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Biomedical subjects

M Davis

Publications and source records attributed to M Davis.

At least 631 records · Page 35Linked to original sources
PubMed1977

The role of the false neurotransmitter octopamine in the hypotension of fulminant hepatic failure.

1. An investigation was carried out into the mechanism of unexplained hypotension in patients with fulminant hepatic failure. The cardiac output and peripheral resistance were compared in normotensive and hypotensive patients. In addition, the serum concentration of the false neurotransmitter octopamine and the pressor response to noradrenaline, and to the indirectly acting sympathomimetic agent tyramine, were measured in hypotensive and normotensive patients with fulminant hepatic failure and in healthy subjects. 2. The cardiac output and the peripheral resistance were decreased in the hypotensive patients, and their mean heart rate was slower than in the normotensive patients. Although the serum octopamine concentration was significantly elevated in the patients compared with the control subjects, the highest octopamine concentrations were unexpectedly found in the normotensive patients and a significant positive correlation could be demonstrated between the resting blood pressure and the serum octopamine concentration. The pressor response to tyramine and noradrenaline were similar in the hypotensive patients, the normotensive patients and control subjects. 3. These results suggest that neither increased serum concentrations of the false neurotransmitter octopamine, nor end-organ insensitivity to released noradrenaline are responsible for the hypotension. A more likely explanation is toxic depression of the vasomotor centre. The opening of peripheral arteriovenous shunts, possibly as a result of endotoxaemia, might be an additional factor.

Cardiac Output↗
PubMed1977

Serum octopamine, coma, and charcoal haemoperfusion in fulminant hepatic failure.

Serum octopamine levels were significantly higher in twenty patients with fulminant hepatic failure (FHF) during the first 48 h of grade IV coma than in health control subjects (3.38 +/- 0.20 ng/ml and 1.75 +/- 0.19 ng/ml respectively, P less than 0.001). Serial measurements in five patients who died without regaining consciousness showed serum octopamine to remain raised, and concentrations in the cerebrospinal fluid at death reflected serum levels. In five patients who regained consciousness, improvement in encephalopathy was associated with a significant reduction in serum octopamine. Renal failure in patients with FHF was found to contribute to raised serum octopamine but could not alone account for the observed levels. Patients given neomycin therapy did not have significantly lower serum octopamine levels than an untreated group. There was, however, a significant correlation between elevated serum octopamine and the occurrence of gestrointestinal bleeding during the previous 24 h. Charcoal haemoperfusion did not appreciably reduce serum octopamine levels.

Charcoal↗
PubMed1977

Vitamin B6 deficiency in chronic liver disease--evidence for increased degradation of pyridoxal-5'-phosphate.

Plasma levels of pyridoxal-5'-phosphate (PLP), the active coenzyme form of vitamin B6, were found to be significantly lower than normal in 22 out of 31 patients with decompensated cirrhosis or subacute hepatic necrosis. There was no significant difference in plasma PLP levels between those with liver disease due to alcohol and those with other varieties. When intravenous supplements with pyridoxine hydrochloride were given only 33% responded with an increase in plasma PLP. In contrast, all patients given PLP responded, although peak plasma levels were variable, the response being significantly less than that found in normal control subjects. After supplementation with pyridoxine hydrochloride, and with PLP, the urinary excretion of 4-pyridoxic acid, which is derived from the degradation of PLP, was higher in patients who showed the least increase in plasma PLP levels. Although impaired phosphorylation of pyridoxine hydrochloride may be one factor, the most likely explanation for these findings is an increased rate of PLP degradation which may be important in the pathogenesis of vitamin B6 deficiency in patients with severe liver disease.

Alcoholism↗
PubMed1977

Early prediction of the outcome of a paracetamol overdose based on an analysis of 163 patients.

