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PubMed2004

Perinatal asphyxia in the rat has lifelong effects on morphology, cognitive functions, and behavior.

Perinatal asphyxia (PA) is a major determinant of neurological morbidity and mortality in the neonatal period. Many studies have been investigating neurological deficits following PA, including seizures, cerebral palsy, mental retardation, as well as psychiatric deficits. Most research performed so far has been focusing on acute or subacute sequelae and has uncovered a variety of morphological, neurochemical, behavioral, and cognitive changes following PA. However, information on long-term sequelae of animals that underwent a period of PA is scanty. Perinatally asphyxiated rats at the end of their life span present with immunohistochemical and synaptic changes as well as changes in brain protein expression. Furthermore, deficits in cognitive function tested in the Morris water maze and changes in social behavior were described. In this review, we are summarizing and discussing reported effects of global PA on morphology, cognitive functions, and behavior in rats at the end of their life span.

Animals↗
PubMed2000

Volatile substance use in sexual asphyxia.

A 38-year-old man was found dead in bed dressed in female clothing with a mouth gag, handcuffs and bindings around the genitals and limbs. A respirator was also covering the mouth and nose. There were no suspicious circumstances and a diagnosis of death due to sexual asphyxia was made. Following the subsequent discovery of bottles of chloroform in the bedroom, head space analysis of blood confirmed the presence of chloroform, with a blood level of 33 mg/L. Death was, therefore, attributed to a combination of chloroform toxicity and upper-airway obstruction. Headspace analysis with follow-up quantitation may, therefore, be a useful adjunct to the investigation of such cases when devices such as respirators or gas masks are found with the body.

Journal Article↗
PubMed1985

Quality of obstetric care and occurrence of fetal asphyxia and cerebral palsy. Is there a relationship?

Whether a relationship exists between the quality of obstetric care and poor fetal outcome, notably cerebral palsy, remains uncertain. We herein report a study which suggests that substandard obstetric care bears little relationship to the etiology of cerebral palsy. In none of our 34 cases of cerebral palsy was there any recognized delay on the physician's part in reacting to evidence of fetal asphyxia.

Cerebral Palsy↗
PubMed1993

Uteroplacental and fetal circulation during extradural bupivacaine-adrenaline and bupivacaine for caesarean section in hypertensive pregnancies with chronic fetal asphyxia.

We have studied the effects of an extradural block during Caesarean section using either bupivacaine plain or with adrenaline 85-100 micrograms on blood velocity waveforms of maternal uterine and placental arcuate arteries and fetal umbilical, renal and middle cerebral arteries, in 20 hypertensive parturients with chronic fetal asphyxia. Fetal myocardial function was investigated at the same time by M-mode echocardiography. Extradural anaesthesia resulted in a significant decrease in maternal mean systolic and diastolic arterial pressures in both groups, but this was more marked after plain bupivacaine. There were no significant differences in any of the Doppler recordings relative to baseline values after plain bupivacaine, but after bupivacaine with adrenaline there were significantly increased blood flow velocity indices for the maternal uterine and placental arcuate arteries and significantly decreased indices in the fetal renal and middle cerebral arteries. Neonatal outcome as evaluated by Apgar scores and acid-base values in the umbilical cord were similar in the two groups. The results suggest that adrenaline added to the solution of bupivacaine increased vascular resistance in the uteroplacental circulation, indicating impaired blood flow.

Anesthesia, Epidural↗
PubMed2005

Pharmacokinetics of the active metabolites of ethyl loflazepate in elderly patients who died of asphyxia associated with benzodiazepine-related toxicity.

We determined the pharmacokinetics of ethyl loflazepate (Lof) in elderly patients who died of benzodiazepine-related toxicity. Three elderly patients with body mass indexes of less than 17 kg/m2 died of asphyxia after having taken maintenance doses of Lof for 2 to 3 weeks. We measured serum concentrations of the active metabolites of Lof using gas chromatography-mass spectrometry and a benzodiazepine receptor assay to determine the pharmacokinetics of each. On admission, the serum concentrations of the active metabolites of Lof ([Lofl) were 256 ng/mL, 425 ng/mL, and 177 ng/mL in cases 1, 2, and 3, respectively. Serum benzodiazepine-receptor binding activities, expressed as diazepam equivalent concentrations ([Bz]), were 1800 ng/mL, 2200 ng/mL, and 1500 ng/mL. The T1/2(beta) of [Lof] were 124 and 121 h in cases 1 and 2 and the T1/2(beta) of [Bz] were 75 and 87 h. The distribution volume in the elderly was reduced due to a small lipid compartment, and total drug clearance was decreased due to the decline in liver and kidney function. These changes did not prolong T1/2(beta) but did increase plasma concentrations of active metabolites, especially in case 2, and a slight decrease in protein binding increased the amount of free active metabolites greatly.

