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PubMed1992

Effects of birth asphyxia on urinary organic acid excretion.

Using capillary gas chromatography-mass spectrometry, the effects of birth asphyxia on the urinary organic acid profile of term babies was investigated. Random urine samples were collected on days 1 and 8 from 19 babies with fetal distress, 19 with moderate birth asphyxia and 12 with severe asphyxia causing encephalopathy. Controls were 27 well neonates. Statistically significant abnormalities were found only for the severely asphyxiated group: increased concentrations of lactic, pyruvic, 3-hydroxybutyric, 4-hydroxyphenyllactic and 4-hydroxy-3-methoxymandelic acids, and excretion of four abnormal metabolites, 2-hydroxybutyric, 2-oxoisocaproic, 2-hydroxyisovaleric and 2-oxo-3-methylvaleric acids. Six other babies had increased lactic acid excretion, associated in four with transient 'jitterness' or hypotonia. Organic acid studies may help to grade the severity of perinatal asphyxia in the outcome or intervention studies.

3-Hydroxybutyric Acid↗

PubMed1981

Cerebrovascular mechanisms in perinatal asphyxia: the role of vasogenic brain edema.

Previous studies from our laboratory have demonstrated penetration of Evan's blue dye into the brain in profound fetal asphyxia, suggesting that vasogenic brain edema (BE) might be an immediate contributing factor in asphyxial brain injury. We modified the 125I-labeled albumin method of Pappius and McCann to quantitate vasogenic BE after acute fetal asphyxia. With 51Cr-labeled red cells to measure intravascular volume, and 125I-labeled albumin to measure total tissue plasma, the equivalent extra vascular plasma volume, i.e., vasogenic BE, was calculated. Twenty chronically prepared animals were studied, six nonasphyxiated controls and 14 asphyxiated (of which sex term animals were normotensive and five term and three premature animals were hypertensive during asphyxia). No difference in extra vascular plasma volume was found between asphyxiated and control animals in any of four brain regions. We conclude that, although blood brain barrier function might be impaired, vasogenic BE is not quantitatively significant immediately after severe fetal asphyxia.

Animals↗

PubMed1981

Blood volume in newborn piglets: effects of time of natural cord rupture, intra-uterine growth retardation, asphyxia, and prostaglandin-induced prematurity.

Blood volume (BV), red cell mass (RCM; Cr-51) and plasma volume (125I-labeled albumin) were measured in 205 piglets from 28 litters shortly after birth. Spontaneous cord rupture in healthy piglets occurred during delivery (n = 25) or within 190 sec of birth (n = 82). Spontaneous and induced delay of cord rupture resulted in a time-dependent increase in BV and RCM. BV (x +/- S.D.) at birth was 72.5 +/- 10.5 ml/kg (RCM, 23.6 +/- 4.6 ml/kg) in the 25 piglets with prenatal cord rupture and 110.5 +/- 12.9 ml/kg (RCM, 38.4 +/- 7.0 ml/kg) in 17 piglets with late spontaneous cord rupture. The mean blood volume of all the 107 healthy piglets with spontaneous cord rupture was 90.2 +/- 12.7 ml/kg (RCM, 30.1 +/- 4.8 ml/kg). RCM was significantly (P less than 0.05) increased in nine piglets with intra-uterine growth retardation (RCM, 35.8 +/- 11.2 ml/kg) and in 13 with metabolic acidosis but without signs of asphyxia (RCM, 35.8 +/- 6.7 ml/kg). In five piglets with cord wrapping, prenatal cord rupture, and acute asphyxia, BV (57.8 +/- 7.3 ml/kg) was significantly decreased. In five other piglets with prenatal cord rupture and acute asphyxia, BV (67.9 +/- 10.0 ml/kg) corresponded to that of the normal piglets with prenatal cord rupture. However, delay of cord rupture to 60 sec after birth did not increase BV (66.0 +/- 11.8 ml/kg) in four piglets with acute asphyxia. Forty-one premature piglets delivered 6 days before normal term had their cords ruptured prenatally or within 5 sec of birth. Their hematocrit at birth (0.337 +/- 0.028 liters/liter) was significantly decreased compared to the normal full-term piglets with corresponding time of cord rupture (0.384 +/- 0.033 liters/liter). RCM in 18 piglets with prostaglandin-induced prematurity (18.9 +/- 3.4 ml/kg) was significantly lower than in 23 piglets whose births had been induced by ovarectomy of their mother (RCM, 22.1 +/- 3.2 ml/kg).

