Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Asphyxia”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed2000

Myelination deficits in brain of rats following perinatal asphyxia.

Perinatal asphyxia remains a major cause of acute mortality and of permanent neurodevelopmental disability in infants and children. However, the pathophysiologic features of hypoxic-ischemic encephalopathy are still incompletely understood. Animal studies have been focussing on grey matter pathology but information on white matter lesions is limited. The aim of the study was to investigate white matter lesions after three months following graded perinatal asphyxia in the rat using a well-documented, reproducible, clinically relevant and simple animal model of perinatal asphyxia. Brains of rat pups (n=10 per group) exposed to asphyctic periods of 10 and 20 minutes were examined histologically and compared to normoxic brain using Kluever-Barrera myelin staining, immunohistochemically with antibodies against myelin basic protein, 2',3'-cyclic-nucleotide'-phosphodiesterase as markers for myelination, antibodies against neurofilaments for the evaluation of axonal density and antibodies against glial fibrillary acidic protein as a marker for astrocytic gliosis. Morphometry three months after perinatal asphyxia showed significant reduction of corpus callosum in asphyctic brains. Patchy myelination deficits were found in hippocampal fimbriae and cerebellum, lobulus L 8, accompanied by reduced axonal density. Hypothalamus and striatum did not show any myelination deficit. Up to now only short term effects of perinatal asphyxia on myelination have been reported and this communication reveals long-term myelination deficit in three brain regions after three months following perinatal asphyxia. As myelination deficit was regularly accompanied by reduction of neurofilament immunoreactivity, we suggest that white matter lesions are paralleling grey matter damage, a subject still controversial in pathophysiology of brain damage in perinatal asphyxia.

Animals↗
PubMed1998

Ventilatory response to asphyxia in conscious rats: effect of ambient and body temperatures.

In many mammals the ventilatory response to hypoxia depends on ambient temperature (Ta), largely because of the hypometabolic effects of hypoxia below thermoneutrality. We questioned whether the ventilatory response to asphyxia also depends upon Ta, and the role played by metabolism and body temperature (Tb). Oxygen consumption (VO2) and pulmonary ventilation (VE) were measured in conscious rats at Ta = 27 degrees C (warm) and 11 degrees C (cold), breathing air or two levels of asphyxic gases, moderate (10% O2-4% CO2), or severe (10% O2-8% CO2), for approximately 30 min each. In the cold, the pattern of the VE response to moderate asphyxia was qualitatively similar to that seen in hypoxia alone, i.e the attained VE/VO2 was similar in warm and cold conditions, with, in the latter, a major drop in VO2 and little or no hyperpnea. During severe asphyxia, however, the VE/VO2 attained in the cold was less than in the warm, and it was accompanied by a large drop in Tb (approximately 6 degrees C). Blood gases confirmed the lower asphyxic hyperventilation in the cold. By maintaining Tb at 38 degrees C with an implanted abdominal heat exchanger, the VE/VO2 levels attained during asphyxia were the same between cold and warm conditions. We conclude that (a) the VE response to asphyxia is Ta-dependent, largely because of the hypometabolic effect of the hypoxic component in the cold, (b) during moderate asphyxia the hypercapnic component is qualitatively unimportant, and (c) with severe asphyxia the hypercapnia becomes an important contributor to the Ta-sensitivity by aggravating the decrease in Tb in the cold and lowering VE sensitivity.

Animals↗
PubMed1997

Perinatal asphyxia-induced changes in rat brain tyrosine hydroxylase-immunoreactive cell body number: effects of nicotine treatment.

Perinatal asphyxia (15-22 min) was induced to male Sprague-Dawley rat pups during the last day of gestation and the surviving pups were sacrificed at 4 weeks of age. Brain sections were stained for tyrosine hydroxylase immunoreactivity and Cresyl violet. With increasing duration of perinatal asphyxia a reduction in the number of tyrosine hydroxylase immunoreactive (TH-IR) nerve cell bodies was found in the locus ceruleus, probably reflecting an increased death of noradrenaline nerve cell bodies. In contrast, perinatal asphyxia (15-20 min) resulted in an increased number of TH-IR nerve cell bodies in the A9 (zona compacta of the substantia nigra) and the A10 (ventral tegmental area) regions of the mesencephalon, probably reflecting an increased survival of dopamine nerve cell bodies. Perinatal asphyxia for longer than 20 min periods reduced the number of TH-IR cell bodies in the 4 week old rat, even below those found in control animals, indicating that when asphyxia is induced for a period leading to almost 100% mortality, a long-term reduction of the number of mesencephalic dopamine neurons is produced. It has previously been shown that a 4 week postnatal nicotine (0.2 micromol/kg per h) treatment counteracts the asphyxia-induced increase in TH-IR cell body number in the substantia nigra and ventral tegmental area. Such nicotine treatment did not influence the reduction in TH-IR cell bodies in the locus ceruleus following 15-20 min of perinatal asphyxia.

