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PubMed2001

Reproductive risk factors of fetal asphyxia at delivery: a population based analysis.

To investigate reproductive maternal risk factors of intrapartum fetal asphyxia, we analyzed 556 women with singleton pregnancies complicated by intrapartum fetal asphyxia who gave birth at Kuopio University Hospital from January 1990 to December 1998. The general obstetric population (N=21746) was selected as the reference group and logistic regression analysis was used to identify independent reproductive risk factors. The incidence of intrapartum fetal asphyxia was 2.5%. Placental abruption, primiparity, alcohol use during pregnancy, low birth weight, preeclampsia, male fetuses, and small-for-gestational age births were independent risk factors of intrapartum asphyxia, with adjusted relative risks of 3.74, 3.10, 1.75, 1.57, 1.49, 1.48 and 1.33, respectively. Most cases of intrapartum fetal asphyxia occur in low-risk pregnancies and, therefore, risk screening in antenatal care cannot accurately predict which women will eventually need emergency care for fetal asphyxia.

Abruptio Placentae↗
PubMed1995

Circulatory responses to acute asphyxia in intact and chemodenervated fetal sheep near term.

The study concerned the role of the carotid sinus nerves in the effects of acute asphyxia on the fetal circulation. Fetal sheep (n = 12) were instrumented at approximately 130 days' gestation for placement of fetal vascular catheters and an occluder around the maternal descending aorta below the renal arteries. In 7 fetuses the carotid sinus nerves were cut. On the third post-operative day, asphyxia was produced by occluding the maternal aorta for 2 min and fetal blood flows were determined by the radio-labelled microsphere technique. In control, there were no differences between intact and denervated fetuses in blood gases, cardiovascular variables or blood flows, with the exception of lower blood flows to the cerebrum, caudate nucleus, kidney, skeletal muscle and scalp in the denervated group (P < 0.01). Fetal heart rate, cardiac output, stroke volume and the rate-pressure product were similar in asphyxia, with the exception that mean arterial pressure was lower in denervated fetuses after 2 min of asphyxia. Noradrenaline and adrenaline concentrations peaked at 2 min, then declined, the increase being smaller (P < 0.01) in denervated fetuses. Regional blood flows were similar in the two groups. Vascular resistance was lower in the placenta and abdominal aorta at 2 min in denervated fetuses. There were few differences in organ blood flows between intact and denervated fetuses, and the differences in flow in normoxia for the kidney, skeletal muscle and scalp (but not cerebrum, caudate nucleus and hippocampus) disappeared in asphyxia. This study confirms that section of the carotid sinus nerves has little effect on arterial blood pressure and fetal heart rate in normoxia but produces small differences in the responses to acute severe asphyxia, e.g. in arterial blood pressure and catecholamines, giving evidence for the operation of chemoreflexes. The lower blood flow to cerebrum, caudate nucleus, kidney, skeletal muscle and scalp in denervated fetuses in normoxia suggests a tonic vasodilatation, part of the drive for which comes from carotid chemo- or baroreceptors.

Animals↗
PubMed2003

Comparison of isoflurane and propofol-fentanyl anaesthesia in a swine model of asphyxia.