Animals↗

PubMed1984

Regulation of upper airway maintaining muscles during progressive asphyxia.

The electromyographic activity of an upper airway muscle (genioglossus, GG) and the diaphragm were studied in 10 adult and three young anesthetized rabbits during progressive asphyxia induced by airway occlusion. Results were similar for both age groups. Peak inspiratory activity of GG muscle increased more than that of the diaphragm during both the hyperpnea and gasping (P less than 0.05). The increase in GG activity during gasping was not significantly different from that during hyperpnea even though an important stimulus, arousal, was absent during gasping. During end stage asphyxia, as the strength of gasps grew weaker, the rate of loss of GG muscle activity was greater than that of the diaphragm. However, GG activity remained greater than that of the diaphragm at the time of the last spontaneous gasp. As asphyxia progressed, inspiratory duration and the inspiratory contour of integrated electromyogram activity of both muscles changed. These data indicate differences in the control mechanism of the genioglossus and diaphragm during acute severe asphyxia. Increased upper airway muscle activity seen during gasping should help preserve upper airway patency and facilitate autoresuscitation by gasping. These observations of coordinated changes in timing and activity of two functionally different respiratory muscles support the concept that gasping is a highly organized function of the respiratory centers.

Airway Resistance↗

PubMed1985

Cerebrovascular hemodynamics during and after recovery from acute asphyxia in the newborn dog.

Cerebrovascular volume and transmural pressure loads accompanying acute increases in cerebral blood flow are implicated in the pathogenesis of periventricular-intraventricular hemorrhage in preterm infants. An acute increase in cerebral blood flow would be expected during acute recovery from asphyxia. Therefore, cerebrovascular hemodynamics, including flow (microspheres), were studied during and after acute recovery from asphyxia in seven newborn dogs in order to study the determinants of these volume and pressure loads. During the acute recovery phase, cerebral hemispheric blood flow was 69.6 +/- 10 ml/100 g/min (mean +/- SEM) representing a 250% increase from baseline values of 19.9 +/- 1.8 ml/100 g/min (p less than 0.005), while combined cerebellar-brainstem flow was 204.3 +/- 19.3 ml/100 g/min representing a 536% increase from baseline values of 32.0 +/- 1.5 ml/100 g/min (p less than 0.005). Blood flow to both areas had returned to baseline levels 20 min after the onset of recovery. Associated with this cerebral hyperemia was an acute increase in mean arterial pressure from 21.3 +/- 4.5 mm Hg at end asphyxia to 69.5 +/- 6.0 mm Hg at peak recovery (p less than 0.01), and parallel acute increases in sagittal sinus pressure (from 4.0 +/- 0.4 to 14.6 +/- 1.9 mm Hg, p less than 0.01) and cerebrospinal fluid pressure (from 3.8 +/- 0.4 to 14.3 +/- 1.9 mm Hg, p less than 0.01). Central venous pressure fell from 4.3 +/- 0.6 mm Hg at end asphyxia to 1.6 +/- 0.5 mm Hg, and thus is not a determinant of the elevation in sagittal sinus pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

PubMed1992

Cerebral histologic and electrocorticographic changes after asphyxia in fetal sheep.

