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 199 records · Page 11Linked to original sources
PubMed2006

Nitrotyrosine in brain tissue of neonates after perinatal asphyxia.

HYPOTHESIS: Nitrotyrosine, a reaction product of peroxynitrite and proteins, could be demonstrated in the postmortem examination of brain tissue of full-term neonates who had severe perinatal asphyxia. METHODS: The brain tissue of 22 full-term neonates who died after severe perinatal asphyxia was examined, including cerebral cortex, basal ganglia, thalamus, hippocampus, brain stem, olives and cerebellum. Median age at death was 52 h. Routine histopathological examination and additional immunohistological staining were carried out with anti-cysteine protease protein 32 antibodies to detect activated caspase 3, anti-nitrotyrosine antibodies to detect nitrotyrosine and anti-CD68 antibodies to detect activated microglia and macrophages, which might be associated with the production of nitric oxide. Staining was scored as none, weak (1-25% positive cells), moderate (26-75% positive cells) or severe (>75% positive cells). RESULTS: 14 patients showed global injury, 4 showed injury of the basal ganglia and thalamus, and 4 showed predominantly parasagittal brain injury. One neonate without perinatal asphyxia served as a control. Nitrotyrosine staining of neurones was shown in all neonates with asphyxia, mostly in the thalamus (70%) and inferior olives (68%). Total nitrotyrosine staining tended to be less in the base of the pons and inferior olives of neonates with parasagittal brain injury. Activated caspase 3 was found mostly in the thalamus (60%) and hippocampus (53%). Positive CD68 staining was mainly present in the thalamus (70% positive). CONCLUSION: Nitrotyrosine was found in brain tissue of full-term neonates, suggesting that nitric oxide toxicity might have a role in hypoxic-ischaemic brain injury at term. This may be relevant for neuroprotective strategies in full-term neonates with perinatal asphyxia.

Antigens, CD↗
PubMed1997

Indices of renal tubular function in perinatal asphyxia.

AIMS: To determine and compare two urinary indices of renal tubular function, N-acetyl-glucosaminidase (NAG) and beta 2-microglobulin (beta 2 M), in healthy term neonates and babies with perinatal asphyxia. METHODS: In a prospective case-control study using asphyxiated (n = 35) and normal control (n = 55) infants, urinary NAG and beta 2 M were assayed at 24-48 hours of life, 4-6 days, and 4-6 weeks. RESULTS: NAG and beta 2 M were significantly increased at 24-48 hours and 4-6 days in the asphyxiated infants compared with the controls. Increased NAG values reflect the degree of perinatal asphyxia more than do beta 2 M. Gentamicin also increased NAG excretion, but to a lesser extent than did perinatal asphyxia. CONCLUSIONS: NAG (+/- beta 2 M) may be a useful marker of perinatal asphyxia. Urinary NAG concentrations correlate with the severity of perinatal asphyxia.

Acetylglucosaminidase↗
PubMed1990

Role of prostanoids in cerebrovascular responses to asphyxia and reventilation in newborn pigs.

Cerebral hemodynamics during asphyxia and reventilation were investigated in normothermic, hypothermic (35 degrees C), and indomethacin-pretreated (5 mg/kg iv) anesthetized, newborn pigs. In the normothermic group, total cerebral blood flow (CBF) measured with radioactive microspheres was 57 +/- 12 ml.min-1 x 100 g-1 during baseline, 104 +/- 19 at 1 min of asphyxia, 39 +/- 5 at 5 min of asphyxia, 186 +/- 16 at 8 min of reventilation, and 95 +/- 20 at 16 min of reventilation. During asphyxia and reventilation blood flow to brain stem was better regulated than to cerebrum or cerebellum. Baseline CBF was similar in the indomethacin and hypothermic groups (32 +/- 2 and 41 +/- 5 ml.min-1 x 100 g-1, respectively; n = 5 for each group). However, during asphyxia, blood flow was never less in either one of these groups than in the normothermic group in spite of a lack of arterial hypercapnia at 1 min in the hypothermia group. During reventilation, blood flow was sometimes lower in the hypothermic and indomethacin groups than the normothermic group but never lower when considered on a percentage change from baseline basis. We conclude that inhibition of prostanoid production with indomethacin did not limit vasodilation during these conditions.