BACKGROUND: There have been few studies comparing the response to asphyxia and the effectiveness of typical cardiopulmonary resuscitation (CPR) using exogenous epinephrine administration and manual closed-chest compression between total intravenous anaesthesia (TIVA) and inhalational anaesthesia. METHODS: Twenty pigs were randomly assigned to two study groups anaesthetized using either 2% end-tidal isoflurane (n=10) or propofol (12 mg x kg(-1) h(-1))-fentanyl (50 microg x kg(-1)) (n=10). Asphyxia was induced by clamping the tracheal tube until the mean arterial pressure (MAP) decreased to 40% of the baseline value (40% MAP time). The tracheal tube was declamped at that point, and CPR was performed. Haemodynamic parameters and blood samples were obtained before the induction of asphyxia, at 1-min intervals during asphyxia, and 1, 2, 3, 5, 10, 30 and 60 min after asphyxia. RESULTS: TIVA maintained the MAP against hypoxia-hypercapnia stress significantly longer than isoflurane anaesthesia (mean (SD) 40% MAP time 498 (95) and 378 (104) s respectively). In all animals in the isoflurane group, spontaneous circulation returned within 1 min of the start of CPR. In six of the TIVA animals, spontaneous circulation returned for 220 (121) s; spontaneous circulation did not return within 5 min in the remaining four animals. CONCLUSIONS: Although TIVA is less prone than isoflurane anaesthesia to primary cardiovascular depression leading to asphyxia, TIVA is associated with reduced effectiveness of CPR in which resuscitation because of asphyxic haemodynamic depression occurs.

Anesthetics, Combined↗
PubMed1997

The effects of bupivacaine, L-nitro-L-arginine-methyl ester, and phenylephrine on cardiovascular adaptations to asphyxia in the preterm fetal lamb.

UNLABELLED: The preterm fetal lamb that is exposed to clinically relevant plasma concentrations of lidocaine loses its cardiovascular adaptations to asphyxia, and its condition deteriorates further. Nitric oxide (NO) is an important regulator of vascular tone, and local anesthetics are known to inhibit endothelium-dependent vasodilation. The purpose of the present study was to determine whether the adverse effects of lidocaine noted in the preterm fetal lamb also occur with bupivacaine and whether the inhibition of NO results in effects similar to those of bupivacaine. Thirty-two chronically prepared pregnant sheep were studied at 117-119 days' gestation. Maternal and fetal blood pressure, heart rate, and acid-base state were evaluated. Fetal organ blood flows were determined using 15-microM diameter dye-labeled microspheres. After a control period, mild to moderate asphyxia (fetal PaO2 15 mm Hg) was induced by partial umbilical cord occlusion and maintained throughout the experiment. Ewes in Group I (n = 13) were given a two-step intravenous infusion of bupivacaine for 180 min. Fetuses in Group II (n = 12) received an intravenous injection of L-nitro-L-arginine-methyl ester (L-NAME) (25 mg/kg), and measurements were taken 10 and 30 min after the injection. A third group (Group III) of fetuses (n = 7) were given an intravenous infusion of phenylephrine to mimic the blood pressure increases noted in L-NAME-treated fetuses. At 90 min of stable asphyxia, there was a significant decrease in fetal PaO2 and pHa and an increase in PaCO2 and mean arterial blood pressure. There was also an increase in blood flow to the adrenals, myocardium, and cerebral cortex, whereas blood flow to the placenta decreased. Administration of bupivacaine during asphyxia did not affect the changes in mean arterial blood pressure and acid-base state but did abolish the increases in blood flows to the myocardium and cerebral cortex. Injection of L-NAME to the asphyxiated fetus resulted in an increase in mean arterial blood pressure above the level noted at 90 min of cord occlusion, and an increase in fetal PaO2 toward control levels. This was accompanied by a reduction in organ blood flows to preasphyxia levels. In asphyxiated Group III fetuses, titration of the phenylephrine infusion to achieve blood pressure increases similar to those noted with L-NAME were also associated with an increase in fetal PaO2. These data indicate that bupivacaine abolishes some of the circulatory adaptations to mild to moderate asphyxia induced by partial cord occlusion in the preterm fetal lamb. It is not clear whether these effects of bupivacaine are due to inhibition of NO. IMPLICATIONS: In the preterm fetal lamb, clinically relevant plasma concentrations of bupivacaine achieved by intravenous infusion to the pregnant ewe (80% gestation) abolished some of the fetal cardiovascular adaptations to asphyxia induced by partial umbilical cord occlusion.

Adaptation, Physiological↗
PubMed1993

The relationship of asphyxia in the mature fetus to long-term neurologic function.