Asphyxia can cause neurologic damage in the fetus, but there are few data relating severity or duration of asphyxia to the degree of cerebral damage. We report cerebral histologic and electrophysiologic changes after asphyxia in chronically instrumented late-gestation fetal sheep. We reduced uterine blood flow to produce an ascending aortic blood oxygen content less than 1.5 mM for either 30 or 60 min (n = 13). In a subsequent protocol (n = 6), if full occlusion of the common uterine artery for 15 min did not reduce the EEG voltage to less than 20% of baseline, supplementary maternal hypoxia was added for a maximum of 120 min. Histologic outcome was assessed 3 d postinsult. Uterine artery occlusion resulted in severe hypoxemia, hypercarbia, acidosis, and an initial hypertension and bradycardia. Eight of 14 surviving fetuses showed neuronal damage, with greatest loss in the parasagittal cortex, striatum, and the CA1/2 region of the hippocampus. Neuronal damage was strongly associated with the percentage of decrease in blood pressure during the insult (r = 0.75, p less than 0.005) but not with the degree of hypoxia. No other factor was independently predictive, but, when considered separately, pH (r = 0.54; p less than 0.05) and loss of intensity of the EEG (r = 0.61, p less than 0.02) at the end of asphyxia were also correlated with outcome. The pH fell to less than 7.0 in six of eight fetuses with damage, whereas it remained greater than 7.0 in five of six without damage (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗

PubMed1997

Reperfusion injury as the mechanism of brain damage after perinatal asphyxia.

Upon reperfusion of ischemic tissues, reactive oxygen metabolites are generated and are responsible for much of the organ damage. Experimental studies have revealed two main sources of these metabolites: 1) the oxidation of hypoxanthine to xanthine and on to uric acid by the oxidase form of xanthine oxidoreductase and 2) neutrophils accumulating in ischemic and reperfused tissue. Blocking either source will reduce reperfusion damage in a number of experimental situations. Although xanthine oxidoreductase activity may be unmeasurably low in organs other than liver and intestine, it may be involved in reperfusion injury elsewhere because of its localization in capillary endothelial cells. Time course considerations suggest that substrate accumulation and NADH inhibition of dehydrogenase activity may be more important in the pathogenesis than conversion of xanthine dehydrogenase into the oxidase form. Neutrophil accumulation may be partly due to oxidants in the first place, suggesting a link between the two sources of reactive oxygen metabolites. In the clinical context, many of the sequelae of perinatal asphyxia may be accounted for by reperfusion damage to organs such as brain, kidney, heart, liver, and lungs. During asphyxia, substrates of xanthine oxidase accumulate, upon resuscitation the cosubstrate oxygen is introduced, and evidence for oxidant production and effects has been obtained. In the pathogenesis of brain damage after asphyxia, both microvascular injury and parenchymal cell damage are important. Oxygen metabolites are involved in the former, but in the latter process their role is less clear because ischemia-reperfusion triggers not only oxidant production but many other phenomena, including gene activation, ATP depletion, glutamate accumulation, and increase of intracellular calcium. A severe insult results in cell necrosis, but more moderate asphyxia may cause delayed neuronal death through apoptosis. The time course of the changes in high energy phosphates as well as of selective neuronal death suggest that in the first hours of life there is a "therapeutic window," with future possibilities for prevention of permanent damage.

Animals↗

PubMed2000

Glucose transporters, hexokinase, and phosphofructokinase in brain of rats with perinatal asphyxia.

Transport by glucose transporters from blood to the brain during hypoxic-ischemic conditions is well studied. However, the recent availability of a clinically related animal model of perinatal asphyxia and the fact that no concomitant determination of glucose transporters, parameters for glucose utilization, brain glucose, and cerebral blood flow (CBF) have been reported and the early phase of perinatal asphyxia has never been studied led us to perform the following study. Cesarean section was performed on full-term pregnant rats. The obtained pups within patent uterus horns were placed into a water bath at 37 degrees C from which they were subsequently removed after 5-20 min of graded asphyxia. Brain pH, brain tissue glucose, CBF, mRNA and activity of hexokinase and phosphofructokinase, and mRNA and protein of the glucose transporters GLUTI and GLUT3 were determined. Brain pH decreased and brain tissue glucose and CBF increased with the length of the asphyctic period; hexokinase and phosphofructokinase mRNA and activity were unchanged during the observation period. The mRNA and protein of both glucose transporters were comparable between normoxic and asphyctic groups. We show that glucose transport and utilization are unchanged in the early phase of perinatal asphyxia at a time point when CBF and brain glucose are already significantly increased and severe acidosis is present.