Animals↗
PubMed1980

Cerebral energy metabolism in mallard ducks during apneic asphyxia: the role of oxygen conservation.

Cerebral energy metabolism during apneic asphyxia was studied in ducks. Fluctuations in the reduced form of respiratory chain nicotinamide adenine dinucleotide (NADH) were monitored from the left cerebral hemisphere and used as an indicator of mitochondrial hypoxia. Electroencephalogram (EEG) and surface PO2 were recorded from the right hemisphere. Forced dives of 4- to 7-min duration on restrained ducks were characterized by bradycardia and an accumulation of NADH, which increased throughout the diving period. NADH returned to the preasphyxic level when breathing was resumed. In later experiments, asphyxia was produced by stopping artificial ventilation in paralyzed ducks. Asphyxia produced by this means caused similar changes in the measured variables (heart rate, blood pressure, and NADH fluorescence) to those obtained in forced submergence of nonparalyzed ducks. The inhibition of cardiovascular adjustments by atropine caused NADH to increase faster and tissue PO2 to decrease faster during apneic asphyxia than in nonatropinized ducks. We conclude that the oxygen-conserving cardiovascular adjustments play a key role in the increased cerebral tolerance to apneic asphyxia in ducks.

Animals↗
PubMed1993

Amiloride blocks the inhibition of fetal lung liquid secretion caused by AVP but not by asphyxia.

We have examined whether the activation of Na+ channels, located on the luminal surface of pulmonary epithelial cells, mediates the inhibitory effects of both arginine vasopressin (AVP) and moderate asphyxia on fetal lung liquid secretion. Lung liquid secretion rates were measured in chronically catheterized fetal sheep during AVP infusions and during periods of asphyxia with and without an Na+ transport blocker (amiloride; 10(-4) M) present in lung liquid. Lung liquid secretion rates were also measured during epinephrine infusions with amiloride present in lung liquid. These secretion rates were compared with measurements made during a preceding control period. Both asphyxia and an infusion of AVP significantly reduced the rate of secretion of fetal lung liquid from 8.4 +/- 1.5 and 18.0 +/- 3.7 to 3.6 +/- 1.0 (P < 0.01) and 5.5 +/- 2.1 ml/h (P < 0.01), respectively. The addition of amiloride to lung liquid did not reverse the inhibitory effects of asphyxia on lung liquid secretion (8.6 +/- 0.8 vs. 0.7 +/- 0.4 ml/h) but did block the inhibitory effects of both epinephrine (14.8 +/- 4.4 vs. 13.8 +/- 3.1 ml/h) and AVP (18.0 +/- 3.7 vs. 19.5 +/- 5.0 ml/h). The addition of amiloride to lung liquid during fetal normoxia did not significantly affect fetal lung liquid secretion rates (8.2 +/- 1.1 vs. 7.4 +/- 0.7 ml/h). We conclude that the inhibitory effect of AVP on fetal lung liquid secretion, like that of epinephrine, involves the activation of luminal surface Na+ channels, whereas the inhibitory effect of asphyxia does not.

Amiloride↗
PubMed1975

Fetal asphyxia due to umbilical cord compression. Metabolic and brain pathologic consequences.

