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PubMed1998

Brain lipid peroxidation and antioxidant levels in fetal lambs 72 hours after asphyxia by partial umbilical cord occlusion.

OBJECTIVES: The purpose of this study was to explain the role of oxidative stress in the pathogenesis of brain damage caused by intrauterine fetal asphyxia. STUDY DESIGN: Six chronically instrumented near-term fetal lambs were subjected to asphyxia by partial umbilical cord occlusion for approximately 60 minutes until fetal arterial pH diminished to less than 6.9 and base excess to less than -20 mEq. Another six fetuses surgically prepared but not occluded were used as control. Fetuses were killed after 72 hours and eight different brain regions (frontal and parietal gray matter, frontal and parietal white matter, basal ganglia, thalamus, hippocampus, and cerebellum) were dissected and assayed for thiobarbituric acid reactive substances, glutathione, and superoxide dismutase. RESULTS: Thiobarbituric acid reactive substance levels in asphyxiated animals were elevated in frontal and parietal white matter, basal ganglia, and thalamus compared with those in controls. The concentrations of superoxide dismutase in the asphyxiated group were also higher in frontal and parietal white matter, basal ganglia, and cerebellum compared with those in the control group. Between the two groups, however, glutathione concentrations did not differ significantly. CONCLUSION: These results suggest that oxidative stress may be a major contributing factor to the development of brain damage in intrauterine fetal asphyxia.

Animals↗
PubMed1996

Suicide by proxy: a case report of juvenile autoerotic sexual asphyxia disguised as suicide. A common occurrence?

The confusion and embarrassment felt by a person discovering a body who has died through sexual asphyxia is likely to be considerable. Attempts may be made to disguise the nature of the death to medical attendants and to investigating police officers. A high level of suspicion and a knowledge of the characteristic findings seen in sexual asphyxia are important for the correct determination of the cause of death. This report describes the death of a 12-year-old boy in the Midlands, UK, in 1977. An open verdict had been recorded by the coroner. I Further evidence coming to light 17 years later appears to suggest that death was in fact due to autoerotic sexual asphyxia.

Journal Article↗
PubMed2002

Neonatal EEG-sleep disruption mimicking hypoxic-ischemic encephalopathy after intrapartum asphyxia.

OBJECTIVES: EEG-sleep organization of asphyxiated and non-asphyxiated full-term neonates was compared during the first 3 days after birth. BACKGROUND: Aggressive fetal and neonatal resuscitative efforts have reduced the severe expression of the neonatal brain disorder termed hypoxic-ischemic encephalopathy. Neonates may alternatively express altered EEG-sleep organization over the first days of life after asphyxia which may mimic mild or moderate hypoxic-ischemic encephalopathy. None of ten asphyxiated infants had EEG-confirmed seizures or pharmacologically-induced encephalopathies. All asphyxiated infants expressed fetal distress on fetal heart monitoring prior to delivery, and required neonatal resuscitation, as reflected in depressed 1, 5, and 10 min Apgar scores. Moderate to severe metabolic acidosis was also documented at birth in the asphyxiated group. All ten asphyxiated infants displayed either hyperalertness/irritability or somnolence/lethargy during the first 24 h after birth, suggesting mild to moderate post-asphyxial encephalopathy. Twenty-two 1 h 21-channel EEG polygraphic studies were obtained from the first through third days of life on nine asphyxiated infants and scored for EEG-sleep states. Studies on 23 non-asphyxiated newborns were also obtained between 1 and 3 days of life and scored for EEG-sleep state. EEG-sleep states were assigned to every minute of each record by visual analyses, without knowledge of the presence or absence of asphyxia. Comparisons of active, quiet, and indeterminate sleep percentages between neonatal groups were performed. Nested MANOVA was used which took into account multiple observations per child in the asphyxiated group. RESULTS: The percent of active sleep was 44.7% (+/-14.7), the percent of quiet sleep was 38.7% (+/-14.3), and the percent of indeterminate sleep was 13.3% (+/-11.4) in the non-asphyxiated group. The percent of active sleep was 18.9% (+/-18.5), the percent of quiet sleep was 46.5% (+/-21.1), and the percent of indeterminate sleep was 33.4% (+/-19.7) in the asphyxiated group. A significant decrease in active sleep (F=39.5, P<0.0001), and significant increases in quiet sleep (F=4.6, P<0.05) and indeterminate sleep (F=21.5, P<0.0005) were noted in the asphyxiated group. Shorter active sleep bout lengths were noted (F=21.8, P<0.001), while the quiet sleep bout lengths remained unchanged for the asphyxiated group. CONCLUSIONS: An increased percentage of quiet sleep and indeterminate sleep at the expense of decreased active sleep reflects postnatal brain adaptation to asphyxia in infants despite the absence of overt clinical or electrographic evidence of hypoxic-ischemic encephalopathy. Brain adaptation in newborns after acute asphyxial stress may be expressed as altered sleep organization, despite clinical signs which may masquerade as mild to moderate post-asphyxial encephalopathy. EEG-sleep studies can assist in a more accurate classification of newborn encephalopathy that does not satisfy the criteria for hypoxic-ischemic encephalopathy.