Animals↗

PubMed2003

Neurodegeneration, neuronal loss, and neurotransmitter changes in the adult guinea pig with perinatal asphyxia.

There is only limited morphologic information on long-term alterations and neurotransmitter changes after perinatal asphyxia, and no long-term study showing neurodegeneration has been reported so far. We used an animal model for perinatal asphyxia well documented in the rat to investigate the guinea pig as a species highly mature at birth. Cesarean section was performed on full-term pregnant guinea pigs, and pups, still in membranes, were placed into a water bath at 37 degrees C for asphyxia periods from 2 to 4 min. Thereafter pups were given to surrogate mothers and examined at 3 mo of age. We studied brain areas reported to be hypoxia-sensitive. Neurodegeneration was evaluated by fluoro-jade, neuronal loss by Nissl, reactive gliosis by glial fibrillary acidic protein staining, and differentiation by neuroendocrine-specific protein C immunoreactivity. We tested tyrosine hydroxylase, the vesicular monoamine transporter, and dopamine beta-hydroxylase, representing the monoaminergic system; the vesicular acetylcholine transporter; and the excitatory amino acid carrier 1. Neurodegeneration was evident in cerebellum, hippocampal area CA1, and hypothalamus, and neuronal loss could be observed in cerebellum and hypothalamus; gliosis was observed in cerebellum, hippocampus, hypothalamus, and parietal cortex; dedifferentiation was found in hypothalamus and striatum; and monoaminergic, cholinergic, and amino acidergic deficits were shown in several brain regions. The major finding of the present study was that neurodegeneration and dedifferentiation evolved in the guinea pig, a species highly mature at birth. The relevance of this contribution is that a simple animal model of perinatal asphyxia resembling the clinical situation of intrauterine hypoxia-ischemia and presenting with neurodegeneration was characterized.

Animals↗

PubMed2003

Increased brain levels of F2-isoprostane are an early marker of behavioral sequels in a rat model of global perinatal asphyxia.

Perinatal asphyxia is a major cause of immediate and postponed brain damage in the newborn. It may be responsible for several delayed neurologic disorders and, in this respect, early markers of brain injury would be relevant for therapeutic intervention as well as for identification of infants at high risk for developmental disabilities. Biochemical measurements (brain F2-isoprostane levels) and behavioral tests (ultrasonic vocalization pattern on postnatal days (pnd) 5, 8, and 11, spontaneous motor behaviors on pnd 7 and 12, and homing response on pnd 10) were performed in a rat model of global perinatal asphyxia in the immature neonate. Caesarean section was performed in rats and the pups, still in uterus horns, were placed into a water bath at 37 degrees C for either 10 or 20 min. Caesarean delivered pups were used as controls. Pups experiencing severe (20 min), in contrast to those undergoing the 10 min, asphyctic insult presented with detectable abnormalities including early (two hours after the insult) increase in brain F2-isoprostane (a direct marker of oxidative injury) without detectable changes in PGE2, COX-2 and iNOS levels, and delayed physical (reduced weight gain on pnd 5 and thereafter) and behavioral disturbances (alterations in ultrasound emission on pnd 11 and spontaneous motricity levels mainly). These findings suggest that increased brain F2-isoprostane levels shortly after the asphyctic insult are predictive of delayed behavioral disturbances in the newborn rat. The present 20-min asphyxia model might serve for the assessment of preventive and curative strategies to treat neurologic/behavioral disturbances associated with perinatal asphyxia.

