed Doppler ultrasound method. In all 11 fetuses, the waveform of the maximum aortic blood velocity was changed in a typical way with elimination of the diastolic flow (zero flow). In 4 of the fetuses, a short-lasting reversal of the diastolic flow occurred. In 5 fetuses, the pulsatility index of the aortic flow was increased, and the aortic volume flow was pathologically low in 3 fetuses. In the umbilical vein, the volume flow was within normal limits in all cases. The umbilical flow, which normally is continuous and nonpulsatile, showed heart-synchronous pulsations in 3 of the fetuses. The typical changes in the aortic diastolic flow occurred 1-3 days before the onset of the cardiotocographic changes. This suggests that the changes in the fetal aortic blood velocity might be a clinically useful early sign of imminent asphyxia.

Amniotic Fluid↗
PubMed1989

Urinary excretion of prostacyclin metabolites in infants born after maternal preeclampsia or with birth asphyxia.

Decreased fetoplacental prostacyclin (PGI2) production has been shown in preeclampsia, and increased pulmonary PGI2 synthesis has been demonstrated in experimental hypoxia. We measured the urinary excretion of the main metabolites of PGI2, 6-keto-prostaglandin F1 alpha (6-keto) and 2,3-dinor-6-keto-prostaglandin F1 alpha (2,3-dinor), during the first day of life in infants born to mothers with preeclampsia (n = 26), in infants with birth asphyxia (n = 12), and in control infants (n = 14). The mean excretion of 6-keto in control infants increased from 9.3 to 14.3 ng/h/1.73 m2 from 0-12 to 12-24 h of age, and a corresponding change from 3.5 to 7.0 ng/h/1.73 m2 was seen in 2,3-dinor excretion. In infants of preeclamptic mothers the excretion values at 0-12 and 12-24 h and the pattern of change were not significantly different from controls. In asphyxiated infants, the mean excretion values at 0-12 and 12-24 h of 6-keto (11.0 and 11.6 ng/h/1.73 m2) and 2,3-dinor (6.0 and 5.8 ng/h/1.73 m2) were not significantly different from control infants, but no increase was seen. We conclude that PGI2 production in infants of preeclamptic mothers is not impaired, but after perinatal asphyxia there is an altered pattern of PGI2 metabolite excretion, suggesting decreased production capacity.

6-Ketoprostaglandin F1 alpha↗
PubMed1995

Monoamine neurotransmitters and metabolites in the cerebrospinal fluid following perinatal asphyxia.

While the release of neurotransmitters is involved in the pathophysiology of brain damage following birth asphyxia, it also plays a role in endogenous defense against such damage. Levels of monoamines and the main cerebral monoamine metabolites in the cerebrospinal fluid (CSF) were measured in asphyxiated and control infants within 24 h after birth. The results indicate an increased turnover of noradrenaline (NA) and dopamine following asphyxia. Furthermore, the NA stores in the brain seem to be exhausted in some cases. We conclude that this increase in catecholamine turnover to some extent explains the clinical symptoms of hypoxic-ischemic encephalopathy and that it may reflect an intrinsic adaptive capacity to perinatal distress.

Asphyxia Neonatorum↗
PubMed1996

Prolactin and growth hormone in perinatal asphyxia.

To assess the pituitary response to perinatal asphyxia, the prolactin (PRL) and growth hormone (hGH) serum concentrations were measured in 55 asphyctic (15 preterm and 40 full-term) and 35 control (15 preterm and 20 full-term) newborns at 2-4, 24, 48 and 98 h of life. At 2-4 h the median PRL in the preterm asphyctic neonates was 5.2 U/l, whereas in the preterm control newborns it was 3.2. In the full-term newborns with and without hypoxic-ischaemic encephalopathy (HIE) it was 5.8 and 3.4, respectively. In the full-term neonates with HIE the PRL remained significantly higher than in the controls up to the fourth day. At 2-4 h the median hGH in the preterm asphyctic and control newborns was 106.2 and 54.8 mU/l, respectively. In full-term newborns it was 85.0 and 40.8, respectively. The lowest hGH concentrations were found in the severe HIE. The increased PRL and hGH in asphyxia may result from a stress-related hormone release, whereas the very low hGH concentrations in severe HIE may result from a damage at the hypothalamic-hypophyseal axis.

Asphyxia Neonatorum↗
PubMed1988

Effect of autonomic nervous system blockade and acute asphyxia on heart rate variability in the fetal rat.

