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Biomedical subjects

D Janowsky

Publications and source records attributed to D Janowsky.

29 records · Page 2Linked to original sources
PubMed1978

Unresponsiveness of catatonic symptoms to naloxone.

A case report of a catatonic patient is presented. Because of the similarity of catatonia to the animal behavior produced by intracerebral administration of beta-endorphin, an endogenous opioid, naloxone was administered. No effect was observed with naloxone, whereas both amobarbital and diazepam were able to reverse catatonic behavior. Testing of catatonic patients with naloxone may help further elucidate naloxone's reported anti-psychotic properties.

Adult↗
PubMed1978

Effects of smoking marihuana on left ventricular performance and plasma norepinephrine: studies in normal men.

In 14 healthy men we assessed the effects of smoking marihuana cigarettes containing 6 mg of delta-9-tetrahydrocannabinol on ultrasound measures of left ventricular function. Four of this group and four additional subjects also had measurements of plasma norepinephrine. Both heart rate and left ventricular performance (mean rate of internal diameter shortening [mean Vcf]) were significantly increased for at least 1 h after drug exposure compared with these values after placebo cigarettes. The immediate tachycardia and increase in mean Vcf were not accompanied by raised plasma norepinephrine levels. However, by 30 min after marihuana exposure, sympathetic neurotransmitter levels were significantly greater than both control values and those after placebo cigarettes, and they remained elevated for at least 2 h. Excessive sympathoadrenal discharge, as evidenced by augmented left ventricular function and prolonged catecholamine release, could adversely affect patients with heart disease.

Adult↗
PubMed1975

Rebound phenomena in manic patients following physostigmine. Preliminary observations.

The authors have administered physostigmine intravenously to three hospitalized manic patients on a double-blind basis. All three individuals showed clinical change both during and after the physostigmine period, which can be clearly delineated into three distinct phases. The behavioral modifications occurring during the physostigmine run did not qualitatively alter the underlying mania. The authors focus on 'rebound' phenomena, or post-physostigmine changes, as a possible clinical index with which chemically to characterize the initial state of amine imbalance responsible for a given affective illness. The data are considered consistent with an adrenergic-dopaminergic-cholinergic balance hypothesis of affective disorders, and may provide a relevant link in understanding the interface or crossover between manic and schizo-affective illness.

Bipolar Disorder↗
PubMedDate not supplied

Verbal memory deficits associated with major affective disorders: a comparison of unipolar and bipolar patients.

The verbal learning and fluency of patients with unipolar and bipolar depression were compared to those of normal controls and patients with Huntington's disease. The data demonstrated that the recall and recognition performance of both groups of depressed patients were impaired relative to the performance of normal control subjects. The bipolar patients, however, were more impaired than the unipolar patients on both tasks (P less than 0.024 and P less than 0.022, respectively). In addition, the unipolar patients generated more correct responses on a test of verbal fluency (P less than 0.04). The performance of the bipolar patients was, in fact, similar to that of patients with Huntington's disease, a progressive degenerative disorder that primarily affects subcortical areas.

Adult↗
PubMedDate not supplied

Lethal effects of reserpine plus physostigmine and neostigmine in mice.

1. The interaction between the reversible cholinesterase inhibitors, physostigmine and neostigmine and reserpine was studied. 2. A combination of reserpine plus a cholinesterase inhibitor significantly increased lethality in adult male Swiss-Webster mice above that caused by either neostigmine, physostigmine, or reserpine alone. 3. Methscopolamine completely reversed this effect. 4. It would appear that the presence of the antiadrenergic agent, reserpine, increases the toxicity of cholinomimetic agents. 5. The above results may have clinical significance, since reserpine and cholinesterase inhibitors are used in the practice of medicine.

Animals↗