Animals↗

PubMed1999

Comparison between creatine kinase brain isoenzyme (CKBB) activity and Sarnat score for prediction of adverse outcome following perinatal asphyxia.

AIM: To assess whether plasma creatine kinase brain isoenzyme (CKBB) levels or Sarnat scores are more accurate for prediction of poor neurological outcome in babies with suspected birth asphyxia. METHODS: In a retrospective study of 97 babies CKBB levels were compared to the presence of severe hypoxic ischaemic encephalopathy (HIE) as a predictive test for these outcomes: developmental delay, cerebral palsy, visual problems, deafness or death from perinatal asphyxia. The tests were compared using positive predictive values (PPV) and likelihood ratios (LR) with confidence intervals (CI). RESULTS: 3 babies had died from perinatal asphyxia and 14 survivors were found to have neurological or developmental problems. CKBB was elevated in babies with severe HIE (p = 0.0004). A receiver operator characteristic (ROC) curve showed the optimal discriminating value for CKBB to be 21 IU/L but the CKBB was a poor predictive test. For prediction of adverse outcome: CKBB > 21 sensitivity 76%, specificity 40%, PPV 21% and LR 1.3 (95% CI 0.8-1.7). Severe HIE sensitivity 53%, specificity 95%, PPV 69% and LR 10.6 (95% CI 3.8-29.2). CONCLUSION: CKBB is elevated following birth asphyxia but is a poor predictor of adverse neurological outcome.

Asphyxia Neonatorum↗

PubMed2000

Changes in fetal plasma adenosine and xanthine concentrations during fetal asphyxia with maternal oxygen administration in ewes.

In this study, we measured fetal plasma adenosine and xanthine concentrations during and after severe asphyxia, and investigated the key issues related to oxygen therapy. Asphyxia was induced by occluding the umbilical cord for 5 minutes in 6 fetal sheep with and without the administration of oxygen to the ewe. Plasma adenosine concentration increased significantly during cord occlusion in the all fetuses, and the differences between the values in the fetuses with and without maternal oxygen administration was not significant. By 30 minutes after cord release, plasma adenosine concentration in all fetuses had returned to levels similar to those at the start of the experiment. Plasma xanthine concentration also increased during cord occlusion in all fetuses. However, 30 minutes after cord release, plasma xanthine concentration had decreased significantly in fetuses without additional oxygen, while it did not change significantly in fetuses with maternal oxygen administration. Thus, we speculated that maternal oxygen administration before fetal asphyxia may not contribute to additional ATP stores in fetal organs and may produce oxygen free radicals following asphyxia.

Adenosine↗

PubMed2001

Perinatal asphyxia: a clinical review, including research with brain hypothermia.

Perinatal asphyxia may occur in utero, during labor and delivery, or in the postnatal period. There are numerous causes, and the clinical manifestations vary. Infants who experience mild asphyxia may show no neurologic injury. Severe asphyxia may be fatal in utero, or immediately after birth, with survivors showing extensive neurologic sequelae, with or without cognitive deficits. Mild brain hypothermia appears promising in the prevention of further neurologic damage in encephalopathic infants following asphyxia. Recent research on newborn animal models has focused on the timing, duration, and depth of hypothermia. Promising new research is now under way in nurseries in the U.S. in an attempt to establish clinical protocols for use of hypothermia in human neonates.

Animals↗

PubMed1991

Response of the endolymphatic sac d.c. potential to asphyxia.

The effect of asphyxia on the endolymphatic sac d.c. potential (ESP) was examined in the guinea pig. Asphyxia was caused for 1.5 min by stopping the respirator. The ESP decreased in amplitude during asphyxia. After the termination of asphyxia the ESP showed a diphasic recovery pattern. When respiration was resumed, the ESP decreased again following a transient recovery. Thereafter, the ESP showed a gradual recovery. beta-blocker (propranolol) inhibited a temporary decrease in the ESP after the resumption of respiration, but not alpha-blocker (phentolamine). The result indicates that the ESP decrease after the resumption of respiration is induced by beta-adrenergic action.

