Biomedical subjects
Publications and source records attributed to Y Eshel.
Phencyclidine (PCP), when given to mice, induces general hyperactivity and rapid circling, similar to that caused by morphine. These effects are partially antagonized by naloxone.
In an effort to explore possible changes in 5-hydroxytryptamine (5-HT) metabolism in idiopathic torsion dystonia (ITD), platelets from patients were studied. Platelet 5-HT concentrations did not differ from those in matched controls. 5-HT uptake by the platelets was also studied, and the results demonstrated significantly higher Km values, but Vmax values were normal among patients. Inhibition by imipramine of 5-HT uptake by platelets taken from ITD patients was also normal. The therapeutic implications of the low affinity of 5-HT to its platelet receptors are discussed.
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Administration of somatostatin intracerebroventricularly to mice produced a dose-dependent mydriasis, whereas intravenous injections were ineffective. Naloxone could prevent or abolish this effect. It is suggested that somatostatin either directly excites opiate receptors or activates endopioid pathways involved in the regulation of pupillary size.
Male albino rats, injected intravenously or intracerebroventricularly with delta 1-tetrahydrocannabinol (THC), develop mudriasis. The median effective dose of the intravenous administration group was 5 mg/kg THC, whereas that for the intracerebroventricular route was 150 microgram/kg THC. Sympathectomy significantly decreased the THC-induced mydriasis. The mydriatic effect was not influenced by naloxone. We conclude that THC produces mydriasis through a central action, the efferent pathway of which is the sympathetic system.
Amantadine, injected into mice, produces dose-dependent mydriasis. The pupillary dilation caused by amantadine is not abolished by pretreatment with reserpine, or by combined pretreatment with reserpine and alpha-methyl-p-tyrosine, although the mydriasis is reduced by approximately 25%. Thus, release of catecholamines from nerve terminals can account for only 25% of amantadine-produced mydriasis. Haloperidol and phentolamine can partially block the effect of amantadine, but, when given after reserpine, neither of the antagonists increases the blockade produced by reserpine alone. We conclude that the catecholaminergic system contributes only partially to the pupillary effect of amantadine, and that other mechanisms appear to be involved.
Morphine is known to produce mydriasis in mice. We have found that enkephalins caused a similar effect. Morphine was twice as active as D-Ala-D-Leu-enkephalin (BW-180C), 5 times as active as Met-enkephalin and 7 times as active as Leu-enkephalin. The time course of the effect was shortest for the enkephalins ( t 1/2 = 8-12 min), intermediate for BW-180C (60 min) and longest for morphine (80 min). Naloxone antagonised the effect of all agents to a similar extent. The question whether enkephalins are involved in the physiological regulation of pupillary diameter was investigated by administering either naloxone or D-phenylalanine to mice. None of these agents changed pupillary size, thus making such an involvement unlikely.
Administration of oxotremorine to mice produced centrally-mediated effects, such as catalepsy and tremor, and peripheral muscarinic actions, such as diarrhoea and lachrymation. Pretreatment with amantadine (25--200 mg/kg) prevented these oxotremorine-induced effects in mice. Catalepsy was most susceptible and tremor most resistant to the administration of amantadine. The possible mechanisms involved are discussed. Our results validate the use of the oxotremorine model in the search for novel antiparkinsonian drugs.
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1. The activity of dopamine-beta-hydroxylase (DBH) was assayed in the serum of 102 patients, mostly with varying degrees of hepatic dysfunction. 2. DBH activity was not elevated in those with liver disorder and did not correlate with serum bilirubin, transaminase, lactic dehydrogenase, alkaline phosphatase or creatine phosphokinase. 3. It is concluded that the liver is not necessarily involved in the inactivation of DBH.
The activity of dopamine-beta-hydroxylase was measured in the serum before and immediately after electroconvulsive treatments. No significant difference was observed, suggesting that the seizures did not cause an increase in the peripheral sympathetic tone.
Dopamine-beta-hydroxylase activity was measured in serum samples that were incubated at 37 degrees C for up to seven days and were compared with preincubation values. No change of activity was observed.
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The activity of dopamine beta-hydroxylase in the serum was measured in patients with acute cardiac disorders who were admitted to a coronary care unit. The activity of the enzyme on admission was similar in patients with acute myocardial infarction and in those with other conditions; on discharge, the activity was reduced significantly. Patients with myocardial infarction had the greatest fall in the activity of dopamine beta-hydroxylase. Patients with multiple signs of sympathetic hyperactivity had significantly higher values for the activity of dopamine beta-hydroxylase on admission. Pain was found to significantly increase the activity of the enzyme. These data confirm findings that the activity of dopamine beta-hydroxylase in the serum reflects the intensity of sympathetic activity. The factors contributing to the elevated sympathetic activity in some patients with acute myocardial infarction seem to be nonspecific, but because of the ominous nature of increased sympathetic tone in this condition, it could be advantageous to identify these patients.
Halothane, but not methoxyflurane, was found to cause specific hepatocellular damage, the hepatotoxicity being prompt but transient. The hepatotoxicity was demonstrated by the elevation in the serum activity of xanthine oxidase, a highly sensitive marker for acute liver damage.
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A randomized, placebo-controlled, double-blind study was performed as a pilot study to examine the benefit of the administration of magnesium sulfate given intravenously as a protective substance during the first 24 hours following a stroke. Patients who had cortical infarction in the middle cerebral artery territory with moderate to severe neurologic deficits lasting for more than 15 minutes with onset less than 24 hours were included. The patients were treated with magnesium sulfate or placebo for 5 days and examined by a blinded investigator. Patients had follow-up for 30 days. The primary efficacy variable was the proportion of patients reaching mild to moderate neurologic deficit on the Orgogozo scale (80 points) and relative functional independence on the Barthel index (60 points). Orgogozo scale and Mathew scale values were obtained on admission and days 2, 4, 8, and 30 after stroke. Barthel activities of daily living index and Rankin disability score were obtained on day 30. Forty-one patients (22 given treatment and 19 given placebo) demonstrated significant beneficial effects on the Orgogozo scale (84 +/- 11 vs. 64 +/- 10, p < 0.0001) and (83 +/- 14 vs. 70 +/- 15, p < 0.009), respectively. At the end of 1-month follow-up, the Barthel ADL index was nonsignificantly higher and the Rankin disability score was marginally significantly lower in the magnesium-treated group (84 +/- 26 vs. 71.8 +/- 26, p < 0.143) than in control subjects (2.3 +/- 1.1 vs. 3 +/- 1.3, p < 0.077). Intravenous magnesium sulfate had significant positive effect on the outcome in patients with acute stroke. Further studies on a larger scale are needed to confirm these findings.