Tuberculosis of the gastrointestinal tract in Bradford, 1967-77.
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Adult↗
Biomedical subjects
D K Stevenson
Publications and source records attributed to D K Stevenson.
Effect of erythrocyte destruction on the pulmonary excretion rate of carbon monoxide in adult male Wistar rats.
One of the major contributory factors to hyperbilirubinemia in the human infant is bilirubin production. Determination of the pulmonary excretion rate of carbon monoxide is used to measure indirectly the rate of bilirubin production by estimating the endogenous production of CO, which is formed in equimolar amounts with bilirubin in the catabolism of heme. There has been no study to confirm that complete recovery of CO produced in vivo from the catabolism of known amounts of heme occurs via pulmonary excretion. We report here quantitative determinations of the pulmonary excretion rate of CO in five adult male Wistar rats after injection of known amounts of heme in the form of red blood cells "damaged" by incubation in a solution containing a sulfhydryl inhibitor, NEM. The mean recovery of "extra" CO above baseline production represented as a molar ratio of extra CO to heme was 0.98 +/- 0.02 (S.E.). Control studies showed no extra CO production after starvation, injection of NEM in an amount comparable to that used in the experimental animals, or injection of undamaged red blood cells.
Animals↗
Pulmonary excretion of carbon monoxide in the human newborn infant as an index of bilirubin production: III. Measurement of pulmonary excretion of carbon monoxide after the first postnatal week in premature infants.
Using a single pass, flow-through system, the excretion rate of endogenously produced carbon monoxide (VeCO) was measured as an index of bilirubin production in 41 Caucasian infants of various gestational ages after the first postnatal week. twenty-one were less than or equal to 32 weeks gestation. The mean slope for the 25 premature infants with multiple VeCO determinations was -0.21 +/- 0.11 (SE) microliters/kg/hour per day (P less than .025, one-tailed). Fifteen premature infants with at least three VeCO determinations during the first 30 days of life had an average decrease in total CO excreted of 1.33% per day compared to the extrapolated initial value of total CO excretion of 27.0 +/- 2.0 (SE) microliters/hour, giving a calculated maximum red cell life span of 75 days.
Bilirubin↗
Hepatic injury in a child caused by trimethoprim-sulfamethoxazole.
Trimethoprim-sulfamethoxazole was given to a 16-year-old boy as prophylaxis for a urinary tract infection. He developed severe cholestatic hepatitis 41 days after administration of the drug. A liver biopsy specimen showed a mixed inflammatory infiltrate in the portal triads and prominent bile stasis. The clinical course in this patient supports the concept of an indirect hypersensitivity reaction to sulfamethoxazole.
Adolescent↗
Necrotizing enterocolitis in the neonate.
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Enterocolitis, Pseudomembranous↗
Pulmonary tuberculosis.
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Adrenal Cortex Hormones↗
A model for detecting early metabolic changes in neonatal asphyxia by 1H-MRS.
In newborn rabbits, the early cerebral metabolic changes caused by hypoxic-ischemic (H-I) insult was examined by using volume localized 1H-MRS (STEAM). Partial ischemia was caused by unilateral carotid artery ligation, and hypoxia was induced by 10% oxygen inspiration for 150 minutes. Lactate immediately increased after hypoxia induction and almost disappeared 120 to 150 minutes after removal of hypoxia in both H-I and hypoxia-only experiments. Lactate production correlated well with decrease of the blood oxygen saturation. More lactate was produced on ischemic side 50 minutes post-hypoxia induction in H-I study. Ischemia alone did not cause any significant lactate production. Lactate caused by hypoxia can be dynamically monitored by localized 1H-MRS. Existence of regional ischemia can induce greater anaerobic glycolysis and may affect the pattern of brain injury under hypoxia. 1H-MRS is a sensitive tool to detect the acute metabolic change caused by H-I insult.
Animals↗
Diffusion and perfusion magnetic resonance imaging of the evolution of hypoxic ischemic encephalopathy in the neonatal rabbit.