Journal Article↗
PubMed1987

Tachycardia of carotid chemoreceptors originates in apneic asphyxia in dogs.

Using various anesthetics, we investigated the heart rate changes resulting from apneic asphyxia in paralyzed artificially ventilated dogs with 1) low control heart rate (LCHR) and 2) high control heart rate (HCHR). We observed that apneic asphyxia produced by stopping the ventilation pump for 1 min evoked tachycardia in dogs with LCHR and bradycardia in dogs with HCHR. In dogs breathing 100% O2 in the preapneic period, the tachycardia response was almost wholly abolished, whereas the bradycardia response was attenuated. Intracarotid injection of sodium cyanide induced a tachycardia response in dogs with LCHR and a bradycardia response in dogs with HCHR. The results suggest that 1) apneic asphyxia evokes tachycardia or bradycardia response depending on whether the resting cardiac vagal tone is high or low, respectively, and 2) both types of heart rate responses are in part due to stimulation of carotid chemoreceptors.

Animals↗
PubMed1984

Newborn puppy cerebral acid-base regulation in experimental asphyxia and recovery.

We hypothesized that part of the newborn tolerance of asphyxia involves strong ion changes that minimize the cerebral acidosis and hasten its correction in recovery. After exposure of newborn puppies to 15 or 30 min experimental asphyxia (inhalation of gas with fractional concentration of CO2 and of O2 in inspired gas = 0.07-0.08 and 0.02-0.03, respectively), blood lactate increased to 13.2 and 23.4 mmol/l, respectively, brain tissue lactate increased to 14.4 and 19.7 mmol/kg, and cerebrospinal fluid (CSF) lactate increased to 7.6 and 14.4 mmol/l. We presume that the tissue lactate increase reflects increases in brain cell and extracellular fluid lactate concentration. The lactate increase, a change that will decrease the strong ion difference (SID), [HCO3-], and pH, was accompanied by increases in Na+ (plasma, CSF, brain), K+ (plasma, CSF), and osmolality without change in Cl-. After 60-min recovery, plasma and brain lactate decreased significantly, but CSF lactate remained unchanged. [H+] recovery was more complete than that of the strong ions due to hyperventilation-induced hypocapnia. We conclude that during asphyxia-induced lactic acidosis, changes in strong ions occur that lessen the decrease in SID and minimize the acidosis in plasma and CSF. To the extent that the increase in brain tissue sodium reflects increases in intra-and extracellular fluid sodium concentration, the decrease in SID will be less in these compartments as well. In recovery, CSF ionic values change little; plasma and brain tissue lactate decrease with a similar time course, and the [H+] is rapidly returned toward normal by hypocapnia even while the SID is below normal.

Acid-Base Equilibrium↗
PubMed1986

Cerebral blood flow and O2 metabolism after asphyxia in neonatal lambs.

