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Biomedical subjects

O B Evans

Publications and source records attributed to O B Evans.

At least 19 recordsLinked to original sources
PubMed1991

Fructose-1,6-bisphosphate, when given immediately before reoxygenation, or before injury, does not ameliorate hypoxic ischemic injury to the central nervous system in the newborn pig.

BACKGROUND AND METHODS: We demonstrated earlier in our laboratories that fructose-1,6-bisphosphate (FDP) would improve the outcome of hypoxic ischemic injury to the brain in the adult rabbit. Since many human newborns suffer hypoxic injury to the brain, with a secondary ischemic component due to hypoxic cardiac failure, we set out to reproduce similar experiments in newborn piglets. Hypoxic ischemic CNS damage was induced by ligating both carotid arteries and reducing BP to 66% of normal for 30 min; in the last 15 min, FIO2 was reduced to 0.6. Twelve piglets were randomized to receive either 175 mg/kg of FDP in the last 5 min before reoxygenation or the equivalent volume of saline. The other 20 piglets received 75 mg/kg of FDP in the 5 min immediately before carotid ligation, followed by 1.8 mg/kg.min continuous infusion for the 30 min of hypoxia and ischemia or an equivalent volume of saline. RESULTS: There were no significant differences in the neurologic exam scores or pathologic exam scores between the FDP and control animals at either dose level. CONCLUSIONS: In this animal model, FDP at the doses given was not effective in ameliorating hypoxic ischemic injury to the CNS.

Animals↗
PubMed1991

Fructose-1,6-diphosphate, when given five minutes after injury, does not ameliorate hypoxic ischemic injury to the central nervous system in the newborn pig.

Hypoxic ischemic injury to the brain was induced in 12 0- to 3-day-old piglets. At time 0, the carotid arteries were ligated, and the blood pressure was reduced by one third by hemorrhage. At 15 min, inspired FIO2 was reduced from 50 to 6%. After 10 min of flat EEG, the FIO2 was changes to 100%, the carotid ligations were released, and the withdrawn blood was reinfused. Five minutes after reoxygenation, the piglets were randomly assigned to either receive 350 mg of fructose-1,6-diphosphate over 5 min, followed by 6 mg/kg/min for the ensuing 50 min, or an equivalent volume of normal saline. 3 days after the experiment, the animals received a neurologic examination by a blinded observer, were then sacrificed, and the brains examined by a blinded observer. There were no significant differences in the degree of damage between the two groups.

Animals↗
PubMed1991

MK-801 does not protect against hypoxic-ischemic brain injury in piglets.

BACKGROUND AND PURPOSE: The excitatory amino acid inhibitor MK-801 has been shown in many animals species to protect against hypoxic-ischemic brain injury. We sought to determine whether hypoxic-ischemic injury to the newborn pig's brain could be prevented by the use of MK-801. METHODS: Hypoxic-ischemic injury to the brain was induced in forty 0-3-day-old piglets. They were randomized to receive either 3 mg/kg MK-801 (MK-801 group, n = 20) or vehicle (control group, n = 19) prior to insult. At time 0, the carotid arteries were ligated and the blood pressure was reduced by one third by hemorrhage. At 15 minutes, inspired oxygen was reduced from 50% to 6%. At 30 minutes, inspired oxygen was changed to 100%, carotid ligatures were released, and the withdrawn blood was reinfused. An additional 14 piglets received 3 mg/kg MK-801 but not hypoxic-ischemic injury (drug-only group), and a final group of 11 piglets were subjected to only a sham operation (sham group). RESULTS: Neurological examination scores at 24, 48, and 72 hours showed that MK-801 and drug-only piglets were significantly worse than the controls. Pathological examination of the brains at 72 hours showed significantly greater damage in the brains of the MK-801 and control pigs relative to the sham and drug-only groups. No differences were found between the control and the MK-801 groups. No differences were found between the sham and drug-only groups. CONCLUSIONS: MK-801, at a dose of 3 mg/kg, causes neurological dysfunction in piglets lasting at least 72 hours, but neither causes brain damage nor ameliorates the effects of hypoxic-ischemic injury to the brain of the newborn pig.

Animals↗
PubMed1989

Hematologic monitoring in children with epilepsy treated with carbamazepine.

