Chronic active hepatitis associated with oxyphenisatin.
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Cathartics↗
Biomedical subjects
J D Reynolds
Publications and source records attributed to J D Reynolds.
Painful sickle cell crisis. Successful treatment with hyperbaric oxygen therapy.
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Abdomen, Acute↗
Treatment of hepatic coma. Treatment of acute hepatic coma with plasmaphoresis and plasma exchange.
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Acute Disease↗
The role of adenosine A1 receptor activation in ethanol-induced inhibition of stimulated glutamate release in the hippocampus of the fetal and adult guinea pig.
The role of adenosine A1 receptor activation in ethanol-induced inhibition of stimulated L-glutamate (Glu) release was determined in transverse hippocampal slices of the near-term fetal guinea pig and the adult guinea pig. Exposure of the slices to 48 mM ethanol inhibited K(+)-stimulated Glu efflux. Pretreatment with 8-cyclopentyltheophylline (CPT), a selective adenosine A1 receptor antagonist, blocked the ethanol-induced inhibition of K(+)-stimulated Glu efflux in the near-term fetal and adult hippocampus. In the near-term fetus, 2-chloro-N6-cyclopentyladenosine (CCPA), a selective adenosine A1 agonist, and exogenous adenosine each blocked K(+)-stimulated Glu efflux similar to that produced by 48 mM ethanol. In the adult, although K+ increased Glu efflux in the presence of CCPA or adenosine, the magnitude of increase was less than that of the K(+)-stimulated Glu efflux for the control conditions. Exposure to ethanol alone or ethanol plus CPT produced a transient increase in endogenous adenosine efflux in the near-term fetal and adult hippocampus, which was not temporally related to the ethanol-induced inhibition of K(+)-stimulated Glu efflux. Overall, the data indicate that adenosine A1 receptor activation mediates ethanol-induced inhibition of stimulated Glu release in the hippocampus of the near-term fetal and adult guinea pig.
Adenosine↗
Effects of acute ethanol exposure on glutamate release in the hippocampus of the fetal and adult guinea pig.
The effects of in vitro and/or acute in vivo ethanol exposure on L-glutamate (GLU) release were determined in transverse hippocampal slices of the adult guinea pig and the immature and mature fetal guinea pig. In vitro ethanol (34-110 mM) exposure produced age-dependent and narrow concentration range-dependent depressant effects on K(+)-stimulated and basal GLU release, in which the fetal hippocampus was more sensitive than the adult. For acute in vivo ethanol exposure, the hippocampal slices were prepared 1 h after oral intubation of 4 g ethanol/kg body weight. In vivo ethanol exposure produced a persistent depressant effect on stimulated GLU release in the fetus and no effect in the adult. After acute in vivo ethanol treatment, in vitro ethanol (48 mM) exposure also decreased stimulated GLU release in the hippocampus of the immature and mature fetus and decreased basal GLU release only in the immature fetus. Furthermore, this acute in vivo/in vitro ethanol regimen did not affect stimulated or basal GLU release in the adult, which is indicative of tolerance development. Overall, the data indicate that ethanol depresses GLU release in the hippocampus of the guinea pig and that the fetal hippocampus is more susceptible to these depressant effects.
Aging↗
Nitric oxide synthase activity in the hippocampus, frontal cerebral cortex, and cerebellum of the guinea pig: ontogeny and in vitro ethanol exposure.
Decreased nitric oxide (NO) formation, resulting from inhibition of NO synthase (NOS), may be important in the pathogenesis of ethanol central nervous system teratogenesis. The objectives of this study were to determine the ontogeny of NOS activity in the hippocampus, frontal cerebral cortex, and cerebellum of the developing guinea pig, and to test the hypothesis that direct exposure to ethanol inhibits NOS activity in these brain regions at selected developmental ages. NOS activity was quantitated by an optimized radiometric assay. The ontogeny study demonstrated that NOS activity in the hippocampus and frontal cortex was not fully developed prenatally, and apparently increased during postnatal life to attain adult level of activity at postnatal day > 60. In the cerebellum, NOS activity increased during prenatal life to an apparent maximum in the mature near-term fetus at gestational day 63 (term, about 68 days), and then apparently declined during postnatal life to attain adult level of activity. In vitro ethanol exposure (25-100 mM) did not affect NOS activity in the hippocampus, frontal cortex, or cerebellum at any developmental age studied. These data indicate that, although the ontogeny of NOS activity varies between brain regions, ethanol does not directly affect NOS activity in the developing guinea pig. The effects of acute and chronic in utero ethanol exposure on NOS activity in these brain regions are currently being investigated.