A neonatal lamb model has been developed to examine the regulation of cerebral blood flow (CBF) and oxygen metabolism during the critical period after an asphyxial insult. Nine newborn lambs had control measurements and timed measurements after asphyxia of CBF (radioactive microsphere technique), arterial and cerebral venous (sagittal sinus) blood gases and oxygen contents performed. Immediately after resuscitation from asphyxia, there was a marked increase in CBF compared to control (239 +/- 22 versus 82 +/- 7 ml X 100 g-1 X min-1, mean +/- SEM; p less than 0.01). Cerebral oxygen delivery (CBF X arterial O2 content) increased from 12.87 +/- 1.20 to 37.40 +/- 3.40 ml X 100 g-1 X min-1 (p less than 0.01), while cerebral O2 consumption was significantly decreased compared to control (4.75 +/- 0.42 to 3.42 +/- 0.46 ml X 100 g-1 X min-1, p less than 0.05). Cerebral fractional O2 extraction, the relationship between oxygen uptake and delivery fell from 0.38 +/- 0.03 to 0.09 +/- 0.02; p less than 0.01. This reactive hyperemia was followed in all animals by a period of hypoperfusion. CBF (52 +/- 4 ml X 100 g-1 X min-1), O2 delivery (7.94 +/- 0.50 ml X 100 g-1 X min-1), and cerebral O2 consumption (3.34 +/- 0.24 ml X 100 g-1 X min-1) were all significantly depressed when compared to control. These data demonstrate important changes in CBF and O2 metabolism after neonatal asphyxia that may be important to the pathogenesis of brain injury.

Animals↗
PubMed1975

[The effect of asphyxia on the electrical and mechanical activities of the rat hindlimb muscles (author's transl)].

After asphyxia by clamping external iliac artery, the changes of electrical and mechanical activities of M. extensor digitorum longus and soleus were followed up. Although the action potential amplitude was decreased monotonously, a transient increase in twitch tension appeared, one or two minutes after start of asphyxia, which was seen more frequently and more remarkable in extensor than soleus. This was attributed to the different metabolic process of components contained in the muscle and also to their different population in two kinds of muscle fibres. It was suggested from the previous results obtained by us that the decrease of action potential amplitude, at least in the early period of asphyxia, was not due to membrane depolarization but to conformational change of Na-channel by anoxia.

Action Potentials↗
PubMed1976

Fetal heart deceleration patterns in relation to asphyxia and weight-gestational age percentile of the fetus.

The relation between fetal heart rate deceleration patterns and fetal asphyxia and the weight-gestational age percentile characteristics of the fetus has been reviewed from data obtained from 533 patients monitored during the intrapartum period. There is a significant relation between the frequency of total and late decelerations and fetal asphyxia, again confirming this as a useful criterion in the identification of fetal asphyxia. There is a significant relation between decreasing weight-gestational age percentile of the fetus and increasing frequency of total and late decelerations, identifying this fetal characteristic as another variable which will influence fetal heart rate deceleration patterns. The appreciation of the effect of this variable is useful in the interpretation of the fetal heart rate record during the intrapartum period.

Birth Weight↗
PubMed1991

Catecholamine concentrations in plasma and organs of the fetal guinea pig during normoxemia, hypoxemia, and asphyxia.

To examine the responses of the sympatho-adrenal system to reduced oxygen supply we studied plasma and tissue concentrations of catecholamines during normoxemia, hypoxemia, and asphyxia in 22 fetal guinea pigs near term. Fetal blood was obtained by cardiopuncture in utero under ketamine/xylazine-anesthesia. Catecholamines were determined in plasma and tissue of 15 organs and 14 brain parts by HPLC-ECD. During normoxemia (SO2 54 +/- 4 (SE) %, pH 7.36 +/- 0.02, n = 5) plasma catecholamine levels were low (norepinephrine 447 +/- 53, epinephrine 42 +/- 12, dopamine 44 +/- 6 pg/ml). During hypoxemia (SO2 27 +/- 3%, pH 7.32 +/- 0.01, n = 6) and asphyxia (SO2 24 +/- 2%, pH 7.23 +/- 0.02, n = 11) tissue catecholamine concentrations changed with changing blood gases and with increasing plasma catecholamines. Norepinephrine concentrations increased in both skin and lung and decreased in liver, pancreas, and scalp; those of epinephrine increased in the heart, lung liver, and scalp and decreased in the adrenal. There were only minor changes in brain catecholamine concentrations except for a 50% reduction in dopamine in the caudate nucleus. Concentrations of dopamine catabolite 3,4-dihydroxyphenylacetic acid decreased in many brain parts, suggesting that cerebral catecholamine metabolism was affected by hypoxemia and asphyxia. We conclude that the sympatho-adrenal system of fetal guinea pigs near term is mature and that its stimulation by reduced fetal oxygen supply leads to changes in both plasma and tissue catecholamine concentrations.

