The cardiovascular and cerebrovascular responses of the immature fetal sheep to acute umbilical cord occlusion.
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1. In premature fetal sheep (89-93 days gestation) we examined the fetal response to asphyxia induced by 30 min of complete umbilical cord occlusion. Fetuses were also studied during the first 3 days after asphyxia. We measured heart rate, blood pressure, carotid and femoral blood flows, vascular resistance, electroencephalographic activity and cerebral changes in haemoglobin concentration by near infrared spectroscopy (NIRS). 2. Fetuses tolerated 30 min of asphyxia and the cardiovascular response was characterized by three phases: initial redistribution of blood flow away from the periphery to maintain vital organ function, partial failure of this redistribution and near terminal cardiovascular collapse, with profound hypotension and cerebral and peripheral hypoperfusion. 3. Post-asphyxia carotid blood flow and NIRS data demonstrated that between 3-5 h there was a significant secondary reduction in cerebral blood flow, blood volume and oxygenation despite normal perfusion pressure and heart rate. There was also a secondary fall in femoral blood flow which persisted throughout recovery. 4. These data demonstrate that the immature fetus can survive a prolonged period of asphyxia, but paradoxically the capacity to survive exposes the fetus to profound hypotension and hypoperfusion. A secondary period of significant cerebral hypoperfusion and reduced oxygen delivery also occurred post-asphyxia. These cardiovascular and cerebrovascular responses may contribute to the patterns of cerebral injury seen in the human preterm fetus. (+info)
Visual function in term infants with hypoxic-ischaemic insults: correlation with neurodevelopment at 2 years of age.
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AIMS: To determine if there is any association between the findings of visual assessment performed at the age of 5 months and neurodevelopmental outcome at the age of 2 years in children who have sustained hypoxic-ischaemic insults. METHODS: Twenty nine term infants with hypoxic-ischaemic encephalopathy and/or brain lesions on neonatal magnetic resonance imaging (MRI) were prospectively evaluated. At 5 months of age all the infants had their visual function assessed using the Atkinson Battery of Child Development for Examining Functional Vision, which includes the assessments of optokinetic nystagmus (OKN), acuity, visual fields, fixation shift and phase and orientation reversal visual evoked potentials. At 2 years of age the children had a structured neurological evaluation and a Griffiths developmental assessment. RESULTS: There was good correlation between the extent of the early detected visual impairment and both neuromotor and global development. Children with more than three out of five abnormal visual tests at 5 months of age tended to have abnormal neurological examination results and abnormal developmental quotients. Children with three or fewer abnormalities tended to have developmental quotients in the normal range; the level of their performance, however, was still related to the number of visual tests passed. CONCLUSIONS: Individual visual tests can provide important prognostic information. While abnormal OKN and acuity were always associated with abnormal outcome, normal results on visual evoked potentials and fixation shift tended to be associated with normal outcome. (+info)
Does endothelin-1 reduce superior mesenteric artery blood flow velocity in preterm neonates?
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AIM: To compare plasma endothelin-1 (ET-1) concentrations in preterm neonates from pre-eclamptic and normal mothers; and to evaluate whether ET-1 has a role in altered arterial blood flow velocity. METHODS: Umbilical arterial blood and neonatal arterial blood were sampled on days 1 and 3 for gas analysis and measurement of plasma ET-1. Doppler ultrasonography of the middle cerebral, renal, and superior mesenteric arteries (SMA) was performed. RESULTS: Neonates in the pre-eclampsia (n = 18) and control (n = 18) groups had mean (SD) gestational ages of 31.1 (2.5) weeks and 30.4 (2.1) weeks; their birth-weights were 1432 (SD 676) g and 1692 (SD 500) g, respectively. In the pre-eclampsia group mean umbilical arterial PO2 was lower--1.88 (0.75) kPa compared with 3.27 (1.41) kPa (p < 0.01)--and mean plasma ET-1 concentration was higher in the umbilical artery--40.6 (SD 15.0) compared with 30.5 (SD 13.8) pg/ml (p = 0.04) and day 1 blood--54.9 (35.0) pg/ml compared with 33.6 (14.6) pg/ml (p = 0.03). Middle cerebral artery peak systolic velocity was higher and SMA time averaged, peak systolic, and mean peak velocities were lower in the pre-eclampsia group. SMA time averaged velocity was inversely related to plasma ET-1 concentration. CONCLUSION: The association between increased production of ET-1 and reduction in SMA time averaged velocity suggests a possible mechanism for hypoperfusion of the intestinal wall in neonates. (+info)
Chronic hypoxemia: effects on developing nitrergic and dopaminergic amacrine cells.