Term monkey fetus 1620 sustained 50 min of rapidly developing severe asphyxia which began immediately after its in utero version. The arterial blood pO2 decreased from a normal value of 34 to 11-12 mm Hg while the blood pH fell from 7.35 to 6.70. During this asphyxia, hemoglobin-oxygen saturations below 5% were recorded. The complete collapse of the umbilical circulation several minutes prior to the reoxygenation of the fetus added an episode of total asphyxia. With reoxygenation following delivery, fetal cardiovascular performance improved rapidly though over an hour was required for recovery from the severe acidosis. The animal prospered but was found moribund on the 13th postnatal day due to dehydration. Brain examination after euthanasia revealed severe paracentral cortical and basal ganglia damage. Damage also appeared symmetrically in nuclei in the lower brain stem and in thalamus. These three zones of injury are attributed to the partial, the partial combined with the total, and the total asphyxia, respectively. The present case makes clear that compression of the umbilical cord may cause damage of a variety of types depending on the severity and duration of the asphyxia induced. It also demonstrates the possibility of recovery from a systemic acidosis where the pH values have fallen to levels below 6.70 for up to an hour.

Animals↗
PubMed1992

Role of excitatory amino acid antagonists in the management of birth asphyxia.

Birth asphyxia is an important cause of permanent neuro-developmental disability. Asphyxia sets in course a progression of intracellular events which culminates in neuronal death, and this process may take up to 48 h to complete. Entry of calcium into the neurone appears to be the key to the cell death, and it is known that during asphyxia, excessive glutamate is released which stimulates the voltage-dependent N-methyl-D-aspartate (NMDA) receptor to open with an accumulation of excess intracellular calcium. MK-801 is a very effective NMDA receptor antagonist, and it has been shown that this drug prevents or significantly reduces the extent of cortical neurone infarction following experimental asphyxia in 7-day-old rat pups. Unfortunately, MK-801 is toxic to the pup, but newer NMDA receptor antagonists may offer the opportunity for neuroprotection in the human infant who has suffered severe birth asphyxia.

Amino Acids↗
PubMed2003

Key neuroprotective role for endogenous adenosine A1 receptor activation during asphyxia in the fetal sheep.

BACKGROUND AND PURPOSE: The fetus is well known to be able to survive prolonged exposure to asphyxia with minimal injury compared with older animals. We and others have observed a rapid suppression of EEG intensity with the onset of asphyxia, suggesting active inhibition that may be a major neuroprotective adaptation to asphyxia. Adenosine is a key regulator of cerebral metabolism in the fetus. METHODS: We therefore tested the hypothesis that infusion of the specific adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), given before 10 minutes of profound asphyxia in near-term fetal sheep, would prevent neural inhibition and lead to increased brain damage. RESULTS: DPCPX treatment was associated with a transient rise and delayed fall in EEG activity in response to cord occlusion (n=8) in contrast with a rapid and sustained suppression of EEG activity in controls (n=8). DPCPX was also associated with an earlier and greater increase in cortical impedance, reflecting earlier onset of primary cytotoxic edema, and a significantly smaller reduction in calculated cortical heat production after the start of cord occlusion. After reperfusion, DPCPX-treated fetuses but not controls developed delayed onset of seizures, which continued for 24 hours, and sustained greater selective hippocampal, striatal, and parasagittal neuronal loss after 72-hour recovery. CONCLUSIONS: These data support the hypothesis that endogenous activation of the adenosine A1 receptor during severe asphyxia mediates the initial suppression of neural activity and is an important mechanism that protects the fetal brain.

Animals↗
PubMed1989

Mitochondrial function after asphyxia in newborn lambs.

We examined mitochondrial oxidative function 5 minutes and 2 hours after a gradual asphyxial insult in newborn lambs. We subjected 16 ventilated newborn lambs to 75-90 minutes of hypoxia and hypercarbia that resulted in bradycardia and systemic hypotension over the final 15 minutes of the insult. At the end of asphyxia, the lambs were resuscitated and returned to control ventilator settings. Samples of brain were removed 5 minutes (n = 8) and 2 hours (n = 8) after asphyxia. Each group of eight lambs was subdivided into those less than 3 or greater than 3 days old to evaluate the effect of age on postasphyxia mitochondrial function. After classification into nonsynaptic and synaptic mitochondria, mitochondrial respiration (oxygen consumption) was measured using five different substrates. Data from asphyxiated lambs were compared with that from a control group of ventilated nonasphyxiated lambs (n = 8). In the lambs less than 3 days old, there was significant depression of mean +/- SEM nonsynaptic mitochondrial state 3 (adenosine diphosphate-dependent) respiration to 29.5 +/- 5.2% of control with four of the five substrates and of state 4 respiration to 33.7 +/- 0.9% of control with three of the five substrates 5 minutes after asphyxia. By 2 hours after asphyxia, mean +/- SEM nonsynaptic mitochondria state 3 respiration increased to 70.4 +/- 6.4% of control while state 4 respiration increased to 58.2 +/- 4.5% of control. In contrast, lambs greater than 3 days old exhibited no inhibition of nonsynaptic mitochondrial function after asphyxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1980