Aged↗
PubMed1987

Prenatal asphyxia, hyperlacticaemia, hypoglycaemia, and erythroblastosis in growth retarded fetuses.

The umbilical venous oxygen and carbon dioxide tensions, pH, lactate and glucose concentrations, nucleated red cell (erythroblast) count, and haemoglobin concentration were measured in 38 cases of intrauterine growth retardation in which fetal blood sampling was performed by cordocentesis. The oxygen tension was below the normal mean for gestational age in 33 cases; in 14 it was below the lower limit of the 95% confidence interval for normal pregnancies. The severity of fetal hypoxia correlated significantly with fetal hypercapnia, acidosis, hyperlacticaemia, hypoglycaemia, and erythroblastosis. These findings indicate that "birth asphyxia" is not necessarily due to the process of birth.

Blood Cell Count↗
PubMed1981

Vascular response of the chicken hindlimb to vasoactive agents, asphyxia, and exercise.

Previous studies in live chickens have measured heart rate, blood pressure, and cardiac output during drug administration or asphyxia and made assumptions concerning the peripheral vasculature. The present study employs a constant-flow, isolated hindlimb perfusion technique to measure directly changes in skeletal muscle vascular resistance induced either by local intra-arterial (i.a.) bolus, or continuous i.a. infusion, of various vasoactive substances. Prostaglandin E1 (0.5 microgram, bolus) produced arteriolar vasodilation lasting 10 min, as indicated by a fall ian perfusion pressure. Bolus injection of histamine (10 microgram diphosphate) or adenosine (5 and 10 microgram) produced vasodilation of less than 2-min duration. Theophylline infusion (5 microM infused at 1 mL/min, i.a.) blocked the effect of adenosine. Norepinephrine (1 microgram) produced vasoconstriction which was reduced 60% by systemic alpha-adrenergic blockade with phenoxybenzamine (7.5-10 mg/kg). Tracheal occlusion produced intense vasoconstriction which was reduced 70% by alpha-adrenergic blockade. Electrical stimulation of the peripheral end of the cut sciatic nerve (6 Hz) produced an immediate vasodilation lasting several minutes.

Acetylcholine↗
PubMed1988

Perinatal cerebral asphyxia: pharmacological intervention.

Perinatal asphyxia is associated with an increased risk of cerebral palsy and significant mortality. We investigated the use of flunarizine, a calcium antagonist and MK-801, an excitatory amino acid antagonist, in preventing the sequelae of severe hypoxic/ischemic insults. Flunarizine was neuroprotective in the infant rat subjected to unilateral carotid ligation and 2 h of hypoxia. Preliminary analysis of experiments in a novel model of cerebral ischemia in the fetal sheep suggests that prophylactic treatment with flunarizine greatly modified the outcome after 30 min of total ischemia. Treatment with MK-801 prevented post-ischemic seizures. The background to these developments is outlined and future prospects considered.

Animals↗
PubMed1996

Plasma endothelin-1 levels during asphyxia in the fetal goat.

The changes in fetal carotid arterial plasma levels of endothelin-1, catecholamines, PO2, PCO2 and pH were measured after intermittent repetitive umbilical cord occlusion in late gestation pregnant goats (n = 9). Endothelin-1 levels increased to 3.58 +/- 0.28 pg/ml immediately after the onset of fetal hypoxia, a level significantly higher than the respective values in the control period (p < 0.05). The elevation of fetal plasma endothelin-1 levels correlated inversely with carotid arterial PO2 (r = -0.41, p < 0.05) and pH (r = - 0.43, p < 0.05). The results suggest that increased endothelin-1 levels may contribute to the maintenance of the fetal circulation during fetal asphyxia.

Animals↗
PubMedDate not supplied

[Effect of perinatal asphyxia on thyroid hormones]

OBJECTIVE: To verify the effect of perinatal asphyxia on thyroid hormone levels in term newborn infants. METHODS: We carried out a case-control study with 17 term and asphyxiated (A) and 17 term and control (N) newborn infants at the Hospital de Clínicas de Porto Alegre. Patients were paired according to color of skin, sex, type of delivery, gestational age, and weight at birth. We collected umbilical cord plasma T4, T3, free T4, reverse T3, and TSH after 18 to 24 hours of life and from asphyxiated and control newborn infants. RESULTS: There were no differences in thyroid hormones of cord blood, with the exception of reverse T3, which was higher in A than in controls [median (25th-75th percentile): A= 2(1.4-2); N= 1.41 (1.13-1.92); P=0.037)]. Thyroid hormone levels were lower in A than in controls on samples collected within 18-24 hours after birth, except for reverse T3, which was similar in both groups [average -/+ SD: T4 A= 9.79 -/+ 2.59; N=14.68 -/+ 3.05; P<0.001; median T3 A= 40.83 (37.4-80.4); N= 164 (56.96-222.5); P=0.003; average -/+ SD: free T4 A=1.85 -/+ 0.92; N= 2.8 -/+ 0.74; P=0.004; median: reverse T3 A=1.54 (1.16-1.91); N=1.31(0.87-2); P=0.507; TSH A=9.1 (6.34-12.95); N=14.5(12.9-17.85); P=0.008]. CONCLUSIONS: Our data suggest that lower T4, free T4, and T3 levels are secondary to lower TSH levels in asphyxiated newborns; also, peripheral metabolism of T4 in asphyxiated infants can be altered due to low T3 and normal reverse T3 levels.