Asphyxia may occur before or during labor in the preterm or term fetus. The development of neuropathologic lesions depends on the degree and duration of the asphyxia. Anoxia may occur, but because of the short duration of the fetal response, it usually will cause the death of the fetus. The common mechanism leading to neuropathologic lesions in the fetus is a significant degree of hypoxia present for a particular period of time. Antepartum asphyxia will cause such lesions and deficits in children. What is missing are measures to establish the prevalence of antepartum asphyxia in a large population and the epidemiologic studies to determine the association between the asphyxia so documented and the deficits in surviving children. The prevalence of intrapartum fetal asphyxia is of the order of 2%. Most of these children will have no evidence of brain damage. The key is the fetal cardiovascular compensatory response that maintains cerebral blood flow and oxygen metabolism. This compensatory phase, subject to the severity of the hypoxia, may continue for several hours. In the clinical setting during labor, this provides the "window of opportunity" when a specific blood gas and acid-base diagnosis can be made, and with appropriate intervention, brain damage can be avoided. However, if the hypoxia persists, a threshold will be reached when fetal cardiovascular decompensation will occur. The compromised cerebral oxygen metabolism will result in brain damage and deficits in the children who survive. The threshold at which brain damage may occur is when the acidosis is severe (pH, < 7.0). At this time, systemic hypotension may occur.(ABSTRACT TRUNCATED AT 250 WORDS)

Asphyxia Neonatorum↗
PubMed2004

Effects of chronic intermittent asphyxia on haematocrit, pulmonary arterial pressure and skeletal muscle structure in rats.

Sleep-disordered breathing in humans is a common condition associated with serious cardiovascular and other abnormalities. The prevalence and pathogenesis of increased haematocrit and pulmonary hypertension is controversial and it has been suggested that these changes only occur in patients who also have daytime continuous hypoxaemia. The hypothesis tested here is that the chronic intermittent hypoxia and asphyxia associated with sleep-disordered breathing causes erythropoiesis and pulmonary hypertension and that this occurs in the absence of periods of continuous hypoxia. In humans and animals with obstructive sleep apnoea, there are abnormalities of upper airway muscle structure that have been ascribed to increased load placed on these muscles. An alternative hypothesis is that chronic intermittent hypoxia and asphyxia cause changes in upper airway muscle structure and function. To test these hypotheses, rats were exposed to intermittent hypoxia and asphyxia for 8 h per day for 5 weeks. This caused an increase in haematocrit, right ventricular weight and pulmonary arterial pressure. There were only slight changes in diaphragm, upper airway and limb muscle structure and force production but in general, muscle fatigability was increased. In conclusion chronic intermittent hypoxia and asphyxia cause an increase in haematocrit and pulmonary arterial pressure in the absence of periods of continuous hypoxia. Chronic intermittent hypoxia and asphyxia have little effect on skeletal muscle structure and force production but increase muscle fatigue. Increased upper airway muscle fatigue could lead to a vicious cycle of further compromise in upper airway patency and further hypoxia and asphyxia.

Animals↗
PubMed2005

Chronic intermittent asphyxia increases platelet reactivity in rats.