The effects of acute total asphyxia and metabolic acidosis on cerebrospinal fluid bicarbonate regulation in newborn puppies.

We evaluated CSF [HCO3-] regulation in lightly anesthetized newborn puppies following: (1) acute total asphyxia; (2) metabolic acidosis; and (3) metabolic acidosis induced after acute asphyxia. Five and one-half min of total asphyxia resulted in a 4.4 mM/liter decrease in mean CSF [HCO3-]. During 65 min of recovery with mechanical ventilation mean CSF [HCO3-] increased 1.7 mM/liter. Mean plasma [HCO3-] decreased 7 mM/liter and recovered 4.5 mM/liter in the same period. We produced a stable metabolic acidosic for 4 hr using a peritoneal dialysis technique with PaCO2 maintained at the normal value. With acidosis in nonasphyxiated control puppies, CSF [HCO3-] decreased steadily. At 4 hr, the ratio, delta CSF [HCO3-]/delta plasma [HCO3-], was 0.43, a value close to that observed in adults of many species with metabolic acid-base disturbances, 0.41. With acidosis in asphyxiated puppies allowed 1 hr of recovery, the time course and mean values of plasma and CSF [HCO3-] were indistinguishable from those of the nonasphyxiated acidotic controls. Newborn puppies appear to regulate CSF [HCO3-] in response to acute asphyxia or metabolic acidosis, and acute asphyxia does not impair the puppy's ability to regulate CSF [HCO3-] in metabolic acidosis.

Acidosis↗
PubMed1988

Cord plasma vasopressin, erythropoietin, and hypoxanthine as indices of asphyxia at birth.

To assess the value of cord plasma arginine vasopressin (AVP), erythropoietin (EP), and hypoxanthine (HX) as indices of asphyxia, we studied 62 infants of mothers with preeclampsia, 34 acutely asphyxiated infants, with 5-min Apgar score less than or equal to 6 and/or umbilical arterial pH less than or equal to 7.05, and 38 control infants. Umbilical arterial AVP in the asphyxia group (geometric mean; 95% confidence interval: 180; 92-350 pg/ml) was higher than in the control group (23; 8-66, p = 0.002) and correlated with umbilical arterial pH (r = -0.447, p = 0.028). AVP levels in the preeclampsia group did not differ from controls. Cord venous EP was higher in infants delivered by elective cesarean section from women with severe preeclampsia (115; 75-177 mU/ml, p less than 0.001) than in control infants (23; 18-27); in the whole group EP correlated with pH (r = -0.493, p less than 0.001). EP in the asphyxia group was similar (46; 35-65) to controls (40; 33-47) and did not correlate with pH. Cord arterial HX in the preeclampsia group was similar to controls (12.3; 9.5-16.0 mumol/liter), but elevated in the asphyxia group (23.7; 17.6-31.8, p = 0.001), in which HX correlated with pH (r = 0.558, p = 0.008) and AVP (r = 0.588, p = 0.005). EP did not correlate with AVP or HX in any group, nor did any of the variables correlate with the Apgar score. We conclude that cord plasma AVP and HX reflect acute asphyxia, whereas EP is elevated after more prolonged hypoxia.