Journal Article↗
PubMed1980

Alterations in the electrocardiogram of the fetal lamb as a sign of fetal asphyxia. A comparison between the scalp lead and the precordial lead.

Progressive changes in the ST-T period of the fetal electrocardiogram (FECG) were studied in 18 lamb fetuses, acutely exteriorized and subjected to graded hypoxia. The aim of the study was to compare the bipolar precordial lead (CR-lead) with the unipolar scalp lead, and to correlate the alterations in the FECG to blood-gas and acid-base status. The scalp lead gave less information regarding fetal condition and was more difficult to interpret than the precordial lead. This might be one factor in the controversy regarding the significance of alterations in the FECG during asphyxia and labor, since the scalp lead is used mainly in clinical situations. Our previous results demonstrating progressive changes in the ST-T period of the FECG during hypoxia in experimental animals and showing the same ECG changes in newborn human infants immediately after birth, were registered with the bipolar precordial lead. It is possible that a bipolar scalp lead might give more information regarding the fetal condition than the unipolar scalp lead mainly used in clinical practice.

Animals↗
PubMed1978

Perinatal asphyxia and outcome of very low birthweight infants.

Seventy-eight very low birthweight (VLBW) infants (whose birthweights were 1500 g or less) were admitted to the Neonatal Special Care Unit in 1977. Seventy-two of them required treatment in the intensive care area; these represented 40% of admissions to that area of the Unit. The mortality rate was 20% for infants weighing 1001 g to 1500 g, and 52% for those weighing 501 g to 1000 g. An Apgar score of 0 to 3 at two minutes and five minutes was reported in 34% and 19% of VLBW infants respectively. Although there was no difference in birthweight between the groups with a high or low Apgar score, the mortality rate of infants with a five-minute Apgar score of 0 to 3 was 79% compared to 22% in those with a score of 4 to 10. Over 50% of the infants developed hyaline membrane disease regardless of Apgar score. However, in the infants with a five-minute Apgar score of 0 to 3, the severity of respiratory insufficiency was increased as indicated by increased requirement for high inspired oxygen, and the need for intermittent positive pressure ventilation. The duration of stay in the neonatal intensive care area, and the total length of hospital stay of the 49 VLBW survivors were shorter in the group with higher two-minute and five-minute Apgar scores. Long-term morbidity cannot yet be ascertained. It is likely that prevention, or prompt detection, and appropriate management of perinatal asphyxia would produce a further decline in mortality as well as morbidity for VLBW infants.

Acute Disease↗
PubMed2001

[The asphyxia-cardiac arrest rat model for developing mechanism of effect oriented therapeutic concepts after cardiopulmonary resuscitation].

In order to expand and combine clinical and basic science research opportunities on cardiac arrest, the Asphyxial Cardiac Arrest Rat Model, originally developed at the International Resuscitation Research Center in Pittsburgh, was introduced and adapted at the University of Magdeburg Medical Center. For better utilization of established morphological and biochemical evaluation techniques, the former Sprague-Dawley rat model was adapted for Wistar rats. Life-support procedures, especially controlled ventilation, had to be adjusted. Wistar rats seem to be more sensitive to asphyxia, resulting in significantly faster-developing cardiac arrest (time from ceasing ventilation to pulselessness: Wistar 2:43 min versus 3:28 min in Sprague-Dawley) and a tendentiously longer resuscitation time (37 versus 23 s). Furthermore, a trend towards a more pronounced secondary blood pressure depression was observed especially during the later half of the first hour after resuscitation. Post-mortem brain evaluations using conventional Nissl and haematoxylin-eosin staining techniques showed--most distinctly in the hippocampal CA1 region--delayed neuronal damage with a peak at 72 hours after resuscitation and with only a few neurons remaining after seven days of survival.

Animals↗
PubMed2002

Proinflammatory cytokines in injured rat brain following perinatal asphyxia.