Sleep-disordered breathing is associated with chronic intermittent asphyxia and with a variety of cardiovascular abnormalities. Cardiovascular morbidity and mortality are linked to altered platelet function, and platelet function is affected in sleep-disordered breathing. As there is evidence that chronic continuous hypoxia may alter platelet number and function, the aim of the present study was to test the hypothesis that chronic intermittent asphyxia affects platelet count, activation and aggregation. Rats were treated with a hypercapnic hypoxic gas mixture (minimum of 6-8% O2, maximum of 10-14% CO2) for 15 s, twice per minute for 8 h per day for 3 weeks. Blood was analysed for platelet count, platelet activation (CD62p expression using flow cytometry), response to low dose ADP, haematocrit, red cell count and haemoglobin concentration. A platelet function analyser measured the closure time of an aperture, dependent on platelet aggregation. Compared to controls (n = 16), chronic intermittent asphyxia (n = 13) reduced body weight and increased right ventricular weight but had no significant effect on platelet count (control, 880.4 +/- 20.1; treated: 914.1 +/- 35.2 x 10(3) microl(-1); mean +/- S.E.M.), on the reduction in platelet count in response to ADP (control, reduced to 206.7 +/- 49.0; treated, reduced to 193.8 +/- 35.9 x 10(3) microl(-1)), or on the percentage of platelets positive for CD62p (control, 5.2 +/- 0.7; treated, 6.0 +/- 0.8%). Chronic intermittent asphyxia significantly (P = 0.037) reduced the closure time (control, 90.9 +/- 7.7; treated, 77.7 +/- 3.8 s), indicating greater adhesion and aggregation. There was no significant difference in haematocrit, red cell count and haemoglobin concentration. In conclusion, chronic intermittent asphyxia has no effect on platelet count but does increase platelet aggegation in rats. These data support the idea that chronic intermittent asphyxia alters platelet function in sleep-disordered breathing.

Animals↗
PubMed1970

Cerebral and cardiac enzymic activity and tolerance to asphyxia during maturation in the rabbit.

The tolerance of neonatal rabbits to asphyxiation in 95% N(2) + 5% CO(2) was studied under conditions of controlled body temperature, and the enzymic activities of succinoxidase and lactic dehydrogenase were quantitatively determined in the heart and brain of untreated litter-mates.1. In new-born rabbits tolerance to asphyxia increases progressively as body temperatures are reduced until at 15 degrees C it is four times that at 39 degrees C. At colonic temperatures below 15 degrees C, tolerance to asphyxia decreases rapidly.2. All new-born rabbits having colonic temperatures of 15 degrees C recover spontaneously from asphyxia two to four times as long as that which is lethal for their warm litter-mates. Recoveries from asphyxia five and six times as long occur in 80%.3. At 39 degrees C colonic temperature, the tolerance of new-born rabbits to asphyxia decreases over ninefold from birth to young adulthood.4. In all tissues studied succinoxidase activity increases during the post-natal period. In the heart and frontal lobe, lactic dehydrogenase activity tends to parallel that of succinoxidase and is lower in the new-born than one might expect in view of the tolerance to asphyxia at this time.5. In the medulla oblongata an increase in succinoxidase activity occurs without a parallel increase in lactic dehydrogenase activity. This may reflect an increased dependence on aerobic pathways during post-natal development, with no parallel increase in the capacity for anaerobic glycolysis. Such changes may explain in part why the sensitivity of the medullary respiratory centre complex to oxygen lack is so much greater in the adult than in the new-born.

Age Factors↗
PubMed1972

On the physiological response of the cerebral cortex to acute stress (reversible asphyxia).