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PURPOSE: Very low birth weight and growth-restricted children have visual impairments including reduced contrast sensitivity, a parameter mediated in part by dopaminergic amacrine cells. The origin of these deficits is uncertain. In experimental fetal growth restriction, induced by placental insufficiency, the morphology and number of dopaminergic amacrine cells as identified by tyrosine hydroxylase staining were examined. In addition, the subclass of nitrergic amacrine cells was examined because nitric oxide released from nitric oxide synthase- containing neurons is proposed as a mediator of neurotoxicity and might contribute to the injury of dopaminergic amacrine cells in this situation. METHODS: Fetal sheep were subjected to 20 or 30 days of placental embolization leading to fetal hypoxemia, hypoglycemia, and growth restriction during the last third of gestation (term, approximately 147 days). Retinal tissue was prepared as wholemounts or cryostat sections and analyzed for retinal area, total number, density, somal size and cell process length of amacrine cells immunoreactive for tyrosine hydroxylase or nitric oxide synthase, and widths of retinal layers. Retinas from fetal sheep at 72, 96, 113, and 140 days' gestation and adults were collected for an ontogenetic study of tyrosine hydroxylase-immunoreactive neurons. RESULTS: In growth-restricted fetuses, the number of tyrosine hydroxylase-immunoreactive neurons and the total length of stained processes per cell were significantly reduced compared to control fetuses. The total number of neuronal nitric oxide synthase- containing neurons was not different between growth-restricted and control fetuses. The thickness of the inner retinal layers was reduced in hypoxemia. CONCLUSIONS: There is damage to tyrosine hydroxylase-immunoreactive amacrine cells during fetal chronic placental insufficiency. This damage might be involved in the altered retinal dopaminergic system observed in very low birth weight infants, some of whom are growth-restricted. Furthermore, a differential susceptibility of tyrosine hydroxylase-immunoreactive and neuronal nitric oxide synthase-containing amacrine cells to hypoxemic injury has been demonstrated. These observations add to the current hypothesis that neuronal nitric oxide synthase- containing neurons are resistant to hypoxemic injury and may be involved in mediating some of the neuronal damage that results from hypoxemic insults. (+info)
Metabolic and cardiorespiratory responses to hypoxia in fetal sheep: adenosine receptor blockade.
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8-Phenyltheophylline (PT), a potent and specific inhibitor of adenosine receptors, was infused intra-arterially into unanesthetized fetal sheep to determine the role of adenosine in hypoxic inhibition of fetal breathing. PT in normoxic fetuses increased heart rate and the incidence of low-voltage electrocortical activity, rapid eye movements (REM), and breathing. Mean breath amplitude increased by 44%. Hypoxia (preductal arterial PO2 = 14 Torr) induced a metabolic acidemia, a transient bradycardia, and hypertension while virtually eliminating REM and breathing. PT administration during hypoxia enhanced the metabolic acidemia, blocked the bradycardia and hypertension, increased the incidence of REM and breathing, and elevated mean breath amplitude. The results indicate that 1) adenosine is involved in fetal glycolytic and cardiovascular responses to hypoxia, 2) activation of central adenosine receptors mediates about one-half the inhibitory effects of hypoxia on REM and breathing, and 3) the depression of breathing may critically depend on a hypoxia-induced reduction in phasic REM sleep. (+info)
Measurement of the urinary lactate:creatinine ratio for the early identification of newborn infants at risk for hypoxic-ischemic encephalopathy.
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BACKGROUND: Newborn infants with perinatal asphyxia are prone to the development of hypoxic-ischemic encephalopathy. There are no reliable methods for identifying infants at risk for this disorder. METHODS: We measured the ratio of lactate to creatinine in urine by proton nuclear magnetic resonance spectroscopy within 6 hours and again 48 to 72 hours after birth in 58 normal infants and 40 infants with asphyxia. The results were correlated with the subsequent presence or absence of hypoxic-ischemic encephalopathy. RESULTS: Hypoxic-ischemic encephalopathy did not develop in any of the normal newborns but did develop in 16 of the 40 newborns with asphyxia. Within six hours after birth, the mean (+/-SD) ratio of urinary lactate to creatinine was 16.75+/-27.38 in the infants who subsequently had hypoxic-ischemic encephalopathy, as compared with 0.09+/-0.02 in the normal infants (P<0.001) and 0.19+/-0.12 in the infants with asphyxia in whom hypoxic-ischemic encephalopathy did not develop (P<0.001). A ratio of 0.64 or higher within six hours after birth had a sensitivity of 94 percent and a specificity of 100 percent for predicting the development of hypoxic-ischemic encephalopathy. The sensitivity and specificity of measurements obtained 48 to 72 hours after birth were much lower. The mean ratio of urinary lactate to creatinine was significantly higher in the infants who had adverse outcomes at one year (25.36+/-32.02) than in the infants with favorable outcomes (0.63+/-1.50) (P<0.001). CONCLUSIONS: Measurement of the urinary lactate: creatinine ratio soon after birth may help identify infants at high risk for hypoxic-ischemic encephalopathy. (+info)
Hemodynamic and metabolic responses to moderate asphyxia in brain and skeletal muscle of late-gestation fetal sheep.
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The purpose of this study was to investigate metabolic and hemodynamic responses in two fetal tissues, hindlimb muscle and brain, to an episode of acute moderate asphyxia. Near-infrared spectroscopy was used to measure changes in total hemoglobin concentration ([tHb]) and the redox state of cytochrome oxidase (COX) simultaneously in the brain and hindlimb of near-term unanesthetized fetal sheep in utero. Oxygen delivery (DO(2)) to, and consumption (VO(2)) by, each tissue was derived from the arteriovenous difference in oxygen content and blood flow, measured by implanted flow probes. One hour of moderate asphyxia (n = 11), caused by occlusion of the maternal common internal iliac artery, led to a significant fall in DO(2) to both tissues and to a significant drop in VO(2) by the head. This was associated with an initial fall in redox state COX in the leg but an increase in the brain. [tHb], and therefore blood volume, fell in the leg and increased in the brain. These data suggest the presence of a fetal metabolic response to hypoxia, which, in the brain, occurs rapidly and could be neuroprotective. (+info)
Fetal complications of obstetric cholestasis.
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Among 56 pregnancies complicated by obstetric cholestasis five intrauterine deaths and one neonatal death occurred between 33 and 39 weeks, and a further six infants required urgent delivery for intrapartum asphyxia. Eighteen spontaneous premature deliveries occurred. Five mothers required specific treatment for unexplained postpartum haemorrhage. Cholestasis of pregnancy is therefore not a condition benign to the fetus, and it may contribute to increased maternal morbidity. (+info)