The effect of parasympathetic (with atropine) and beta-adrenergic (with propranolol) blockade on fetal heart rate variability (HRV) was studied in 162 term fetal Wistar rats. Administration of 1.3 mg of atropine into the jugular vein of the female rat led to an identical decrease of the RR interval in adult rats and in fetuses (about 10%). Administration of 2 mg of propranolol caused a rise in the RR interval by 19% in rats and by 7-9% in fetuses. Overall HRV indices (RMSM, CV) decrease was more pronounced in adult rats than in fetuses. Upon simultaneous administration of both blocking agents the RR interval in adult rats did not differ from the control values; in fetuses it was reduced by 6%. In adult rats HRV indices decreased considerably (by 70%) and their values were within the limits of the estimation error; in fetuses, HRV indices were no higher than upon the administration of any of the blocking agents. Umbilical cord clamping caused a decrease of PO2 in brain tissue from 24.7 +/- 1.7 to 4.7 +/- 0.8 mm Hg within 15 min and led to an immediate increase of the RR interval and the HRV indices if blocking agents were not used. The administration of one or both blocking agents abolished the initial (during the first 7 min of asphyxia) increase of RMSM and CV. Thus, HRV in fetal rats depends to a great extent on the activity of the autonomic nervous system, though it is not fully determined by it. Acute asphyxia causes stimulation of the autonomic nervous system leading to fetal distress.

Animals↗
PubMed1980

Medication use and deaths attributed to asphyxia among psychiatric patients.

In a review of the charts of inpatients who died in 1969-1977 the author found 49 whose death could be attributed to asphyxia. Compared with a matched control group, 48 of the asphyxia patients represented three distinct pathologic categories: 1) older patients with a history of serious physical illness whose deaths appeared unrelated to psychotropic medication use (40%), 2) a group whose deaths were associated with seizures (31%), raising questions about subtherapeutic anticonvulsant levels in association with the use of psychotropic drugs, and 3) a group of patients who choked to death (29%). Choking has been theoretically linked to a combination of dopamine blockade plus strong anticholinergic effects leading to impairment of swallowing. The third category appears to have been virtually eliminated by the use of a drug monitoring system and the Heimlich maneuver.

Adolescent↗
PubMed2002

Delayed onset of status epilepticus after transient asphyxia in an asymptomatic full-term neonate.

A full-term neonate presented with status epilepticus at 12 hours of age after a symptom-free interval following transient asphyxia at birth. Conventional neuroimaging failed to detect structural correlates to support recent injury. However, diffusion-weighted magnetic resonance imaging studies revealed recent ischemic brain injury. Placental examination documented multiple subacute and chronic findings indicative of decreased maternal/fetal perfusion. These antepartum placental abnormalities may have been associated with this child's inability to withstand the stress of a prolonged second stage of labor, resulting in intrapartum asphyxia leading to brain injury. This child's clinical presentation highlights the delayed reperfusion phase after ischemia-induced brain injury.

Asphyxia↗
PubMed1995

Differential involvement of the brain in neonatal asphyxia: a pathogenic explanation.

Multiple cystic lesions in brain parenchyma supplied by the anterior cerebral circulation is a recognized pattern of cerebral injury associated with hypoxic-ischemic encephalopathy in the term infant. This report presents a series of seven infants (gestational age, 39.3 +/- 2.8 weeks; range, 36 to 44 weeks) who developed multicystic encephalomalacia in the distribution of the anterior cerebral circulation after severe neonatal asphyxia. Cerebral imaging and pathologic studies demonstrate relative preservation of the cerebellum, brain stem, and cerebral structures supplied by the vertebrobasilar circulation. Compared to the vertebrobasilar vasculature, the anterior cerebral vessels in the term infant have dense sympathetic innervation. Asphyxia, a potent sympathetic stimulator, may induce vasoconstriction in the anterior circulation and differentially accentuate the effects of hypoxia/ischemia on cerebral tissue.

Asphyxia Neonatorum↗
PubMed1991

Age, transvestism, bondage, and concurrent paraphilic activities in 117 fatal cases of autoerotic asphyxia.

Autoerotic asphyxia is the practice of self-inducing cerebral anoxia, usually by hanging, strangulation, or suffocation, during masturbation. This study investigated the relationships between: asphyxiators' ages; two paraphilias commonly accompanying autoerotic asphyxia, bondage and transvestism; and various other types of simultaneous sexual behaviour. Subjects were two concurrent series totalling 117 males aged 10-56 who died accidentally during autoerotic asphyxial activities. Data concerning sexual paraphernalia at the scene of death or among the deceased's effects were extracted from coronors' files using standardised protocols. Anal self-stimulation with dildos, etc., and self-observation with mirrors or cameras were correlated with transvestism. Older asphyxiators were more likely to have been simultaneously engaged in bondage or transvestism, suggesting elaboration of the masturbatory ritual over time. The greatest degree of transvestism was associated with intermediate rather than high levels of bondage, suggesting that response competition from bondage may limit asphyxiators' involvement in a third paraphilia like transvestism.