1. Rhesus monkey (Macaca mulatta) foetuses were delivered by Caesarean section 3-10 days before term. Aortic blood and cerebrospinal fluid (c.s.f.) samples were taken, the latter from the cortical subarachnoid space and the cisterna magna. The umbilical cord was clamped and foetal breathing prevented for 14-17 min. Blood and c.s.f. were sampled further during this total asphyxiation and for up to 24 hr thereafter.2. The [K(+)] in the cortical subarachnoid fluid started to rise within 2-3 min after the onset of asphyxia and increased up to 7 times the normal level. The [K(+)] of blood plasma and cisternal fluid also increased, but much more moderately. All these effects reversed rapidly upon resuscitation of the foetus.3. A pronounced rise in the cortical subarachnoid fluid [glucose] and a lesser effect on cisternal fluid [glucose] were noted in most cases by the end of, or immediately following, the period of asphyxia. The onset, magnitude and reversal of these effects on [glucose] were less predictable than the observed effects on [K(+)].4. There were no significant changes in the [Mg(2+)], [Ca(2+)] or [Na(+)] of any of these fluids. The calculated total osmolarity of the cortical subarachnoid fluid and, to a much lesser extent, of cisternal fluid and plasma, increased during asphyxia mainly as a result of increased [K(+)].5. The results are interpreted as indicative of a rapid release of K(+) from cortical cells during total asphyxia. The (immature) haematoencephalic K(+) transport system becomes saturated and thus K(+) accumulates in the extracellular fluid (e.c.f.) whence it diffuses into adjacent regions of the c.s.f. system.6. The intracellular fluid of apical dendrites must become even more hypertonic than the e.c.f., since these cellular processes are known to swell during asphyxia at the expense of the e.c.f. space. This apparent increase in intracellular osmolarity could be accounted for by the release of normally bound intracellular cations.7. On the basis of our results and review of the relevant literature, the following sequence of events is proposed: the cortex responds to acute physiological stress (asphyxia, overstimulation, chemical or physical irritation, etc.) by releasing intracellularly bound cations (K(+) and possibly Na(+)). The increased intracellular osmolarity results in the absorption of water from the e.c.f. space. Passage of water across the blood-brain barrier is restricted; thus the e.c.f. space of the cortex does not swell, but becomes hyperosmotic. Under these circumstances, swelling of the cortical cells is limited by the volume of e.c.f. available.8. It is proposed that the release of intracellularly bound cations is a result of their displacement from their binding sites by NH(4) (+) which is released to, and recovered from, these cation binding sites by a glutamate-glutamine interconversion.9. It is concluded that the apparent organized ;shutdown' of the cortical cells in response to acute stress may contribute to the relative insensitivity of this area of the brain to permanent histopathological damage.

Animals↗
PubMed1980

Cerebral metabolism during hypoglycemia dn asphyxia in newborn dogs.

The cerebral metabolic responses to perinatal hypoglycemia (blood glucose less than or equal to 1 mmol/l) combined with asphyxia were studied in paralyzed, lightly anesthetized newborn dogs. No major differences in heart rate, blood pressure or arterial acid-base balance between control and hypoglycemic animals occurred either prior to or during asphyxia. The electroencephalogram, unaltered by hypoglycermia alone, became isoelectric at the same intervals in both groups following respiratory arrest. Intravenous carbon black infusion at 5 min of asphyxia demonstrated no relationship between blood glucose level and cerebral perfusion (p > 0.05), whereas a positive correlation did exist between systemic blood pressure and cerebral perfusion (p < 0.01). During asphyxia, anaerobic glycolysis in brain was less enhanced in hypoglycemic dogs, resulting in a more rapid exhaustion of high-energy phosphate reserves (phosphocreatine, ATP and ADP). Thus, the cerebral metabolic responses to asphyxia superimposed upon hypoglycemia were the direct consequence of insufficient cerebral glucose stores coupled with deficient circulating glucose to brain. These metabolic disturbances were no more the result of cerebral ischemia than that which occurs during asphyxia alone. The findings also suggest that systemic physiological monitoring may be an inadequate means of appraising cerebral homeostasis during combined hypoglycemia ad hypoxia.

Animals↗
PubMed1982

Effect of acute perinatal asphyxia on development of the lung and brain in the rat.

Fetal rats were exposed to asphyxia by compression of the umbilical vessels, and the animals were studied shortly after delivery, close to term (21st fetal day). Following asphyxia on the 20th fetal day, the lungs appeared immature. The surface active phospholipids, disaturated lecithin and phosphatidylglycerol, as well as the elastic tissue around the alveoli were lower than in the control littermates. However, lung maturity was little affected following asphyxia on the 17th-18th fetal day. As studied in the brain, hemorrhages in the periventricular area, sometimes intraventricular hemorrhages, were evident (asphyxia on the 17-18 and 20th fetal days). In addition, cells in cerebral cortex were altered following asphyxia of 17 - to 18-day-old fetuses. The present animal model clarifies the mechanism of increased incidence of respiratory distress syndrome following acute asphyxia and may prove to be useful in studies of pathogenesis of periventricular hemorrhages.