Animals↗
PubMed1999

Cerebrospinal nerve growth factor--a marker of asphyxia?

Asphyxia in neonates is characterized by different degrees of hypoxia-ischemia, with the outcome depending on the severity of the underlying brain cell damage. Neurotrophic factors rescue neurons from cell death after injury and promote neuronal survival during development. The authors have used enzyme-linked immunosorbent assay to study levels of nerve growth factor in the cerebrospinal fluid of children with asphyxia at birth (n = 10) and of controls (n = 23). Compared with reference groups the children who had had severe asphyxia had lower or negligible levels of cerebrospinal fluid nerve growth factor in the neonatal period or later. The level of cerebrospinal fluid nerve growth factor measured in the neonatal period was 3.76+/-4.13 pg/mL in children with asphyxia (n = 8), which is significantly lower than in children without asphyxia or infection (n = 10) 9.42+/-4.09 pg/mL or in those without asphyxia but with infection (n = 13) 17.63+/-11.48 pg/mL (P = 0.0186 and P = 0.0013, respectively). However, in some children with asphyxia the cerebrospinal fluid nerve growth factor levels were virtually normal, and most importantly these children subsequently had normal neurologic development. These results suggest that cerebrospinal fluid nerve growth factor might be used as a biochemical marker for early estimates of hypoxic-ischemic brain damage in asphyxiated neonates.

Adolescent↗
PubMed1994

Asphyxia-related infant mortality rates.

We present an epidemiological study of asphyxia-related infant mortality. Via linkage of birth and death certificates, infant mortality data were analyzed for all infants born in Israel from 1985 through 1988. During this period, there were 397,083 live births in Israel, and 4392 infants subsequently died within the first year of life (total infant death rate of 11.1/1000 live births). Of the deaths, 176 (4.0%) were associated with a diagnosis of perinatal asphyxia, resulting in an overall asphyxia-related infant mortality rate of 0.44/1000 live births. The percent of deaths attributable to asphyxia was calculated by birthweight, maternal age, and birth order and was compared with overall infant mortality rates analyzed for the same variables. Interesting results include the following: (1) Asphyxia-related mortality within the low birthweight group was proportional to overall birthweight-specific mortality for that group; (2) birthweight more than 4.5 kg disproportionately increased the risk of asphyxia-related mortality; and (3) perinatal asphyxia did not add to the risk of mortality subsequent to teenage pregnancy.

Adolescent↗
PubMed2003

Positional asphyxia: reflection on 2 cases.

Positional asphyxia, a fatal condition arising because of the adoption of particular body positions, causing mechanical interference with pulmonary ventilation, can occur in various circumstances that are likely to come under the observation of the specialist in legal medicine (work, car accidents, torture, kidnapping, etc.). It is difficult to diagnose the cause of death in such cases because they generally present with an aspecific anatomopathologic picture. In some situations, positional asphyxia can be hard to distinguish from asphyxia because of chest compression. The main difference is in the way the event occurred: whether the particular position causing the asphyxia had been adopted by choice or by compulsion or necessity when an extrinsic mechanical action would result in traumatic asphyxia. The diagnosis of positional asphyxia is essentially based on 3 criteria: the body position must obstruct normal gas exchange, it must be impossible to move to another position, and other causes of natural or violent death must be excluded. To illustrate the main physiopathologic and diagnostic causes of positional asphyxia, the authors report 2 cases taken from the records of events that came under the observation of the Medico-Legal Sector of Bari University Hospital throughout the last 10 years.

Adult↗
PubMed1995

Birth asphyxia: incidence, clinical course and outcome in a Swedish population.