Hypoxic-ischemic encephalopathy (HIE) can result from neonatal asphyxia, the pathophysiology of which is poorly understood. We studied the acute evolution of this disease, using magnetic resonance imaging in an established animal model. HIE was induced in neonatal rabbits by a combination of common carotid artery (CCA) ligation and hypoxia. Serial diffusion and perfusion-weighted magnetic resonance images were acquired before, during, and after the hypoxic interval. Focal areas of decreased apparent diffusion coefficient (ADC) were detected initially in the cortex ipsilateral to CCA ligation within 62 +/- 48 min from the onset of hypoxia. Subsequently, these areas of decreased ADC spread to the subcortical white matter, basal ganglia (ipsilateral side), and then to the contralateral side. Corresponding perfusion-weighted images showed relative cerebral blood volume deficits which closely matched those regions of ADC change. Our results show that MRI diffusion and perfusion-weighted imaging can detect acute cell swelling post-hypoxia in this HIE model.
Animals↗
Clinical observations on mechanical ventilation for respiratory failure in bronchiolitis.
An unusually large number of infants (82) were admitted to Stanford University Hospital from November 1, 1983, through May 31, 1985, with a diagnosis of bronchiolitis requiring oxygen therapy. A larger percentage of these infants (17/82 = 21%) than generally expected required mechanical ventilation for respiratory failure. Fourteen infants had respiratory syncytial virus (RSV) infections, and three had parainfluenza virus infections. Ten patients had respiratory difficulties as neonates. The mechanical ventilation of the children requiring respiratory assistance was characterized by high minute ventilation with high tidal volumes (15 to 20 ml/kg) and slow respiratory rates (16 to 22 breaths/min). Peak inspiratory pressure averaged (mean +/- SD) 35 +/- 6 cm H2O in the RSV group and 34 +/- 6 cm H2O in the parainfluenza group. The mean number of days on the ventilator was 9.7 +/- 3.1 for the RSV group and 8.3 +/- 2.9 for the parainfluenza group. All were extubated within 17 days of presentation and discharged within 28 days. The complications encountered included pneumothorax and acute pulmonary hypertension.
Bronchiolitis, Viral↗
Heme oxygenase activity and acute and chronic ethanol exposure in the hippocampus, frontal cerebral cortex, and cerebellum of the near-term fetal guinea pig.
Heme oxygenase (HO) catalyzes the oxidation of heme to produce carbon monoxide, which is considered to be a novel neuronal messenger in the brain and may play a role in neuronal development. The objective of this study was to determine the effects of in vitro, acute in vivo, and chronic in vivo ethanol exposure on HO activity in the hippocampus, frontal cerebral cortex, and cerebellum of the near-term fetal guinea pig. HO activity was determined using a gas chromatographic method to quantitate CO formation in the microsomal fraction of the homogenate of each selected brain region, incubated with saturating concentrations of heme, NADPH, and O2. Fetal body, brain, hippocampal, and cerebellar weights were recorded. In vitro ethanol exposure (25-100 mM) did not affect hippocampal, cerebral cortical, or cerebellar HO activity of the fetal guinea pig at gestational day (GD) 62 (term, about GD 68). Acute maternal oral administration of 4 g ethanol/kg maternal body weight at GD 62 did not affect HO activity in these three fetal brain areas compared with control fetuses (maternal administration of isocaloric sucrose or water). For chronic daily maternal oral administration of 4 g ethanol/kg maternal body weight throughout gestation, fetal body, brain, hippocampal, and cerebellar weights were decreased at GD 62 compared with isocaloric-sucrose/pair-fed and water treatment control groups. Furthermore, isocaloric-sucrose/pair-feeding treatment decreased fetal body and brain weights compared with water treatment. Chronic in vivo ethanol exposure did not alter HO activity in the near-term fetal hippocampus, frontal cerebral cortex, or cerebellum. This is the first study of the effect of ethanol exposure on HO activity in the developing brain of any species. The data demonstrate, for ethanol CNS teratogenesis in the guinea pig manifesting as fetal brain growth restriction, there is no associated change in HO activity in the hippocampus, frontal cerebral cortex, or cerebellum.
Animals↗
Bilirubin toxicity and differentiation of cultured astrocytes.