Animals↗
PubMed2000

Hydroxyethyl starch reduces leukocyte adherence and vascular injury in the newborn pig cerebral circulation after asphyxia.

BACKGROUND AND PURPOSE: Hydroxyethyl starch (HES) has beneficial effects on ischemic brain injury; however, its mechanism of action remains unclear. The present study was undertaken to test the hypothesis that HES can attenuate increases in leukocyte adherence and vascular permeability in the cerebral vasculature after global cerebral ischemia induced by asphyxia. METHODS: Pial venular leukocyte adherence and permeability to sodium fluorescein were quantified in anesthetized newborn piglets by in situ fluorescence videomicroscopy through closed cranial windows during basal conditions and during 2 hours of reperfusion after global ischemia induced by 9 minutes of asphyxia. Experimental animals received HES after the asphyxial insult (10% HES 257/0.47, 600 mg/kg IV bolus 5 minutes after asphyxia, followed by 600 mg/kg per hour IV drip during reperfusion; n=9). RESULTS: A progressive and significant (P:<0.05) increase in adherent leukocytes was observed during the initial 2 hours of reperfusion after asphyxia compared with nonasphyxial controls. In this model, vascular injury, as determined by significant (P:<0.05) increases in fluorescein permeability at 2 hours of reperfusion, is largely dependent on adherent leukocytes. HES significantly reduced (P:<0.05) leukocyte adherence at 1 hour and 2 hours of reperfusion and reduced fluorescein permeability at 2 hours. HES did not change hematocrit or alter pial arteriolar diameter. CONCLUSIONS: These findings indicate that a vascular anti-inflammatory action may underlie the beneficial effects of HES in global cerebral ischemia secondary to asphyxia. Since this compound is well tolerated by patients, future preclinical and clinical studies may reveal improvements in functional outcome with the early introduction of this or similar agents after perinatal asphyxia or global ischemia.

Animals↗
PubMed1984

Effects of asphyxia on lung fluid balance in baby lambs.

The purpose of this study was to assess the effects of combined hypoxia and hypercapnia and of severe asphyxia on lung water balance and protein transport in newborn lambs. We studied ten 2-4-wk-old anesthetized lambs which were mechanically ventilated first with air for 2-3 h, then with 10-12% oxygen in nitrogen for 2-4 h, and then with 10-12% oxygen and 10-12% carbon dioxide in nitrogen for 2-4 h. Next we stopped their breathing for 1-2 min to produce severe asphyxia, after which we followed their recovery in air for 2-4 h. In 5 of the 10 lambs we intravenously injected radioactive albumin and measured its turnover time between plasma and lymph during the baseline period and after recovery from asphyxia. During alveolar hypoxia alone, mean pulmonary arterial pressure increased 60% and lung lymph flow increased 74%, whereas lymph protein concentration decreased from 3.47 +/- 0.13 to 2.83 +/- 0.15 g/dl. Cardiac output, left atrial pressure, and plasma protein concentration did not change. When carbon dioxide was added to the inspired gas mixture, pulmonary arterial pressure increased 22%, cardiac output increased 13%, lung lymph flow increased 33%, and lymph protein concentration decreased from 2.83 +/- 0.15 to 2.41 +/- 0.13 g/dl. Left atrial pressure and plasma protein concentration did not change. After 60-90 s of induced asphyxia, vascular pressures and lung lymph flow rapidly returned to values the same as those obtained during the baseline period. The turnover time for radioactive albumin between plasma and lymph was the same between the baseline and recovery periods (185 +/- 16 vs. 179 +/- 12 min). The ratio of albumin to globulin in lymph relative to the same ratio in plasma did not change during any phase of these experiments. Five lambs killed after recovery from asphyxia had significantly less blood and extravascular water in their lungs than control lambs had. We conclude that in the newborn lamb both alveolar hypoxia and alveolar hypoxia with hypercapnia increase lung lymph flow by increasing filtration pressure in the microcirculation, but neither hypoxia with hypercapnia nor brief severe asphyxia alters the protein permeability of the pulmonary microcirculation.