A total of 42,203 live infants were born in Göteborg in 1985-1991, and 292 term infants had Apgar scores < 7 at 5 min. Infants with congenital malformations, infections and opioid-induced respiratory depression were excluded and thus 227 infants were included in the birth asphyxia group, which formed the basis of this retrospective study. Clinical signs of mild, moderate or severe hypoxic-ischemic encephalopathy (HIE) were present in 65 infants, and in another 10 infants, sedated and on controlled ventilation, HIE was assumed but grading was not possible. The incidences of Apgar scores < 7 at 5 min, birth asphyxia and birth asphyxia with HIE were 6.9, 5.4 and 1.8 per 1,000 live born infants: 95% of infants resuscitated with bag and mask ventilation only, did well, compared with 1 of 11 in whom resuscitation included adrenaline. Seizures occurred in 27 of 227 infants, beginning in 18 infants within 12 h of birth. Small-for-gestational-age (SGA) infants were overrepresented in the birth asphyxia group but not in the birth asphyxia-HIE group. All infants with severe HIE died or developed neurological damage. Half of the infants with moderate, and all of the infants with mild, HIE were reported to be normal at 18 months of age. A total of 0.3 per 1,000 live born infants died and 0.2 per 1,000 developed a neurological disability related to birth asphyxia. The disabilities were dyskinetic (4), tetraplegic (2), spastic diplegic (2), cerebral palsy and mild neuromotor dysfunction (1). The relatively low incidences of birth asphyxia and HIE were probably due to effective antenatal care.

Apgar Score↗
PubMed1991

Sympathetic nerve modulation of regional cerebral blood flow during asphyxia in newborn piglets.

Regional cerebral blood flow (rCBF) during asphyxia suggests a reflex vasoconstrictor mechanism active principally in brain cortex. Present studies in newborn piglets investigate sympathetic modulation of the cerebrovasculature both during and after acute asphyxia. Unilateral superior cervical sympathetic ganglionectomy (SCSG) was performed in 13 newborn piglets, after which asphyxia was produced by discontinuing ventilation. In 8 animals, blood flow was measured during control and sequentially 1, 2, and 3 min after ventilation was stopped. In 5 piglets with unilateral SCSG, cortical flow decreased in the innervated hemisphere, -34 +/- 14% after 2 min, and -25 +/- 9% at 3 min of asphyxia compared with control (104 +/- 22 ml.min-1.100 g-1; mean +/- SE). In contrast, the sympathetically denervated hemisphere showed -13 +/- 17% at 2 min and +7 +/- 23% at 3 min, representing 45 +/- 6% and 30 +/- 9% left-right (L-R) flow differences, respectively. Bilateral SCSG (3 piglets) similarly attenuated the cortical CBF vasoconstrictor response to asphyxia, +6 +/- 21% at 2 min and -8 +/- 5% at 3 min. Significant innervated-denervated rCBF differences were present during asphyxia in cerebral gray (55% +/- 24), cerebral white (41% +/- 16), caudate (25% +/- 7), hippocampus (36% +/- 12), and choroid plexus (145% +/- 42), indicating sympathetic nerve modulation. Brain stem structures showed increasing rCBF throughout asphyxia and no L-R differences.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Nonimmune hydrops fetalis and activation of the renin-angiotensin system after asphyxia in preterm fetal sheep.

This study examined the hypothesis that the development of hydrops fetalis after asphyxia in the 0.6 gestation sheep fetus would be associated with activation of the fetal renin-angiotensin system (RAS). Fetuses were randomly assigned to either sham occlusion (n = 7) or to 30 min of asphyxia induced by complete umbilical cord occlusion for 30 min (n = 8). Asphyxia led to severe bradycardia and hypotension that resolved after release of occlusion. After occlusion, plasma renin concentration was significantly increased in the asphyxia group compared with controls (P < 0.005) after 3 min (16.3 +/- 5.3 vs. 4.1 +/- 1.3 ng. ml(-1). h(-1)), and 72 h (30.6 +/- 6.3 vs. 3.7 +/- 1.2 ng. ml(-1). h(-1)). Renal renin concentrations and mRNA levels were significantly greater in the asphyxia group after 72 h of recovery. All fetuses in the asphyxia group showed generalized tissue edema, ascites, and pleural effusions after 72 h of recovery. In conclusion, asphyxia in the preterm fetus caused sustained activation of the RAS, which was associated with hydrops fetalis.

Animals↗
PubMed2001

Neonatal asphyxia in rats: acute effects on cerebral kynurenine metabolism.