One hundred seventy-six children treated with carbamazepine for epilepsy were monitored over a 12-month period to determine the effects of carbamazepine on the hematologic system. There were no significant changes within the total population in the mean hematocrit or platelet count. The white blood cell count and total neutrophil count showed declines at 1, 8, and 12 months, but the differences did not achieve statistical significance. There was no correlation between the hematologic parameters and carbamazepine blood level, age or sex, or the presence of other drugs. Pretreatment leukopenia and neutropenia were present in 2.8% and 4.0% of children, respectively. During carbamazepine therapy, 8.0% and 17.0% of the children developed leukopenia and neutropenia, respectively, and it was persistent in 1.7% and 2.8%, respectively. The changes in the white blood cell count could be attributed to the changes in the total neutrophil count.

Agranulocytosis↗
PubMed1984

Glycogen-membrane complexes in denervated human skeletal muscle.

We describe an unusual intracellular complex of glycogen with smooth, cisternal, cytoplasmic membranes (glycogen-membrane complexes, GMC) in denervated human skeletal muscle. Glycogen particles were always intimately associated with these structures, although the staining intensity varied markedly with different fixation conditions. This may account for previous investigations of similar structures in which an association with glycogen was not recognized. Electron micrographs of tannic acid-enhanced specimens, and of freeze-fracture replicas, showed similarities between the GMCs and the terminal cisternae of the sarcoplasmic reticulum: (i) GMCs resembled the terminal cisternae of the sarcoplasmic reticulum in the size and asymmetric distribution of intramembranous particles seen in freeze-fracture replicas; (ii) tannic acid-enhanced thin sections of GMCs showed intense staining of the cisternal contents and irregular staining of the cytoplasmic leaflet, similar to the appearance of the sarcoplasmic reticulum terminal cisternae; and (iii) triad-like junctions were seen between the glycogen-membrane complexes and elements of the transverse tubule system.

Cell Membrane↗
PubMed1984

Ischemia of the brain stem as a cause of sudden infant death syndrome.

Recent evidence indicates that the sudden infant death syndrome (SIDS) is related to abnormal control of respiration. Focal morphologic changes have not been noted. In a case of SIDS, ischemic degeneration was noted bilaterally in the medulla, particularly in the dorsal motor nucleus of the vagus nerve. Pathologic changes were not found elsewhere in the CNS. To our knowledge, this is the first description of a focal brain-stem lesion in SIDS that had enough of a role in altered respiratory control to cause death.

Brain Ischemia↗
PubMed1983

Muscle pyruvate oxidation following denervation and reinnervation.

Muscle pyruvate metabolism was studied in rats following sciatic nerve crush. Control studies showed high pyruvate dehydrogenase and lipoamide dehydrogenase enzyme activity in muscle with type 1 fiber predominance (soleus) and low activities in muscle with type 2 fiber predominance (extensor digitorum longus), whereas lactate dehydrogenase was much higher in the latter. Following denervation, both muscles showed a significant reduction in pyruvate dehydrogenase enzyme activity. During reinnervation, muscle with type 2 predominance developed significantly elevated pyruvate oxidation enzyme activities.

Animals↗
PubMed1983

Effects of dichloroacetate on brain tissue pyruvate dehydrogenase.

The activation of the pyruvate dehydrogenase complex (PDHC) by dichloroacetate (DCA) was studied in brain tissue. Chronic administration of DCA to rats caused no significant change of PDHC activation in brain. DCA brain concentrations were comparable to those of other tissues in which activation is known to occur. No effect of DCA on PDHC could be demonstrated from isolated brain mitochondria, whereas DCA reversed the deactivation of PDHC by ATP, alpha-ketoglutarate plus malate, and succinate in liver mitochondria. This study suggests that the regulation of PDHC activation in neural tissue differs from that in other tissues.

Acetates↗
PubMed1983

Improvement of muscle function in acid maltase deficiency by high-protein therapy.

Progressive muscle weakness in acid maltase deficiency (AMD) is associated with intralysosomal accumulation of glycogen and altered myofibrillar morphology. A rapid fall in circulating branched chain amino acids after protein ingestion in a child with AMD suggested that increased net muscle protein catabolism may play a part in the pathogenesis of this condition. To reduce this muscle catabolism, the patient was treated with a high-protein diet for 12 months. This has reversed the weakness and wasting, with improvement in muscle function, exercise tolerance, and growth.

Amino Acids, Branched-Chain↗