Aging↗
Ethanol increases uterine blood flow and fetal arterial blood oxygen tension in the near-term pregnant ewe.
Fetal hypoxia is a hypothesized mechanism of ethanol teratogenesis. The objective of this study was to test this hypothesis by determining the effects of maternal ethanol infusion on uterine blood flow (UBF) and fetal oxygen status. UBF was measured with an electromagnetic flow probe placed around the left maternal uterine artery of the surgically recovered instrumented near-term pregnant sheep at 124 +/- 3 days of gestation (term = 147 days). Experimental treatment involved maternal infusion of 2 g (n = 3) or 4 g (n = 5) ethanol/kg maternal body weight, or 0.9% saline (n = 4) over a 5-h period. Arterial blood samples were collected at regular intervals to monitor maternal ethanol concentration and fetal PO2. Maternal ethanol infusion produced a dose-dependent increase (p = 0.0009) in UBF. Ethanol infusion also increased (p = 0.03) fetal arterial PO2. Overall, these findings indicate that fetal hypoxia is not a mechanism of ethanol teratogenesis.
Abnormalities, Drug-Induced↗
Bolus maternal cocaine administration does not produce a large increase in fetal sheep cerebral cortical glutamate concentration.
Human cocaine use during pregnancy may result in postnatal neurologic dysfunction and abnormal behavior. L-Glutamate, the major excitatory neurotransmitter in the brain, plays an important role in cerebral cortical development. An optimal level of glutamate is required for normal neuronal development. We tested whether acute cocaine exposure produces large increases in glutamate release in the intact cerebral cortex of the near-term fetal sheep. Cocaine 3.0 mg kg(-1) IV bolus produced the expected increase in maternal and fetal mean arterial pressure, increase in fetal heart rate, decrease in uterine blood flow, and decrease in fetal arterial blood pO2 (N = 5). The percentage increases in extracellular glutamate concentration in the fetal cerebral cortex measured by in utero microdialysis were 7%, 15%, 17%, 17%, and 43% in each fetus (upper 95% confidence bound for the median = 43%). We conclude that if cocaine increases glutamate concentration in the developing cerebral cortex, the increase in magnitude is small relative to the changes produced by other interventions such as ethanol or umbilical cord occlusion. Mechanisms other than increases in cerebral cortical glutamate concentration probably contribute to the neurologic injury associated with prenatal cocaine exposure.
Animals↗
Chronic ethanol exposure during late gestation produces behavioral anomalies in neonatal lambs.
A total of 45 pregnant ewes were assigned to one of three treatment groups: 1 g ethanol/kg maternal body weight (n = 18); pair-fed control (n = 15); and ad lib control (n = 12). Dosing started at gestational day (GD) 106, and was administered every other day until GD 134. Parturition occurred between GD 144 and 147. Analysis of the placentas indicated that ethanol exposure decreased cotyledon diameter and cotyledon weight compared to the control groups (p < 0. 05). At birth, lambs were given a Vigor Score and then behavior was assessed using a videotape monitoring system for 24 h. Offspring in the ethanol treatment group were significantly less vigorous at birth (p < 0.05). This finding reversed during the subsequent 24 h such that the ethanol-exposed lambs were significantly more active (p = 0.001) than the control lambs. Morphometric and histologic examination of the cerebral cortex and hippocampus revealed no differences amongst the three treatment groups. Collectively, the data demonstrate that moderate ethanol exposure during the third-trimester equivalent of gestation can produce placental dysmorphology and postnatal behavioral anomalies in neonatal lambs in the absence of gross neurologic injury.
Abortion, Spontaneous↗
An eleven-year study of chlorinated hydrocarbon insecticide residues in bovine fat in Illinois, 1972-1982.
Bovine fat samples in Illinois were monitored for residues of chlorinated hydrocarbon insecticides from 1972 through 1982. The percentage of fat samples that were contaminated with all chlorinated hydrocarbons decreased during the 11-year study. The percentage of samples contaminated with DDT and its analogs decreased most markedly from 82.4% in 1972 to 2.1% in 1982. The percentage of samples contaminated with aldrin/dieldrin and heptachlor/heptachlor epoxide began to decline in 1980 and continued to decrease through 1982.