Two tryptophan metabolites, the anti-excitotoxic N-methyl-D-aspartate (NMDA) receptor antagonist kynurenic acid (KYNA) and the free radical generator 3-hydroxykynurenine (3-HK), have been proposed to influence neuronal viability in the mammalian brain. In rats, the brain content of both KYNA and 3-HK decreases immediately after birth, possibly to ensure normal postnatal functioning of NMDA receptors. Because complications of birth asphyxia have been suggested to be associated with anomalous NMDA receptor function, we examined the acute effects of an asphyctic insult on the brain levels of KYNA and 3-HK in neonatal rats. Asphyxia was induced in animals delivered by cesarean section on the last day of gestation, using the procedure introduced by Bjelke et al. (Brain Res 543: 1-9, 1991). KYNA and 3-HK levels were determined in the brain at seven time points between 10 min and 24 h after asphyxia. Up to 6 h, asphyxia caused 160-267% increases in KYNA levels. In the same tissues, 3-HK levels decreased (significantly at five of the seven time points), demonstrating an asphyxia-induced shift in kynurenine pathway metabolism toward the neuroprotectant KYNA. This shift might constitute the brain's attempt to counter the ill effects of birth asphyxia. Furthermore, the transient increase in the brain KYNA/3-HK ratio in these animals might be causally related to the well-documented detrimental long-term effects of asphyxia.

Animals↗
PubMed1994

Diagnosis of severe birth asphyxia and early prediction of neonatal neurological outcome in term asphyxiated newborns.

Ten indicators available during the first two hours of life, such as clinical criteria of neonatal distress and postnatal arterial blood gases, were compared with the neonatal neurological course in sixty full term newborns with significant birth asphyxia in order to test their value for the diagnosis and the short-term prognosis of severe birth asphyxia. Birth asphyxia was defined as severe when it was followed by symptoms of moderate or severe post-asphyxial encephalopathy. We calculated a sensitivity lower than fifty percent for clinical criteria such as delay in establishing regular respiration and Apgar scores. It was clear that normal delay in establishing regular respiration and normal Apgar scores do not exclude severe birth asphyxia. Arterial pH and base deficit at thirty minutes of life were found to be the best criteria for the diagnosis of severe birth asphyxia, but lacked positive predictive value. The best predictive tool for the short-term neurological prognosis of birth asphyxia was a single score established at 30 minutes of life and based on the evaluation of consciousness, respiration and neonatal reflexes. Some aspects of the pathophysiology of birth asphyxia and the rationale for treatment of post-asphyxial metabolic acidosis are discussed.

Acidosis, Lactic↗
PubMed1996

Effects of the level of asphyxia during delivery on viability at birth and early postnatal vitality of newborn pigs.

Newborn pigs (n = 117) were used to provide information on the relationships of degree of asphyxia during delivery, viability at birth, and some striking aspects of postnatal vitality including survival, interval between birth and first udder contact and between birth and first suckling, rectal temperature at 24 h of life (RT24), and growth rate over the first 10 d of life. The degree of asphyxia at birth was estimated from cord blood pCO2, pH, and lactate levels. Onset of respiration, heart rate, skin color, and attempts to stand during the first minute after birth were used to estimate the viability score. Neonatal asphyxia, i.e., decreased blood pH and increased blood pCO2 and lactate, was associated with the production of unusually high levels of catecholamines. The degree of asphyxia increased with late position in the birth order (P < .01) and was higher in piglets born posteriorly (P < 0.5). Further, the average blood pCO2 within a litter increased (P < .05) with litter size. The was an inverse relationship between the degree of asphyxia and the viability score (P < .001). Highly viable piglets reached the udder more rapidly (P < .001) and had a higher RT24 (P < .001) than those of low viability. Plasma glucose concentrations increased with blood pCO2 and plasma epinephrine concentrations (P < .001). Neonatal asphyxia reduced postnatal vitality by delaying the first contact with the udder (P < .03) and was associated with a lower RT24 (P < .05), growth rate (P < .001), and survival over 10 d (P < 0.06). These variables, i.e., interval between birth and first udder contact, RT24, and growth rate, were correlated with birth weight (P < .001); RT24 was also shown to decrease (P < .001) with the time taken to reach the udder. Overall, results suggest that piglet suffering from asphyxia during delivery are less viable at birth and less prone to adapt to extrauterine life.