Apgar Score↗
PubMed1994

Effects of surgery and asphyxia on levels of nucleosides, purine bases, and lactate in cerebrospinal fluid of fetal lambs.

During severe oxygen shortage, the fetal brain resorts to anaerobic metabolism and ATP becomes catabolized. High levels of nucleosides, hypoxanthine, and xanthine (ATP catabolites) in cerebrospinal fluid (CSF) may therefore be associated with increased neonatal neurologic morbidity. In 22 fetal lambs (3 to 5 d after surgery, gestational age 123.5 +/- 3.5 d), arterial oxygen content was progressively reduced to 35% of the baseline value with a balloon occluder around the maternal common internal iliac artery. This resulted in a 1-h period of asphyxia, leading to a pH of 7.02 +/- 0.03 and a base excess of -17.0 +/- 1.0 mM. Mortality was 50%. CSF was sampled from the spinal cistern and analyzed using HPLC. During reoxygenation, hypoxanthine and xanthine may serve as substrate for xanthine oxidase with concomitant production of oxygen-derived free radicals, which may aggravate cerebral damage. The main difference between surviving and nonsurviving animals was the speed of increment of ATP catabolites in CSF: in the surviving group levels increased steadily, recovery values being significantly elevated compared with asphyxia values, whereas in the nonsurviving group the rise was rapid and levels during asphyxia did not differ significantly from levels during recovery. We conclude that 1) catheterization of the spinal cistern leads to increased levels of CSF hypoxanthine, xanthine, and inosine, and 2) during fetal asphyxia, levels of these ATP catabolites and lactate in CSF increase. 3) Maximum levels are reached during the recovery period and are similar for surviving and nonsurviving animals, but during asphyxia CSF levels of hypoxanthine and lactate were higher in the nonsurviving fetuses.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed2001

Impaired early neurologic outcome in newborn piglets reoxygenated with 100% oxygen compared with room air after pneumothorax-induced asphyxia.

Birth asphyxia is a serious problem worldwide, resulting in 1 million deaths and an equal number of neurologic sequelae annually. It is therefore important to develop new and better ways to treat asphyxia. In the present study we tested the effects of reoxygenation with room air or with 100% oxygen (O2) after experimental pneumothorax-induced asphyxia on the blood oxidative stress indicators, early neurologic outcome, and cerebral histopathology of newborn piglets. Twenty-six animals were studied in three experimental groups: 1) sham-operated animals (SHAM, n = 6), 2) animals reoxygenated with room air after pneumothorax (R21, n = 10), and 3) animals reoxygenated with 100% O2 after pneumothorax (R100, n = 10). In groups R21 and R100, asphyxia was induced under anesthesia with bilateral intrapleural room air insufflation. Gasping, bradyarrhythmia, arterial hypotension, hypoxemia, hypercarbia, and combined acidosis occurred 62 +/- 6 min (R21) or 65 +/- 7 min (R100; mean +/- SD) after the start of the experiments; then pneumothorax was relieved, and a 10-min reoxygenation period was started with mechanical ventilation with room air (R21) or with 100% O2 (R100). The newborn piglets then breathed room air spontaneously during the next 3 h. Blood oxidative stress indicators (oxidized and reduced glutathione, plasma Hb, and malondialdehyde concentrations) were measured at different stages of the experiments. Early neurologic outcome examinations (neurologic score of 20 indicates normal, 5 indicates brain-dead) were performed at the end of the study. The brains were next fixed, and various regions were stained for cerebral histopathology. In the SHAM group, the blood gas and acid-base status differed significantly from those measured in groups R21 and R100. In group R100, arterial PO2 was significantly higher after 5 (13.8 +/- 5.6 kPa) and 10 min (13.2 +/- 6.3 kPa) of reoxygenation than in group R21 (8.7 +/- 2.8 kPa and 9.2 +/- 3.1 kPa). The levels of all oxidative stress indicators remained unchanged in the study groups (SHAM, R21, and R100). The neurologic examination score in the SHAM group was 18 +/- 0, in group R21 it was 13.5 +/- 3.1, and in group R100 it was 9.5 +/- 4.1 (significant differences between SHAM and R21 or R100, and between R21 and R100). Cerebral histopathology revealed marked damage of similar severity in both asphyxiated groups. We conclude that the blood oxidative stress indicators and cerebral histopathology did not differ significantly after a 10-min period of reoxygenation with room air or with 100% O2 after pneumothorax-induced asphyxia, but reoxygenation with 100% O2 might impair the early neurologic outcome of newborn piglets.