Acid-Base Equilibrium↗
PubMed1978

Relation of amniotic fluid lecithin/sphingomyelin ratio and fetal asphyxia to respiratory distress syndrome in premature infants.

In a group of 81 prematurely delivered infants the amniotic fluid lecithin/sphingomyelin ratio was related to functional fetal lung maturity. Intrapartum fetal asphyxia occurred in 33% of the group. An association between fetal asphyxia and the development of respiratory distress syndrome (RDS) in the infant was observed. When pulmonary maturity was borderline according to the amniotic fluid assessment, intrapartum fetal asphyxia was associated with an increased risk for development of RDS in the infant.

Acid-Base Equilibrium↗
PubMed1993

Relationship of fetal asphyxia to neuropathology and deficits in children.

Neuropathological studies suggest that the majority of the fetal asphyxial complications resulting in brain damage in either preterm or term fetus occur before the onset of labor. Anoxia because of the rapid sequence of events will usually result in death of the fetus. Hypoxia of 1-3 h duration may account for brain damage and deficits in children who survive. The threshold for brain damage is a severe acidosis with a pH < 7.0 in conjunction with systemic hypotension. The prevalence of antepartum fetal asphyxia and the frequency of deficits in such children have not been established. The prevalence of intrapartum fetal asphyxia determined biochemically is 2%. The majority of these children develop normally because of fetal cardiovascular compensatory mechanisms which protect the brain. However, beyond the threshold of asphyxia in either the preterm or term fetus, neuropathology may develop leading to deficits in some children.

Animals↗
PubMed1977

Activities of some peptidases and glycolytic enzymes in cells of the amniotic fluid. II. Pregnancies complicated by threatening intrauterine fetal asphyxia.

Activities of leucylaminopeptidase, aspartyl aminopeptidase, gamma-glutamyl transpeptidase, oxytocinase, phosphohexoisomerase, phosphofructokinase and aldolase were studied in amniotic cells from cases of pregnancy complicated by threatening intrauterine fetal asphyxia. Leucylaminopeptidase and oxytocinase activities were much higher in the group of pregnancies complicated by threatening fetal asphyxia than in the control group. It was concluded that elevated activity of the aforementioned enzymes in cells of the amniotic fluid from pregnancies complicated by threatening intrauterine asphyxia is due to acute hypoxia of the fetus.

Adult↗
PubMed1998

Responses to an increasing asphyxia in infants: effects of age and sleep state.

Infants aged 0-6 months were assessed for respiratory and arousal responses to mild asphyxia during sleep. Ventilatory sensitivity was assessed from the relationship between inspired carbon dioxide (FICO2) and ventilation. Arousal and ventilatory sensitivity were significantly related. Respiratory response increased with age and was greater in quiet sleep than in REM sleep. Arousal occurred more frequently in REM sleep (55/102) than quiet sleep (38/165, P < 0.05) and more frequently at the newborn age (54/117) than at 6 months (13/58, P < 0.05). Arousal in quiet sleep occurred in babies with high ventilatory sensitivities (mean ventilatory asphyxial sensitivity (VAS) 0.476 +/- 0.288) and in REM sleep was more associated with low ventilatory sensitivities (mean VAS 0.194 +/- 0.334, P <0.05). We conclude infants respond to mild asphyxia during sleep with an increase in ventilation, an arousal or both. The exact response is dependent on age and sleep state.

Arousal↗
PubMed1964

HYPOTHERMIA, ASPHYXIA, AND CARDIAC GLYCOGEN IN GUINEA PIGS.

Cardiac glycogen was not affected by cooling guinea pigs for short periods. In normothermic animals it was reduced 75 percent or more at the time of death from asphyxia. Quickly cooled animals asphyxiated until the time of death of warm controls showed no significant losses of cardiac glycogen; animals cooled while breathing 10 percent oxygen plus 5 percent carbon dioxide showed slight reductions. Therefore, hypothermia spares cardiac glycogen during asphyxia, but there are factors other than cardiac glycogen which influence survival of asphyxiated animals.