Action Potentials↗

PubMed1994

Consequences of perinatal asphyxia.

Perinatal asphyxia occurs in 3-9 of every 1,000 births. The risk for perinatal asphyxia is present in every pregnancy. When asphyxia is diagnosed in a newborn, the effects on the infant are potentially life-threatening. Management of the asphyxia focuses on initial stabilization and support based on identified organ system dysfunction as well as support for the infant's family. Long-term outcome for the asphyxiated infant is related to the degree, duration, and resolution of organ system dysfunction.

Asphyxia Neonatorum↗

PubMed2000

Traumatic asphyxia complicated by unwitnessed cardiac arrest.

We report a case of traumatic asphyxia complicated by unwitnessed cardiac arrest in which the patient has made a good, functional recovery. Traumatic asphyxia is an uncommon clinical syndrome usually occurring after chest compression. Associated physical findings include subconjunctival hemorrhage and purple-blue neck and face discoloration. These facial changes can mimic those seen with massive closed head injury; however, cerebral injury after traumatic asphyxia usually occurs due to cerebral hypoxia. When such features are observed, the diagnosis of traumatic asphyxia should be considered. Prompt treatment with attention to the reestablishment of oxygenation and perfusion may result in good outcomes.

Adult↗

PubMedDate not supplied

Endotoxemia severely affects circulation during normoxia and asphyxia in immature fetal sheep.

OBJECTIVE: The purpose of the present study was to determine whether endotoxins (lipopolysaccharides, LPS) affect the fetal cardiovascular system in a way likely to cause brain damage. METHODS: Thirteen fetal sheep were chronically instrumented at a mean gestational age of 107 +/- 1 days. After control measurements of organ blood flow (microsphere method), blood gases, and acid base balance were obtained, seven of 13 fetuses received LPS (53 +/- 3 microg/kg fetal weight) intravenously. Sixty minutes later, asphyxia was induced by occlusion of the maternal aorta for 2 minutes. Measurements of organ blood flows were made at -60, -1, +2, +4, +30, and +60 minutes. RESULTS: Unlike in the control group, after LPS infusion there was a significant decrease in arterial oxygen saturation (-46%; P <.001) and pH (P <.001). In LPS-treated fetuses the portion of combined ventricular output directed to the placenta decreased significantly (-76%; P <.001), whereas output to the fetal body (+60%; P <.001), heart (+167%; P <.05), and adrenals (+229%; P <.01) increased. Furthermore, during asphyxia circulatory centralization was impaired considerably in LPS-treated fetuses, and there was clear evidence of circulatory decentralization. This decentralization caused a severe decrease in cerebral oxygen delivery by 70%. Within 30 minutes after induction of asphyxia five of seven LPS-treated fetuses died, whereas all control fetuses recovered completely. CONCLUSIONS: Endotoxemia severely impaired fetal cardiovascular control during normoxia and asphyxia, resulting in a considerable decrease in cerebral oxygen delivery. These effects might have important effects in the development of fetal brain damage associated with intrauterine infection.

Animals↗

PubMedDate not supplied

[Cognitive deficit in perinatal asphyxia].

INTRODUCTION: During the period 1950 1970 the relation between perinatal asphyxia and cognitive alterations was studied. More recently the neuropsychological approach has been introduced to detect more subtle defects. DEVELOPMENT: With regard to intelligence, alterations in the intelligence quotient resulting from anoxia are more commonly seen in young children than in adolescents, probably because of compensation mechanisms. It is widely accepted that severe asphyxia causes motor and cognitive alterations and leads to cerebral palsy, epilepsy and intellectual retardation. The effects of mild or moderate asphyxia are still controversial. CONCLUSION: Thorough neuropsychological examination, particularly assessment of memory and frontal function, helps to identify subtle deficits which may explain some learning problems observed in children who have a history of moderate asphyxia but previously no clear neurological diagnosis.

Animals↗