Animals↗
PubMed1984

The regional distribution and determinants of myocardial blood flow during asphyxia in the fetal lamb.

The syndrome of hypoxemia-related myocardial dysfunction in the newborn is generally associated with severe intrapartum asphyxia. We investigated the changes in total and regional distribution of myocardial blood flow (MBF) that occur during asphyxia and the factors that regulate MBF, in the chronically prepared, near term, fetal lamb. Studies were done in the awake, physiologically stable state 36-72 h after surgical preparation. In utero asphyxia was produced by partial cord occlusion and blood flow to fetal organs was measured by the radioactive microsphere technique. A complete set of control measurements was made, and then an occlusion loop was inflated to partially occlude the umbilical vessels. After 30-60 min of partial occlusion, all measurements were repeated. The third set of measurements was made after release of the occlusion loop. Six animals were studied and 17 sets of measurements obtained. Partial umbilical cord constriction produced a progressive asphyxia and acidosis. Cardiac output was severely depressed, although the increase in percentage of cardiac output directed to the myocardium (%F) was very significant. Release resulted in improved cardiac output and O2 and CO2 exchange, although the metabolic acidosis was worse. No change occurred in the intramyocardial distribution of MBF during asphyxia or recovery. Total MBF was not significantly increased during asphyxia. Multiple linear regression analysis indicated that arterial oxygen saturation (SaO2) and heart rate were statistically significant predictor variables for absolute MBF, accounting for about 45% of the variation in MBF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Comparison of the effect of asphyxia, hypoxia, and acidosis on intestinal blood flow and O2 uptake in newborn piglets.

The aim of our study was to compare the effects of asphyxia and the two components of asphyxia, i.e. hypoxia and acidosis, on intestinal blood flow and oxygen consumption in anesthetized newborn piglets less than 3 days old. The first series of experiments, consisting of four groups of piglets, showed that blood flow to the proximal and distal small intestine and colon (as determined by the microsphere technique) significantly decreased after piglets were subjected to a sustained hypoxic hypoxemia (PaO2 50% of control) or asphyxia (acidosis plus hypoxia) for 90 min. A sustained acidosis (arterial pH = 7.0-7.15 for 90 min), however, decreased blood flow only to the proximal small intestine, and sham operation did not significantly alter any intestinal blood flow. All animals subjected to asphyxia and two of five of the animals subjected to hypoxia alone in this series, produced gross and microscopic intestinal lesions similar to those seen in human newborn with necrotizing enterocolitis. Acidosis alone, however, did not produce any pathologic lesions. The second series of experiments showed that the 90-min hypoxic hypoxemia decreased blood flow to both the mucosa and muscularis layers of the small intestine. The third series of experiments, consisting of four groups of piglets, determined the effects of 60-min acidosis, hypoxic hypoxemia, asphyxia, or sham operation on venous outflow and oxygen consumption of the isolated in situ terminal ileum. Acidosis or sham operation altered neither ileal blood flow nor oxygen consumption. Hypoxia or asphyxia, however, decreased ileal oxygen consumption without significantly decreasing blood flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1995

Effects of a period of asphyxia during birth on spatial learning in the rat.