Animals↗
PubMed1986

Similarities between lethal asphyxia in postneonatal rats and the terminal episode in SIDS.

The age-related decrease in asphyxia tolerance was examined in young rats under conditions that mimic prolonged apnea. A precise end point of asphyxia tolerance was determined by calculation of LD50 values for exposed groups. Daily exposure to episodes of sublethal asphyxia did not alter the age-related decrease in asphyxia tolerance. These results permitted further studies in which groups of 10-day-old rats were exposed to 10 min of asphyxia resulting in partial mortality of the group. The postmortem findings in these animals were compared to figures for unexposed littermates. The age-related changes in response to asphyxia and the postmortem findings in asphyxiated animals were compared to the age distribution of sudden infant death syndrome (SIDS) and the postmortem findings in these infants. The comparison showed that the terminal event in SIDS shares many features with lethal asphyxia.

Age Factors↗
PubMedDate not supplied

Role of asphyxia and feeding in a neonatal rat model of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a common gastrointestinal disorder affecting premature infants. To investigate critically the importance of the purported risk factors of NEC (formula feeding, asphyxia, bacteria, and prematurity), we developed a neonatal rat model that closely mimics the human disease. Full-term and premature newborn rats were stressed with formula feeding, asphyxia, and/or exogenous bacterial colonization and subsequently evaluated grossly and histologically for the development of intestinal injury. We found that most animals treated with asphyxia, formula feeding, and bacteria developed NEC (77%) and died (86%) by 96 h. All maternally fed animals treated with asphyxia and bacterial colonization survived and had normal intestinal histology. Furthermore, asphyxia was a critical instigating factor, because formula and bacterial exposure without asphyxia resulted in normal intestine and minimal mortality (12%). Enteral bacterial colonization was not a significant determinant of NEC in this model. We conclude that the neonatal rat model is an excellent test system for the study of NEC. As in the human disease, asphyxia and formula feeding play an important role in the pathophysiology of experimental NEC.

Animal Nutritional Physiological Phenomena↗
PubMed2003

Antenatal and intrapartum risk factors for birth asphyxia among emergency obstetric referrals in Mulago Hospital, Kampala, Uganda.

BACKGROUND: Many perinatal deaths follow birth asphyxia that occurs in newborn babies of women who are referred on developing life-threatening obstetric complications. OBJECTIVE: To determine the antenatal and intrapartum risk factors for severe birth asphyxia among babies delivered by women admitted as emergency obstetric referrals. DESIGN: Case-control study. SETTING: Mulago hospital, the National Referral Hospital, Kampala, Uganda. SUBJECTS: Cases were newborn term babies (and their mothers) with a 5-minute Apgar score 4 or less (birth asphyxia). Controls were term newborn babies with a 5-minute Apgar score more than 4. MAIN OUTCOME MEASURES: Antepartum and intrapartum risk factors among newborn babies (and their mothers) from socio-demographic characteristics, obstetric complications or labour management. The Odds ratios (OR) for various outcomes were calculated using the Statistical Assistance Software (SAS) version 6.2 (Windows), and are presented with their 95% confidence intervals (C1) and p-values. RESULTS: There was no association between socio-demographic factors and birth asphyxia. Antepartum hospitalization, antepartum or intrapartum anaemia, antepartum hemorrhage and severe pre-eclampsia/eclampsia were significantly associated with birth asphyxia; the respective ORs and 95% C1 were 1.73 (1.09-2.75), 5.65 (3.36-9.50), 2.12 (1.11-4.05) and 10.62 (2.92-38.47). Augmentation of labour with oxytocin, premature rupture of membranes, meconium staining of liquor amnii, vacuum extraction, caesarean section, low birth weight and mal-presentations were significantly associated with birth asphyxia with ORs of 5.76 (2.20-15.05), 2.23 (1.31 -3.37), 6.40 (2.76-14.82), 2.16 (1.28-3.67), 2.36 (1.07-5.20) and 6.32 (3.57-11.20) respectively. CONCLUSIONS: Early recognition of these complications among emergency obstetric referrals, followed by prompt and appropriate management, may reduce the perinatal deaths from birth asphyxia.

Apgar Score↗
PubMed1999

Cerebral hemodynamic measurements in acute versus chronic asphyxia.