Clinical and biochemical data obtained from 163 patients who had taken an overdose of paracetamol were examined to determine which factors or measurements were of value in predicting the severity of ensuing liver damage early after ingestion of tablets. Although the overall severity of hepatic necrosis was found to increase with the dose of paracetamol ingested, correlation was not sufficiently close to provide an accurate prognostic index in individuals. Severe hepatic damage was less likely if the patient had vomited or had a stomach wash-out within 6 hr of overdose. The plasma concentrations of paracetamol, measured at known times after overdose, distinguished those who developed hepatic dysfunction from those who did not, but there was a poor correlation, particularly in the first 6 hr after ingestion of tablets, between these values and the severity of ensuing liver damage. Estimates of early plasma paracetamol half-lives from three or more samples taken within 4 hr of admission showed that all patients developing moderate or severe liver damage had half-lives greater than 4 hr, but this was also the case in nearly one-third of those with minimal liver lesions only. It is concluded that there is no completely reliable early prognostic test for individual patients with paracetamol overdose. If each patient is selected for treatment with cysteamine (mercaptamine) or other agents on the basis of plasma paracetamol levels, up to 30% may receive this agent who are at risk from trivial hepatic damage only.

Acetaminophen↗
PubMed1977

Intraluminal diverticulum of the esophagus.

Two patients with intraluminal esophageal diverticulum are described and illustrated. Both had chronic esophagitis. One had a distal esophageal stricture, while the other showed persistent retrograde gastroesophageal reflux following hiatal hernia repair. Possible causes are considered, based on the presumption of intermittently or chronically increased intraluminal pressure associated with an area of congenital or acquired weakness of the esophageal wall.

Adult↗
PubMed1977

Affinity chromatography systems for artificial liver support.

The physical, adsorptive, and flow properties of two albumin conjugated agarose materials have been investigated in vitro to determine whether they could be used in artificial liver support systems to enhance the removal of toxic protein-bound substances. The results of binding of chenodeoxycholic acid and unconjugated bilirubin and flow experiments with blood and saline suggested that there could be advantages in using the SepharoseR rather than Bio--GelR albumin agarose in future haemoperfusion systems. However, further modifications are needed before the former can be successfully scaled up for human use.

Chromatography, Affinity↗
PubMed1977

Plasma pyridoxal phosphate levels in fulminant hepatic failure and the effects of parenteral supplementation.

Plasma concentrations of pyridoxal-5'-phosphate (PLP), the active coenzyme form of vitamin B6, were found to be markedly raised in patients with fulminant hepatic failure, when estimated within one week of the onset of symptoms. In parallel with the rise in plasma PLP, there was an increase in serum aminotransferase activity, suggesting that as a result of the severe hepatocyte injury, vitamin is released from theliver in the form of transaminase holoenzymes. There was no correlation between plasma levels of PLP and the urinary excretion of 4-pyridoxic acid, its main metabolite, either in the patients or normal control subjects. There was a progressive decline in plasma PLP levels after the initial period, which was not prevented by administration of high doses of pyridoxine hydrochloride (100 mg intravenously daily), suggesting that thseepatients are either unable to convert pyridoxine to PLP, or that degradation of PLP occurs at a pathologically incrased rate in this condition.

Hepatic Encephalopathy↗
PubMed1977

Thiamine deficiency in fulminant hepatic failure and effects of supplementation.

Nine out of 24 patients with acute hepatocellular necrosis leading to fulminant hepatic failure showed biochemical evidence of thiamine deficiency early in the course of their illness, probably as a result of inadequate intake of the vitamin. This was corrected by twice daily administration of intravenous vitamin supplements containing thiamine hydrochloride (100 mg b.d.). These studies indicate that conversion of thiamine hydrochloride to its biologically active co-enzyme form, thiamine pyrophosphate, is possible even in the presence of severe acute hepatocellular necrosis, and it is suggested that supplements of the vitamin should be included in the routine management of patients with acute hepatic failure.

Acute Disease↗
PubMed1977

Vision tests as predictors of learning disabilities.

Three relatively new screeening tests for visual problems are described. They are color matching, visual language field development, and the speed of the visual language field development, and the speed of the visual scan. The visual problems so measured were found to be associated with poor school achievement. In color matching, only blue was involved, not red or green, and proficiency was relatively undeveloped before age 10. Throughout, blue matching difficulty was associated with poor visual language field development, but not with slow scanning. Early screening with these tests offers possibilities for early detection of students with potential learning problems.

Adolescent↗