Animals↗
PubMedDate not supplied

MR and CT evaluation of profound neonatal and infantile asphyxia.

PURPOSE: To determine the CT and MR characteristics of the brains of infants who have suffered profound asphyxia and correlate those characteristics with pathophysiologic processes. METHODS: MR and CT scans of 16 patients who suffered profound hypoxic-ischemic injury in the perinatal (12 patients) and postnatal (4 patients) periods were retrospectively reviewed in a search for characteristic imaging features. RESULTS: Injury in the perinatal period: subacute MR showed short T1 and T2 in the ventral lateral thalami, posterolateral lentiform nuclei, posterior mesencephali, and hippocampi; MR 1 to 16 years after injury showed atrophy or T2 prolongation in the aforementioned regions, the lateral geniculate nuclei and perirolandic cerebral cortex. Asphyxia later in infancy: subacute MR showed T2 prolongation in the corpus striatum and most of the cerebral cortex (perirolandic sparing); MR weeks to months later showed atrophy of the aforementioned areas, the lateral geniculate nuclei and hippocampi. Acute CT in both groups showed basal ganglia hypodensity. CONCLUSIONS: The injury patterns observed in neonates and infants with profound hypoxic-ischemic injury vary with the age of the patient at the time of the injury. The change in pattern of damage is suggested to be the result of structural and physiologic changes in the maturing brain. The patterns appear to be consistent and are well demonstrated by MR.

Adolescent↗
PubMed1991

Visual evoked potentials and visual prognosis following perinatal asphyxia.

Twenty-five children born at term with perinatal asphyxia were studied at age 2.5 to 4.5 years to evaluate visual function and to determine the prognostic value of postnatal assessments of visual outcome. Postnatal assessments included several visual evoked potentials and electroretinograms in the first week of life. Follow-up assessments included flash and pattern visual evoked potentials, visual evoked potential threshold measurements, and clinical eye examinations. Nineteen children had normal visual function, three were visually impaired, and three remained blind. A strong association was found between normal, abnormal, or absent visual evoked potentials in the early postnatal period and long-term visual outcome (P less than .0001). Other perinatal indicators of asphyxia, including neurologic status, Apgar scores, and arterial pH values, were poor predictors of visual outcome. The risk of visual impairment was limited to those survivors with neurodevelopmental deficits.

Asphyxia Neonatorum↗
PubMed1988

Fetal lamb coagulation system during birth asphyxia.

Levels of many coagulation factors are low in the healthy infant and even lower in the asphyxiated premature infant. We investigated whether a brief exposure to asphyxia at the time of birth causes the activation and consumption of coagulation factors. Following delivery by caesarean section, premature lambs were asphyxiated by occluding the endotracheal tube for 10 min and then resuscitated. Blood was obtained prior to and following birth for measurement of blood gases and the coagulation system. Birth asphyxia in the premature lamb resulted in thrombin generation and rapid consumption of specific coagulation factors.

Animals↗
PubMed2005

Xenon and hypothermia combine to provide neuroprotection from neonatal asphyxia.

Perinatal asphyxia can result in neuronal injury with long-term neurological and behavioral consequences. Although hypothermia may provide some modest benefit, the intervention itself can produce adverse consequences. We have investigated whether xenon, an antagonist of the N-methyl-D-aspartate subtype of the glutamate receptor, can enhance the neuroprotection provided by mild hypothermia. Cultured neurons injured by oxygen-glucose deprivation were protected by combinations of interventions of xenon and hypothermia that, when administered alone, were not efficacious. A combination of xenon and hypothermia administered 4 hours after hypoxic-ischemic injury in neonatal rats provided synergistic neuroprotection assessed by morphological criteria, by hemispheric weight, and by functional neurological studies up to 30 days after the injury. The protective mechanism of the combination, in both in vitro and in vivo models, involved an antiapoptotic action. If applied to humans, these data suggest that low (subanesthetic) concentrations of xenon in combination with mild hypothermia may provide a safe and effective therapy for perinatal asphyxia.

Analysis of Variance↗