In most reports of asphyxia in newborn infants, the occurrence, duration, frequency of episodes, or severity of the asphyxic insult is usually not known, and yet abnormal neurologic outcomes have been observed. The fetus has several innate characteristics that allow compensatory response to lack of oxygen over a reasonable duration of time; however, these inherent capabilities differ among individuals. Therefore, for a given asphyxic insult, the aftermath may be intact survival, some neurologic sequelae, or death. In an asphyxiated infant, an abnormal cerebral blood velocity flow pattern, especially if consistent with vasoparalysis, probably signals that an asphyxic or ischemic neuronal insult has occurred; the integrity of the neurons and their function are dependent on an appropriate uptake of oxygen and nutrients in the presence of adequate perfusion. Hemodynamic changes associated with acute asphyxia are different from those observed in chronic asphyxia. Based on information from experimental studies, less severe but prolonged asphyxia is associated with severer brain injury than when an insult is brief but severe. Thus, when asphyxia or ischemia is suspected based on obstetric monitoring, the fetus should be delivered under appropriate optimal conditions and resuscitative measures initiated if indicated. If all of ACOG's criteria for defining asphyxia are met, it could be assumed that a severe acute asphyxic insult or a repetitive insult has occurred. In cases where the only findings are abnormally low Apgar score and pH, the insult is most probably acute and brief. Thus, survival is likely not associated with any neurologic abnormality. With a likelihood that asphyxia has occurred, available therapeutic intervention should be initiated early, in the first 48 to 72 hours of life, without waiting for neurologic complications or multiorgan system failure to develop.

Acute Disease↗
PubMed2000

[Birth asphyxia as a cause of cerebral palsy].

Birth asphyxia is O2i CO2 exchange disorder during the labour, with consequent hypoxia and ischemia. The term "asphyxia" has been used unprecisely quite often. The most frequently used criteria for birth asphyxia have been: fetal bradycardia, meconium stained amniotic fluid, fetal acido-base status with umbilical artery pH value below 7.10, low Apgar score and need for endotracheal intubation. The correct Apgar score quantification depends on the examiner. Fetal acido-base status measured in umbilical artery could be useful biochemical parameter of birth asphyxia. Only if the fetal oxygen supply during the labour is severe and long enough disturbed, the neurological abnormalities will develop later. Our study has enrolled 70 children with various degree of motor impairment, detected during neonatal period and/or infancy. They have been followed up till 24 months chronological age for term neonates and 24 months corrected age for prematures. 34 children out of them have developed clear clinical signs of cerebral palsy. Birth asphyxia as a possible cause of cerebral palsy has been documented in 10 cases, e.g. 29.4%. The criteria for birth asphyxia have been low Apgar score, meconium stained amniotic fluid and clinical signs of hypoxic-ischemic encephalopathy. Fetal blood gas and acido-base measurements obtained from umbilical artery at delivery have been an important parameter of intrapartal asphyxia. Those measurements should be introduced as a routine method in our practice, in the cases of fetal heart deceleration, to asses the extent of fetal acidosis.

Asphyxia Neonatorum↗
PubMed2003

[Change in the level of inflammatory cytokines and their relationship to the indicator in evaluating renal tubules injury of urinary in neonates with asphyxia].

OBJECTIVE: To explore the relationship between amount of inflammatory cytokines in urine and neonatal postasphyxia renal tubules injury. METHODS: The level of inflammatory cytokines such as interleukin (IL-8, IL-6), tumor necrosis factor-alpha (TNF-alpha) and the indicators of evaluating renal tubules injury [N-acetyl-glucosaminidase(NAG), gamma-glutamyltranspeptidase (gamma-GT), beta(2)-microglobulin (beta(2)-MG)] in urine were detected in neonates with asphyxia. RESULTS: Compared with control, the levels of IL-8, IL-6, TNF-alpha and NAG, gamma-GT, beta2-MG were obviously increased in mild asphyxia group. In severe asphyxia group, the parameters above were all significantly increased compared with mild asphyxia group and the control group. Within the asphyxia group, there were positive relationship between inflammatory cytokines and the indicator of evaluating renal tubules injury. CONCLUSION: The asphyxia may induce systemic inflammatory response syndrome (SIRS), which result in postasphyxia renal injury in neonates. The level of inflammatory cytokines in urine may be used as the indicators of evaluating the severity of asphyxia and postasphyxia renal injury in neonates.

Acetylglucosaminidase↗