OBJECTIVE: To study the toxicity of bilirubin in primary cultures of newborn rat cerebral cortical astrocytes. STUDY DESIGN: Primary cultures of newborn rat astrocytes were incubated at bilirubin concentrations of 0, 1, 5, 10, 25, 50, 100, 200, and 2000 microM, at a bilirubin:albumin molar ratio of 1.7. Bilirubin toxicity was determined by changes in cellular morphology, trypan blue staining, and lactate dehydrogenase (LDH) release into the culture medium at various times of incubation. To determine if differentiation of astrocytes affects bilirubin toxicity, cultures were treated with dibutyryl cyclic adenosine monophosphate. RESULTS: All three indices of toxicity showed a bilirubin concentration dependence. LDH release in experimental cultures was significantly elevated (p < 0.05) above that of control cultures by 24 hours at bilirubin concentrations of > or = 100 microM. The absolute amount of LDH release differed significantly between the 200 and 2000 microM cultures from 1.5 to 24 hours, after which duration of exposure appeared to take over and all cultures approached maximum. LDH release for the lower concentrations all reached maximum by 120 hours, except for the 1 microM cultures, which showed no significant elevation above control throughout the study period. At 100 and 200 microM bilirubin, LDH release by untreated cells was significantly higher (p < 0.05) than release by treated cells by 36 hours. CONCLUSION: Undifferentiated astrocytes appeared to be more sensitive to bilirubin toxicity, which may correlate with the greater susceptibility of newborns to kernicteric injury. Studies with primary astrocyte culture may provide insight into how bilirubin sensitivity changes with brain development as well as the cellular and biochemical mechanisms of bilirubin encephalopathy.
Animals↗
Noninvasive validation of tobacco smoke exposure in late pregnancy using end-tidal carbon monoxide measurements.
OBJECTIVE: To determine whether exposure to tobacco smoke in late pregnancy can be reliably estimated by measuring carbon monoxide (CO) in the mother and newborn breath. STUDY DESIGN: Sixty-eight mothers and their healthy term singleton newborns, delivered at a university-affiliated community hospital in Jerusalem, were enrolled. End-tidal CO (corrected for inhaled air [ETCOc] was measured with a portable automated bedside CO analyzer. ETCOc, cotinine, and carboxyhemoglobin (COHb) levels were compared in 17 smoking, 31 passively exposed, and 20 nonsmoking mothers and their offspring. RESULTS: The mean +/- SD ETCOc was significantly higher in women who smoked than in passively exposed and nonsmoking mothers (8.42 +/- 5.65 vs 1.95 +/- 0.98 vs 1.33 +/- 0.84 ppm. p < 0.0001, respectively). Newborns whose mothers smoked had higher ETCOc levels than those of infants of passively exposed and nonsmoking mothers (10.0 +/- 7.7 vs 2.51 +/- 1.4 vs 1.74 +/- 0.98 ppm, p < 0.0001, respectively). The number of cigarettes smoked by the mother was significantly correlated with maternal ETCOc (r = 0.755, p < 0.00001), and neonatal ETCOc (r = 0.805, p < 0.00001). Maternal ETCOc was highly correlated with neonatal ETCOc (r = 0.857, p < 0.00001), cotinine (r = 0.645, p < 0.00001), and COHb (r = 0.9, p < 0.00001) levels. Birth weight was significantly associated with neonatal ETCOc (p < 0.006) and maternal ETCOc (p < 0.007). CONCLUSION: ETCOc levels in the newborn are well correlated with maternal smoking. Measurements of newborn ETCOc may be used as a noninvasive means to estimate exposure to maternal tobacco smoke immediately before delivery. These measurements will be useful for patient education and research.
Birth Weight↗
On the 25th anniversary of the Section on Perinatal Pediatrics: historical foresight.
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Forecasting↗
Hyperbilirubinemia and early discharge.
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Humans↗
Gd-DTPA MR detection of blood-brain barrier opening in rats after hyperosmotic shock.