Acid-Base Equilibrium↗
PubMed2006

Fetal brain injury in experimental intrauterine asphyxia and inflammation in Göttingen minipigs.

OBJECTIVE: To examine fetal brain injury in the Göttingen minipig following intrauterine asphyxia and infection/inflammation induced at 3/4 of gestational length. METHODS: We performed laparotomy after anesthesia in six pregnant sows. We randomized 29 fetuses to one of four groups: pretreatment with saline or endotoxin followed by 30 min of umbilical cord occlusion or no occlusion. After 48 h we performed a re-laparotomy and examined the fetal brains. RESULTS: After total asphyxia, brain stem injury was present in the group pretreated with saline (P < 0.01 vs. controls) and with endotoxin (P < 0.005 vs. controls). Microglia activation was more marked in the brain stem (P < 0.05) and posterior white matter (P < 0.05) in the asphyxia group than in controls. Two of five fetuses in the asphyxia group had white matter injury, while no white matter lesions were found in the asphyxia/inflammation or endotoxin only groups. CONCLUSIONS: In this Göttingen minipig model, a species closer to humans than animals commonly used in experimental studies of perinatal brain injuries, intrauterine asphyxia following pretreatment with saline caused brain stem and white matter injury. This model can be further developed to study the impact of other intrauterine exposures on brain injury.

Animals↗
PubMed1978

Body colour response of the carp (Cyprinus carpio) during asphyxia.

The body colour of immobilized carp was photoelectrically measured simultaneously with heart rate in order to examine one of the effects of asphyxia on autonomic functions of the cutaneous region. 1) Asphyxia induced marked body colour darkening and bradycardia. 2) Adequate increase in cardiac vagal activity was recorded during asphyxic bradycardia. 3) After atropine injection, body colour darkening, as in intact fish, was observed during asphyxia while heart rate was not changed. 4) After transection of anterior spinal cord, asphyxic stimulation did not induce body colour darkening. It is concluded that body colour darkening mediated by nervous pathways was observed during asphyxia simultaneously with the definite bradycardia. This response of body colour has provided the first indication for responses in cutaneous autonomic systems within the responses of the fish co-ordinated as a whole to asphyxia.

Animals↗
PubMed1996

Petechial hemorrhage of the conjunctiva and histological findings of the lung and pancreas in infantile asphyxia--evaluation of 85 cases.

Eighty-five cases of infantile asphyxia were examined in relation to the degree of conjunctivae petechial hemorrhages and histological and immunohistochemical findings of the lungs and the pancreas. In very young cases, even in the strangulation cases, conjunctivae petechial hemorrhages were unremarkable and sometimes absent. The lungs showed remarkable to moderate congestion, while the pancreas showed only slight to moderate edema and cell infiltrations. Many pancreata of cases of accidental and homicidal asphyxia had hyperplasia and nesidioblastosis of islet cells. In adult asphyxia cases, remarkable congestion has been the main finding in the lungs and the pancreas. This study shows many similarities between the findings in homicidal suffocation and in genuinely accidental suffocation, both in inspection and on histological examination. So, we here, stressed on the necessity of legal necropsy for various infantile asphyxia cases, in the speculation of the cause of death, in order to not only study infantile sudden death cause but also not to mis-diagnose genuine accidental asphyxia cases or homicidal cases using suffocation for Sudden Infant Death Syndrome (SIDS).