Adipose Tissue↗
Intravenous magnesium sulfate does not increase ventricular CSF ionized magnesium concentration of patients with intracranial hypertension.
Magnesium sulfate has attracted interest as a potential neuroprotectant but passage of magnesium ion into the central nervous system has not been well documented. For this study, we quantified plasma and cerebrospinal fluid (CSF) ionized magnesium concentration after systemic magnesium sulfate infusion in patients with intracranial hypertension. Patients ( N = 9) received an intravenous infusion of 5 g/20 mmol magnesium sulfate (125 mL of a 4% wt/vol solution) over 30 minutes. Before and after dosing, CSF (from an indwelling ventricular catheter) and blood samples were collected at hourly intervals. Ionized magnesium concentration in all samples was determined using an electrolyte analyzer. Baseline plasma and CSF ionized magnesium concentrations were 0.58 +/- 0.05 and 0.82 +/- 0.06 mmol/L, respectively. Intravenous magnesium sulfate infusion significantly increased plasma ionized magnesium concentration (peak, 0.89 +/- 0.11 mmol/L), but CSF magnesium levels did not change during the 4-hour study. Systemic administration of magnesium sulfate failed to increase CSF ionized magnesium concentration in patients with intracranial hypertension despite increasing plasma magnesium levels by >50%.
Adolescent↗
Hyperplastic persistent pupillary membrane--surgical management.
Two infants, aged three days and six weeks, respectively, presented with dense extensive persistent pupillary membranes as sporadic isolated findings. A clear central pupillary aperture was unable to be achieved with mydriatic agents. The patients were treated by surgical removal of the membranes at age five days and six months respectively. Surgery was without complication and visual development has been normal. We suggest that early intervention in the first weeks or months of life is necessary to prevent the development of amblyopia. If mydriasis is unsuccessful, surgery is recommended followed by optical correction and occlusion therapy as necessary.
Anterior Chamber↗
Ocular abnormalities in terminal deletion of the long arm of chromosome seven.
Patients with distal deletions of the long arm of chromosome 7q have been reported with a variety of non-specific findings. Ocular findings have been limited to hypertelorism, palpebral fissure abnormalities, strabismus and speckled irides and no intraocular pathology with the exception of one case with unilateral optic nerve coloboma. We report a patient with terminal deletion of the long arm of chromosome 7 with marked ocular abnormalities including severe microphthalmus and large retinal colobomas.
Chromosome Deletion↗
Blood oxygen, carbon dioxide and pH levels prior to diagnosis of retinopathy of prematurity.
We examined the eyes of all infants in our Neonatal Intensive Care Unit from 1979 to 1981 who were premature and/or had exposure to increased ambient oxygen. From these 1,012 neonates, 19 were found to have Grade III or worse acute retinopathy of prematurity (ROP) in at least one eye. We studied the graphic relationship of the mean daily values for blood Pc02, Pa02, PC02, and pH and the production of retinopathy of prematurity in these infants and compared the results with a similar group of infants who had similar birthweight, gestational age and Vitamin E administration. The comparison group patients were in the hospital during this same period of time and did not have Grade III ROP. There was no characteristic level, peak or pattern of these values that could identify or predict which infants would develop ROP.
Age Factors↗
Subnormal binocular vision in the Williams syndrome.
PURPOSE: Patients with Williams syndrome have been found to have a high prevalence of strabismus. This may be due to a primary sensory abnormality. The purpose of this study was to determine the prevalence of subnormal binocular vision in patients with Williams syndrome. METHODS: Patients being followed in an interdisciplinary Williams syndrome clinic were prospectively evaluated to determine their binocular status. RESULTS: Eleven patients with Williams syndrome underwent an ophthalmologic evaluation. Twenty-seven percent of patients had strabismus (3/11). Eight patients demonstrated no measurable strabismus. Six of these patients were found to have monofixation syndrome. CONCLUSIONS: There is a high prevalence of subnormal binocular vision in Williams syndrome. This subnormal binocular vision may explain the high prevalence of strabismus in this syndrome.
Adolescent↗
Perioperative care of the strabismus patient.
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Follow-Up Studies↗