Accidents↗
PubMed2001

Signs of asphyxia at birth and risk of schizophrenia. Population-based case-control study.

BACKGROUND: Previous research has found an association between obstetric complications and schizophrenia, but in many studies the sample size was limited, and no assessment of specific exposures was possible. AIMS: To assess the role of different complications, and in particular to distinguish between disordered foetal development and hypoxia at birth. METHOD: From the Stockholm County In-Patient Register and community registers, we identified 524 cases of schizophrenia and 1043 controls, matched for age, gender, hospital and parish of birth. Data on obstetric complications were obtained from birth records. RESULTS: There was a strong association between signs of asphyxia at birth and schizophrenia (OR 4.4; 95% C11.9-10.3) after adjustment for other obstetric complications, maternal history of psychotic illness and social class. CONCLUSIONS: Signs of asphyxia at birth are associated with an increased risk of schizophrenia in adults.

Adolescent↗
PubMed1981

Birth asphyxia. I. Measurement of visual evoked potential (VEP) in the healthy fetus and newborn lamb.

The visual evoked potential (VEP) of five healthy, near-term exteriorized fetal lambs was compared with the VEP obtained from the same animals during the first hour after ventilation. Characteristics of the individual wave components and their relationship to blood pressure, heart rate, and arterial blood gas measurements concomitantly obtained were examined. Results show that the VEP of the healthy fetus is a stable, reproducible signal consisting of four basic components, and that the latencies (msec) and the amplitude (mu V) of the individual components of the VEP are similar to those of the newborn. In two related experiments, fetal asphyxia of unknown duration was encountered during fetal exteriorization an instrumentation. In the first case, neonatal, acidosis persisted despite aggressive resuscitation efforts and was accompanied by an atypical VEP. In the second case, the neonatal VEP obtained after 15 min of resuscitation was markedly depressed despite restoration of acid-base balance but gradually recovered during the remainder of the 1-hr newborn period. In conclusion, the VEP is a reproducible measure of cortical function in the healthy fetus and neonate and may reflect the acute status of cerebral function during fetal asphyxia and neonatal resuscitation.

Animals↗
PubMed1990

Brain superoxide anion generation during asphyxia and reventilation in newborn pigs.

Superoxide anion generation during severe asphyxia and reventilation was assessed in newborn pigs. Using closed cranial windows over the parietal cortices, superoxide dismutase (SOD)-inhibitable nitroblue tetrazolium (NBT) reduction was determined during asphyxia/reventilation. Asphyxia was induced by turning off the respirator and occluding the endotracheal tube. In each animal, 2.4 mM NBT dissolved in artificial cerebrospinal fluid was placed under one window and under the opposite window, NBT (2.4 mM) plus SOD (60 U/mL) dissolved in artificial cerebrospinal fluid was used. A significant increase in SOD-inhibitable NBT reduction was observed in asphyxiated piglets (14.67 +/- 4.5 pmol/mm2 x 20 min) when compared with control piglets (2.82 +/- 1.1 pmol/mm2 x 20 min). In another group in which the animals were treated with indomethacin (5 mg/kg i.v.) before asphyxia/reventilation, there was minimal SOD-inhibitable NBT reduction. Our results indicate that superoxide anion is generated on the cerebral cortex during asphyxia/reventilation via the prostaglandin endoperoxide synthase pathway.

Animals↗
PubMed1998

Cytokine response in cerebrospinal fluid after birth asphyxia.

Experimental studies suggest that cytokine-mediated inflammatory reactions are important in the cascade leading to hypoxic-ischemic brain injury. The purpose was to study the content of pro- and antiinflammatory cytokines in cerebrospinal fluid (CSF) of asphyxiated and control infants. Samples of CSF were obtained from 20 infants who fulfilled the criteria of birth asphyxia and from seven newborn control subjects. The concentrations of IL-1beta, IL-8, IL-10, tumor necrosis factor (TNF)-alpha, and granulocyte/monocyte colony-stimulating factor (GM-CSF) were determined with ELISA and of IL-6 using a bioassay. The concentration of IL-6 (pg/mL) was higher in asphyxiated (250, 35-543; median, interquartile range) than in control (0, 0-18) infants (p = 0.001). There was also a significant relationship between IL-6 and the degree of HIE, and between IL-6 and outcome. In addition, the content of IL-8 (pg/mL) was higher (p = 0.009) in the asphyxia group (170, 70-1440), than in the the control group (10, 0-30) and there was an association between IL-8 and degree of HIE. The levels of IL-10, TNF-alpha, GM-CSF, and IL-1beta did not differ between groups. In conclusion, the proinflammatory cytokines IL-6 and IL-8 were markedly elevated in CSF of asphyxiated infants, and the intrathecal levels of these cytokines corresponded to the degree of HIE.

Apgar Score↗