In contrast to astrogliosis, which is common to injuries of the adult CNS, in the developing brain this process is minimal. Reasons postulated for this include the relative immaturity of the immune system and the consequent insufficient production of cytokines to evoke astrogliosis. To explore this hypothesis, the study was undertaken to detect the presence of some proinflammatory cytokines in the injured rat brain following perinatal asphyxia (ischaemia/hypoxia). The localisation of TNF-alpha, IL-15, IL-17 and IL-17 receptors was visualised by means of immunohistochemistry. In numerous neurones of the rat brain, the IL-17 appeared to be constitutively expressed. In the early period of inflammation the IL-15 was produced mainly by the blood cells penetrating the injured brain but later it was synthesised also by reactive astrocytes surrounding brain cysts and forming dense astrogliosis around necrotic brain regions. The direct effect on astrogliosis of other estimated cytokines seems to be negligible. All the results lead to the conclusion that from all cytokines identified in the injured immature rat brain the IL-15 plays the most important role during inflammatory response and participates in the gliosis of reactive astrocytes.

Animals↗
PubMedDate not supplied

[Asphyxia protracted after shaking trauma].

A case of "shaken baby syndrome" (SBS) is reported. A 3 1/2 months old female baby has been found by his mother death in bed. The circumstances predicted a case of Sudden Infant Death Syndrome (SIDS), but the father, a disc-jockey, who had to look for the baby, had left a notice: "Gitti--i didn't want it, I don't know what had happened, I'm sorry!". The corpse of the baby had no external signs of violence. At the medicolegal examination we found small subarachnoidal and subdural hemorrhage from ruptured bridge veins and signs of prolonged asphyxia. Few hours later the father could be arrested. He told that he had shaken the baby, because she didn't stop crying. The infant lost conscious and he layed him down to the bed with his face below. Then he looked TV for at least a few minutes. After insufficient reanimation he had left the house. The court found the man to be guilty of fatal infant child abuse and convicted him to detention of 8 months. The main signs of SBS are discussed (subarachnoidal and subdural hemorrhage, intraretinal and periretinal hemorrhages, brain edema). Especially in the german speaking Europe many medical examiners are not familiar with this form of infant child abuse.

Child Abuse↗
PubMed1986

Alterations in the fetal electrocardiogram as a sign of fetal asphyxia--experimental data with a clinical implementation.

Although considerable progress occurred with the introduction of electronic fetal monitoring it is now clear that the fetal heart rate alone does not provide optimal information about the fetus. Thus, a question arises whether additional information could be gained by further analyzing the fetal ECG as this is likely to be the parameter presently most easily accessible during labor. For the past 10 years work by our group in Göteborg has been focused on the evaluation of ST waveform changes in the fetal ECG as a method for fetal surveillance. Fetal hypoxemia results in a reproducible pattern of changes with the progressive increase in T wave amplitude as the main response. The ratio between the amplitude of the T wave and QRS complex, the so called T/QRS ratio, quantifies this T wave alteration. Considerable information has been gained, using this parameter, by conducting experiments on the fetal lamb and guinea-pig. The closest relationship was found between the rate of breakdown of myocardial glycogen and the increase in T wave amplitude. This utilization of myocardial glycogen during hypoxia is stimulated by beta-adrenoreceptors. The data also indicate a close link between the adrenaline surge and the appearance of high T waves in the fetal ECG. Relating T wave changes to other biochemical parameters shows a relationship during marked asphyxia with the appearance of a metabolic acidosis which is a result of an increase in blood lactate concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1977

[Dynamics of spinal cord changes under the influence of asphyxia sustained in utero].

Changes of the neurons and nerve fibers of the spinal cord at the C4-C5 level were studied in rats exposed to intra-uterine asphyxia and sacrificed at various periods. A gradual increase of the neuronal changes was observed the first 10 days. Although the majority of the neurons were normalized by the 1st-2nd month microscopy showed changed nerve cells in every 100 fields of vision. The abnormal neurons were mainly confined to the areas of colateral circulation. Some of the myelin fibers were vacuolated, and their sheaths--disintegrated.

Animals↗
PubMed1981

[Diaplacental influence on the disseminated intravascular coagulation (DIC) in an asphyxia model. I. Influence on the vasal tonus and on the vasal wall (author's transl)].

With the aid of an asphyxia model in rabbit fetuses the possibility of diaplacental influence on the hypoxic effects of the fetal organism has been investigated. The trial to change the vasotonia during the asphyctic shock by sympathicomimetic or -lytic drugs (Dilatol, Obsidan, Ergocomb, Regitin) remained to be without any effect on the DIC in the fetal organism. Trying to seal the vascular wall by the high-molecular-weight basic polypeptide Aprotinin there seemed rather to be an increase of the intravascular fibrin sedimentation.

Adrenergic alpha-Antagonists↗