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Biomedical subjects

M Davis

Publications and source records attributed to M Davis.

At least 667 records · Page 37Linked to original sources
PubMed1975

Effects of d- and l-amphetamine on habituation and sensitization of the acoustic startle response in rats.

In a series of 3 experiments the effects of 2, 4, 8, or 16 mg/kg d-amphetamine and 4, 8, 16, or 32 mg/kg l-amphetamine on acoustic startle amplitude in the rat were investigated. d-Amphetamine was 4--5 times as potent as l-amphetamine in augmenting startle amplitude. Startle potentiation was associated with vigorous stereotypies but the resultant cage movement could not account for the change in startle. Pretreatment with alpha-methyl-p-tyrosine (100 mg/kg, 1 hr before) had only a slight depressant effect on startle but essentially eliminated augmentation of startle by either d-amphetamine (8 mg/kg) or l-amphetamine (32 mg/kg). d-Amphetamine did not have a direct effect on startle but instead enhanced sensitization produced by the startle stimuli without altering sensitization produced by background white noise or habituation. The results suggest that startle sensitization is enhanced by increased availability of catecholamines and, by virtue of the different potencies of the d- and l-isomers, that dopamine and norepinephrine may affect startle differently.

Acoustic Stimulation↗
PubMed1975

Hepatic glutathione depletion and impaired bromosulphthalein clearance early after paracetamol overdose in man and the rat.

1. Plasma clearance of bromosulphthalein was impaired in patients within 8 h, and in rats within 2 h , of paracetamol overdose, before biochemical signs of liver damage had appeared. 2. Paracetamol and bromosulphthalein competed for uptake into the liver and excretion into the bile. Impaired hepatic uptake of bromosulphthalein could also be demonstrated in man at doses of the drug within the therapeutic range. 3. In patients studied a smaller proportion of bromosulphthalein was retained in the plasma as the glutathione conjugate after an overdose than after therapeutic doses. This effect could be reproduced in the rat and shown to be due to depletion of hepatic glutathione and to impairment in the activity of the enzyme glutathione-S-aryl transferase. 4. These studies provide further evidence that depletion of hepatic glutathione occurs after paracetamol overdose in man, as in the experimental animal, allowing the subsequent accumulation and binding of a toxic metabolite of the drug within liver cells. Impaired enzymic conjugation of the toxic metabolite with hepatic reduced glutathione may also be important in this situation.

Acetaminophen↗
PubMed1975

Early inhibition of hepatic bilirubin conjugation after paracetamol (acetaminophen) administration in the rat.

Administration of paracetamol (acetaminophen) 13.3 mmol kg-1 body weight to rats led 2 h later to an impaired capacity to conjugate an intravenous load of bilirubin, in the absence of biochemical signs of liver damage and before the reactive metabolite of the drug had become bound within the liver. In addition, paracetamol inhibited the excretion into the bile of conjugated bilirubin, although the plasma levels of the uncomjugated pigment only were elevated. This study provides additional evidence that hepatic glucuronide conjugation is impaired early after paracetamol overdose, and that this precedes the accumulation and binding of the hepatotoxic metabolite of the drug within the liver cells.

Acetaminophen↗
PubMed1974

Emergency endoscopy after gastrointestinal haemorrhage in 50 patients with portal hypertension.

Endoscopy was carried out in 50 patients with oesophageal varices within 24 hours of a major haematemesis or melaena. Sources of bleeding were identified in 42 of the cases and in only 19 patients was bleeding due to oesophageal varices. Bleeding from gastric varices was present in 11 patients, and a variety of acute and chronic lesions made up the remainder. In contrast with previous series haemorrhage from erosive gastric lesions was seen in only five patients and was no more common in 23 patients with alcoholic cirrhosis than in the group as a whole.

Adolescent↗