Asphyxia↗
PubMed2000

[Reoxigenation after neonatal asphyxia with 21% or 100% oxygen in piglets].

Birth asphyxia represents a serious problem worldwide, resulting in 1 million deaths and an equal number of neurologic sequelae annually. It is therefore important to develop new and better ways to treat asphyxia. In the present study we tested the effect of reoxygenation with room air or 100% oxygen following experimental pneumothorax induced asphyxia on blood oxidative stress indicators, early neurologic outcome and cerebral histopathology of newborn piglets. 26 animals were studied in three experimental groups: sham-operated (SHAM, n = 6), reoxygenation with room air after pneumothorax (RORA, n = 10) and reoxygenation with 100% oxygen after pneumothorax (RO100, n = 10). In RORA and RO100 asphyxia was induced under anesthesia with bilateral intrapleural room air insufflation. Gasping, bradyarrhythmia, arterial hypotension, hypoxemia, hypercarbia and severe combined acidosis occurred 62 +/- 6 (RORA) and 65 +/- 7 min (RO100) after the start of the experiments, when the pneumothorax was relieved and ten min of reoxygenation period was started with mechanical ventilation with room air (RORA) or 100% oxygen (RO100). Then the spontaneously breathing animals were followed on room air during the next three hours. Blood oxidative stress indicators--as oxidized and reduced glutathione, plasma hemoglobin and malondialdehyde concentrations--were also measured at different stages of the experiments and early neurologic examinations (neurological score: 20 = normal, 5 = brain dead) were performed at the end of the study. Then the brains were fixed and stained. In SHAM blood gases and acid/base status differed significantly from values measured in RORA and RO100. In RO100 PaO2 was significantly higher at 5 (13.8 +/- 1.8 kPa) and 10 min (13.2 +/- 2.0 kPa) than in RORA (8.7 +/- 0.9, 9.2 +/- 1.0 kPa), respectively. All the measures of oxidative stress indicators remained unchanged in the study groups (SHAM, RORA, RO100). Neurologic examination scores from SHAM were 18 +/- 0, from RORA 13.5 +/- 1.0 and from RO100 9.5 +/- 1.3 (significant differences between SHAM and RORA and RO100, significant difference between RORA and RO100). Cerebral histopathology showed marked damage with similar severity in both asphyxiated groups. We conclude that blood oxidative stress indicators and cerebral histopathology did not differ significantly after 10 min reoxygenation either with room air or with 100% oxygen following pneumothorax induced asphyxia, but reoxygenation with 100% oxygen might impair the early neurologic outcome of newborn pigs.

Animals↗
PubMed2001

Autoerotic asphyxia (a case report).

The authors report the case of a young man, 18 years of age, who died as a result of autoerotic asphyxia. In the practice of forensic medicine such cases are presented as deaths from mechanic asphyxia in which, using various means and devices, the neck is constricted or the external respiratory orifices are obstructed with the purpose of achieving sexual gratification as a result of the induced hypoxia. These cases pose serious difficulties to the forensic medicine expert and the coroner because of the difficulties of distinguishing it as homicide, suicide or accident. The young man was found hanging by the neck, suspended on a leather belt attached on the door of his room. A mirror was placed in front of the door, reflecting him in full height. He was dressed in women's clothing (a skirt, a blouse, bikini) and a brassiere padded to resemble female breasts. Pornographic pictures from newspapers and magazines were spread on the floor. The young man had no known history of mental disorders, but there was evidence for bisexual tendencies and behaviour. On the basis of a comprehensive evaluation of the data it was accepted that the death was accidental and was attributed to autoerotic asphyxia. All the characteristic features for an act of autoerotic asphyxia, described in the forensic medicine literature, were found in this case. Autoerotic asphyxia is almost unknown as a distinctive psychopathological entity in this country's forensic medicine practice. The deficiency of theoretical knowledge in this field, as well as the lack of personal practical experience in most of the legal physicians and pathologists could result in erroneous interpretation of such case.

Accidents↗