OBJECTIVE: Detection of blood-brain barrier (BBB) opening in neonates has required invasive methods not clinically applicable. We set out to develop a noninvasive approach to detect such opening. MATERIALS AND METHODS: Wistar rats were studied using MRI with Gd-DTPA contrast before and after injection of hyperosmotic solutions known to produce barrier opening. Arabinose was given via right carotid artery to produce unilateral barrier opening; urea was given via tail vein to produce bilateral opening; controls received normal saline. Next, all animals received Gd-DTPA via tail vein. RESULTS: Animals receiving carotid hyperosmotic injections showed increased signal in the ipsilateral brain hemisphere; those receiving venous hyperosmotic injections showed increased signal bilaterally. Similar increases were not found prior to administration of hyperosmotic agent or in saline controls. In both cases, barrier opening was detectable using the relative partitioning of Gd-DTPA between intrabarrier and extrabarrier structures, even in the absence of a hemispheric control. CONCLUSION: We conclude that MRI with Gd-DTPA contrast allows noninvasive detection of BBB opening in the rat.
Animals↗
Red cell destruction and bilirubin production in adult rats with short-term biliary obstruction.
The rate of total bilirubin production and the concomitant relative rate of early-labeled bilirubin (ELB) formation were studied in adult Wistar rats with short-term common bile duct ligation. The pulmonary excretion rate of CO (VeCO), an index of total bilirubin production, was measured preoperatively and postoperatively on day 3 and on day 5 or 6. While the VeCO measurements of control and experimental animals were similar preoperatively, the postoperative VeCO measurements of the experimental animals averaged 30% higher than those of control animals. On postoperative day 3, the relative rate of ELB formation was measured by the recovery of excreted 14CO after the administration of 14C-labeled delta-aminolevulinic acid (ALA) or glycine as nonerythropoietic or total heme synthesis precursor, respectively. No significant differences were found in the 14CO recovered from either compound during the study period between the experimental and control animals. The half-life of 51Cr-labeled transfused red blood cells was decreased by nearly 50% in bile duct ligated rats compared to that in the sham operated ones. We conclude that hemolysis is a major factor contributing to the increase in total bilirubin production even after short-term biliary obstruction in the rat.
Animals↗
Recovery of exogenous heme as carbon monoxide and biliary heme in adult rats after tin protoporphyrin treatment.
We studied the effect of tin protoporphyrin (TP) on bilirubin production in adult Wistar rats by quantifying in vivo carbon monoxide (CO) excretion and the simultaneous excretion of biliary heme after common bile duct cannulation. A known amount of heme was injected intravenously as red blood cells (RBC) damaged with a sulfhydryl inhibitor, N-ethylmaleimide. The recovery of heme as CO or biliary heme in the cannulated animals was calculated as the molar percent of heme recovered over heme injected. For cannulated controls (n = 4), the recovery was 89 +/- 6% SD, and no heme appeared in bile. Cannulated rats treated with TP (n = 4) had 64 +/- 11% recovered as CO and 30 +/- 11% as heme in bile. Our findings suggest that TP is an effective in vivo inhibitor of exogenous heme catabolism and bilirubin production in adult rats. Furthermore, this inhibition results in increased excretion of heme into the bile proportional to the degree of inhibition.
Animals↗
Carboxyhemoglobin concentration as an index of bilirubin production in neonates with birth weights less than 1,500 grams: a randomized double-blind comparison of supplemental oral vitamin E and placebo.
A randomized double-blind study of the efficacy of oral vitamin E supplementation as a prophylactic treatment for hyperbilirubinemia was undertaken in preterm infants weighing less than 1,500 g. Hemoglobin (Hb) levels, blood carboxyhemoglobin saturation (HbCOc), end-tidal carbon monoxide concentration (ETCO), and serum total bilirubin levels were determined in each subject on the first and third days of the study. We found no differences between the vitamin E-treated and placebo-treated groups with respect to Hb, HbCOc, ETCO, or serum bilirubin levels on day 1 or 3. In addition, we reanalyzed our data to compare those infants who had low vitamin E levels at birth with those who had vitamin E levels greater than 0.4 mg/dl on day 1. We still observed no differences in Hb, HbCOc, ETCO, or serum bilirubin levels on day 1 or 3. The results of our study suggest that supplemental oral vitamin E therapy has no major effect on bilirubin production during the first 3 days of life in premature infants weighing less than 1,500 g at birth.
Administration, Oral↗