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Biomedical subjects

M E Charness

Publications and source records attributed to M E Charness.

48 records · Page 3Linked to original sources
PubMed1984

Interaction of ethanol with neural cells in culture: a model of intoxication, tolerance and withdrawal.

The interaction of ethanol with the nervous system produces acute intoxication, tolerance and withdrawal phenomena. Additionally, there are several alcohol-related neurological disorders which develop in alcoholic patients. Current evidence suggests that ethanol produces some of these changes by altering the structure and function of neural membranes. Therefore, neurotransmitter receptors and receptor-dependent molecular events in the nervous system may be highly sensitive to ethanol. The murine neuroblastoma X glioma hybrid cell line NG108-15 was used to study the acute and chronic interactions of ethanol with intact cells. Ethanol acutely inhibited opiate receptor binding, but after chronic exposure the cells exhibited an apparent adaptive increase in the number of opiate binding sites; this was reversible when ethanol was withdrawn. High levels of ethanol (200 mM) increased opiate binding after 18-24 hours; lower concentrations (25-50 mM) produced similar changes after two weeks. This model system has great potential for exploring the cellular and molecular mechanisms which underlie ethanol intoxication, tolerance and withdrawal.

Adaptation, Physiological↗
PubMed1984

Frequent neurologic toxicity associated with amiodarone therapy.

Fifty-four consecutive patients were treated with amiodarone for symptomatic ventricular tachycardia or ventricular fibrillation refractory to treatment with conventional antiarrhythmic drugs. A reversible neurologic syndrome of tremor, ataxia, and occasionally peripheral neuropathy without nystagmus, dizziness, encephalopathy, or long-tract signs developed in 54% of the patients and was the most common reason for altering or discontinuing drug therapy. Neurologic side effects improved or resolved within 2 days to 4 weeks of decreasing or discontinuing amiodarone. Frequent neurologic toxicity is a hitherto undescribed complication of amiodarone therapy. Wider recognition of this syndrome will avoid unnecessary and costly diagnostic evaluation.

Amiodarone↗
PubMed1983

Ethanol modulation of opiate receptors in cultured neural cells.

The mouse neuroblastoma-rat glioma hybrid cell line NG108-15 was used to study the acute and chronic interaction of ethanol with intact neural cells. In the short term, ethanol inhibited opiate receptor binding, but after long-term exposure the cells exhibited an apparent adaptive increase in the number of opiate binding sites; this was reversible when ethanol was withdrawn. High concentrations of ethanol (200 mM) increased opiate binding after 18 to 24 hours, whereas lower concentrations (25 to 50 mM) produced similar changes after 2 weeks. This model system has potential for exploring the cellular and molecular mechanisms underlying ethanol intoxication, tolerance, and withdrawal.

Animals↗
PubMed1979

Exacerbation of angina pectoris by prazosin.

A case of angina pectoris worsened by prazosin is presented. Since a hypertensive population includes many patients with known or occult coronary artery disease, physicians should use prazosin cautiously in this subgroup, particularly when beta-adrenergic antagonists cannot be used concurrently.

Acute Disease↗
PubMed1977

Beta adrenergic receptor labeling in intact animals with 125I-hydroxybenzylpindolol.

After the intravenous administration to mice of 125I-hydroxybenzylpindolol (125I-HYP), a potent beta adrenergic antagonist, particulate bound radioactivity in brain, heart and lung is selectively associated with beta adrenergic receptor binding sites. The amount of total and bound radioactivity in these tissues is time dependent, reaching peak values at about 5 minutes after injection, and increases approximately linearly with increasing 125I-HYP doses. The lung has the highest levels of radioactivity as well as the highest proportion of bound to total radioactivity. The amount of specifically bound 125I-HYP is markedly reduced by simultaneously injecting a beta adrenergic bound 125I-HYP is markedly reduced by simultaneously injecting a beta adrenergic agonist or antagonist, although the total amount of radioactivity in the tissues is not affected. The beta antagonist (-)-propranolol reduces specific 125I-HYP binding 50% at doses of 0.01, 0.03 and 0.004 mg/kg in brain, heart and lung, respectively. Specific 125I-HYP binding is stereospecific in these tissues as (+)-propranolol is only 1 to 2% as effective as (-)-propranolol in reducing binding. The beta agonist (-)-isoproterenol has ID50 values in the range of 2 to 20 mg/kg, whereas the alpha adrenergic antagonist, phentolamine does not reduce 125I-HYP binding. Although some radioactivity is associated with particulate fractions from the liver, little, if any, specific binding of 125I-HYP to a beta adrenergic receptor is demonstrable. The characteristics of 125I-HYP binding in mouse heart, lung and brain are those expected for the recognition site of the beta adrenergic receptor and thus provide a method for labeling the beta adrenergic receptor in vivo.

Animals↗