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Biomedical subjects

D A Trauner

Publications and source records attributed to D A Trauner.

At least 55 records · Page 3Linked to original sources
PubMed1980

Treatment of Reye syndrome.

Although the underlying cause of Reye syndrome is not understood, an effective approach to treatment is based on reversing the known metabolic and pathological abnormalities. A multifaceted therapeutic approach aimed at correcting metabolic derangements and combating intracranial hypertension can result in complete recovery from severe cases of Reye syndrome.

Brain Diseases↗
PubMed1980

Regional cerebral Na+K+ ATPase activity following octanoate administration.

Sodium octanoate in an 0.2 M solution was administered to rabbits by continuous slow IV infusion over 4 hr. Controls were given identical infusions of normal saline. The animals were then sacrificed, brains were removed, and specific areas were isolated and assayed for Na+K+ ATPase activity. Significant inhibition of regional Na+K+ ATPase activity was detected in cortex, thalamus, hypothalamus, pons, and medulla of rabbits given octanoate when compared to controls.

Animals↗
PubMed1978

Treatment of elevated intracranial pressure in Reye syndrome.

Continuous intraventricular monitoring of intracranial pressure appears to be a useful aid in the management of patients with Reye syndrome, especially those in stage 3 or 4 coma, in which the mortality rate remains high. Elevations in intracranial pressure can be treated promptly and before the patient shows clinical signs of deterioration. Careful attention to adequate airway care is essential. The use of paralytic agents to reduce pressure secondary to muscle movement is useful. The minimum dose of mannitol required can be carefully titrated, and sudden pressure changes can be combated by release of small amounts of cerebrospinal fluid.

Adolescent↗
PubMed1978

Short chain fatty acid-induced central hyperventilation in rabbits.

The short chain fatty acid sodium octanoate was infused into rabbits as an 0.2 M solution over 4 hours, resulting in blood and brain levels of 200 to 700 mumoles per liter. During the infusion, animals exhibited marked hyperventilation, resulting in a mild respiratory alkalosis. Octanoate infusion also resulted in significant hyperammonemia and lactic acidemia. Saline-treated control animals demonstrated no clinical or chemical abnormalities. Several short chain fatty acids, including octanoate, are increased in the plasma of patients with hepatic encephalopathies and Reye syndrome. The present study suggests that short chain fatty acids may be endogenous toxins in these clinical disorders. In particular, the central hyperventilation in these conditions may be due to the neurotoxic effect of short chain fatty acids.

Animals↗
PubMed1978

Reye's syndrome in infancy.

Reye's syndrome in infancy is not a well-defined entity and is infrequently diagnosed. Eight infants 6 months of age or younger had a prodromal viral illness followed by the rapid onset of lethargy, seizures, and coma, resulting in the diagnosis of Reye's syndrome. All had abnormal results of liver function tests including elevations of blood ammonia level. Three patients had pathological studies that confirmed fatty visceral infiltration. The data on these patients, as well as a review of the literature, indicate that the most prominent clinical findings in Reye's syndrome in infancy include marked respiratory abnormalities with tachypnea and apneic episodes; frequent occurrence of seizures in the early stages of the illness; and hypoglycemia in most cases. A strong socioeconomic bias was noted in these patients, with the infants coming primarily from lower socioeconomic, urban environments, while older children with Reye's syndrome have been observed to be predominantly middle-class and from suburban or rural areas.

Black or African American↗
PubMed1977

EEG correlations with biochemical abnormalities in Reye syndrome.

A patient with Reye syndrome was studied throughout the course of the illness with continuous EEG monitoring, and these patterns were correlated with serial determinations of serum ammonia and short-chain fatty acid concentrations. There was high correlation between degree of EEG abnormality, clinical symptoms, and elevations of the short-chain fatty acids, while serum ammonia concentrations correlated poorly with the EEG and with the clinical state.

Ammonia↗
PubMed1975

Short-chain organic acidemia and Reye's syndrome.

Short-chain fatty acids were determined prior to therapy in seven patients with Reye's syndrome. Elevated concentrations of propionate, butyrate, and isobutyrate were found in all patients. Isovalerate concentrations were high in three patients. In view of the fact that the administration of certain short-chain fatty acids to experimental animals results in coma, electroencephalographic changes, and fatty accumulation in the viscera, the elevations of short-chain fatty acid concentrations observed in the present study suggest that these fatty acids may play a role in the clinical manifestations of Reye's syndrome.

Adolescent↗
PubMedDate not supplied

Effect of octanoate injection on rat blood-brain barrier.

Serum concentrations of short and medium chain fatty acids, including octanoate, are elevated in hepatic encephalopathy and Reye syndrome. Injection of octanoate into animals produces features reminiscent of Reye syndrome, but the mechanisms are unknown. To evaluate the effect of octanoate on blood-brain barrier permeability, three techniques were used. Entry of horseradish peroxidase and trypan blue into brain was not observed after octanoate injection. Brain uptake of tryptamine, tyrosine and methionine was increased significantly by octanoate, while uptake of insulin was unchanged. This study suggests that octanoate may produce central nervous system alterations by facilitating entry of certain low molecular weight compounds into brain. This may represent one mechanism for the development of encephalopathy in liver disease and Reye syndrome.

Animals↗
PubMedDate not supplied

Alterations in serum glucose and hepatic glycogen concentrations during octanoate administration in rabbits.

During continuous administration of sodium octanoate (0.2 M) into weanling and mature rabbits, a significant decrease in serum glucose concentration was observed within 15 minutes after onset of the infusion. This relative hypoglycemia persisted for as long as one hour, after which there was a rebound to normoglycemia. Hepatic glycogen concentrations were correspondingly reduced by one-half in octanoate-treated versus control animals. Previous studies in an octanoate model have demonstrated clinical, biochemical, and pathologic features similar to those found in Reye syndrome. The current findings may have implications for the hypoglycemia observed in children with Reye syndrome.

Age Factors↗