The present study aimed to test whether an acute period of asphyxia during birth in the rat results in long-term alterations in CNS function. Morphologic studies have indicated that the hippocampus is particularly vulnerable to perinatal anoxia. Thus, the present study tested adult rats, which had undergone acute birth asphyxia, for their performance in spatial learning and memory tasks associated with the hippocampus. Rat fetuses on the day of birth were submitted to an acute period of complete asphyxia by submersion of the isolated uterus into a water bath for 5-20 min before delivery of the pups. Control animals were either born vaginally or delivered by rapid cesarean section. At 1.5 mo of age, rats that had undergone 15 min of birth asphyxia showed no deficit in acquisition of spatial learning, measured as latency to find a hidden platform in the Morris water maze. However, at 4 mo of age, separate groups of rats, which had undergone 10, 15, or 20 min of birth asphyxia, showed a deficit in initial acquisition of the spatial learning task compared with vaginally born controls, whereas the 5-min group performed similarly to controls. After overtraining, there was no difference among groups on short-term (1 wk) retention of the spatial navigation task; however, asphytic animals tested at 1.5 mo and retested at 4 mo showed a slight deficit in retention on retest. Animals that had undergone 15 min of birth asphyxia weighed less than did vaginally born animals, but showed no deficit in swimming ability, spontaneous alternation in a T maze, or other sensorimotor indices.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Cerebral metabolism within 18 hours of birth asphyxia: a proton magnetic resonance spectroscopy study.

Proton magnetic resonance spectroscopy (1H MRS) was performed within 18 h of birth (median 13, range 4-18 h) on 16 term infants with clinical features of birth asphyxia. Ten infants with no evidence of birth asphyxia were studied as controls at 5-18 (median 8) h after birth. To detect delayed impairments in cerebral energy metabolism, 15 infants suspected of asphyxia underwent 31P MRS at 33-106 (median 62) h of age. Choline, creatine, and N-acetylaspartate (NAA) were detected in spectra located to the basal ganglia in all infants. Lactate was detected in 15 of the 16 infants suspected of asphyxia, but in only 4 of the 10 controls (p < 0.05, chi 2). Glutamine and glutamate (Glx) was detected in 11 infants suspected of asphyxia and in three controls, but this difference was not significant at the 5% level. The spectra revealed no other significant differences between asphyxiated infants and controls. In the asphyxiated infants, there was a negative correlation between the ratio of lactate to creatine in the first 18 h of life and phosphocreatine/inorganic phosphate (PCr/ P(i)) at 33-106 h (p < 0.001). Five severely asphyxiated infants had PCr/P(i) < 0.75 (median 0.53, range 0.14-0.65), indicating a poor neurodevelopmental prognosis, and a further infant died before PCr/Pi could be measured. Ten infants had PCr/P(i) > 0.75 (1.03, 0.76-1.49). Median lactate/creatine was 1.47 (range 0.67-3.81) in the six severely affected subjects, 0.38 (0-1.51) in the latter group, and 0 (0-0.6) in controls (p < 0.0005, Kruskall-Wallis). These results suggest that, after birth asphyxia, cerebral energy metabolism is abnormal during the period when 31P MRS characteristically gives normal results. 1H MRS might be of value in predicting which infants are likely to suffer a decline in cerebral high energy phosphate concentrations and subsequent neurodevelopmental impairment.

Asphyxia Neonatorum↗
PubMed1976

[Fetal and neonatal asphyxia].

The literature data and the author's own observations justify the conclusion that asphyxia of the fetus and newborn is the most common cause of death in the perinatal period. The author discusses the significance of asphyxia of the fetus and newborn as the main disease or the principal cause of death. The author suggests that the type of asphyxia of the fetus or newborn in every concrete case should be indicated in the pathologoanatomic diagnosis on the basis of physiology of intrauterine and extrauterine life. In case of asphyxia it is suggested that the question concerning the presence (or absence) of the underlying disease--fetopathy, pre-existing the asphyxia condition--should be considered. In case of asphyxia of the newborn the author recommends to bear in mind the anatomic substrate responsible for impairment of the act of breathing of the newborn. In most cases this substrate is represented by pneumopathies--noninflammatory changes in the lungs of the newborn. Pneumopathies of the newborn include deep aspiration of the amniotic content, atelectasis, edema and hemorrhages, hyaline membranes.

Asphyxia Neonatorum↗