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PubMed · 7312889

Caffeine-induced stimulus control.

Abstract

Six rats were trained to discriminate the effects of caffeine (60 mg/kg, pretreatment time: 1 hour) and saline in a two-lever choice task using a fixed ratio 10 schedule of water reinforcement. Stimulus control was assumed to be present when 80% or more of the first ten responses were appropriate for the treatment condition on each of five consecutive days. The mean number of sessions prior to the onset of criterion performance was 22 (SE = 3; range = 11--32). In trained subjects, doses of caffeine of 30, 10, and 3 mg/kg were followed by a progressively smaller proportion of responses on the caffeine-appropriate lever. Stimulus control by caffeine began to diminish about four hours after administration and was completely absent after 24 hours. The caffeine cue generalized partially to d-amphetamine and completely to aminophylline. Neither pizotyline nor spiperone antagonized stimulus control induced by caffeine.

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BibTeXRIS

J C Winter. 1981. Caffeine-induced stimulus control.. https://doi.org/10.1016/0091-3057(81)90170-2

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Aminophylline

Effects of short-term aminophylline administration on cardiac functional reserve in patients with syndrome X.

OBJECTIVES: This study sought to evaluate the effect of adenosine receptor blockade by aminophylline on cardiac functional reserve in patients with syndrome X. BACKGROUND: Aminophylline may have a potentially antiischemic effect through the inhibition of adenosine and, thus, the coronary steal phenomenon in patients with syndrome X. METHODS: A single-blind, placebo-controlled study of an intravenous infusion of aminophylline (6 mg/kg body weight over 15 min) or placebo (20 ml of saline solution over 15 min) was performed during continuous radionuclide monitoring of left ventricular ejection fraction in 12 patients performing supine bicycle ergometric exercise. RESULTS: Aminophylline increased exercise time (aminophylline 400 s vs. placebo 355 s, p < 0.01), decreased degree of ST segment depression (aminophylline 1.6 mm vs. placebo 2.4 mm, p < 0.01) and either abolished (seven patients) or diminished (five patients) chest pain during exercise. Aminophylline also increased left ventricular ejection fraction at rest (aminophylline 66.5% vs. placebo 62.3%, p < 0.05) but did not improve its deterioration at peak exercise (aminophylline 60.1% vs. placebo 56.6%, p = NS) or shorten the abnormally prolonged interval between the end of exercise and the overshoot (aminophylline 115 s vs. placebo 130 s, p = NS). CONCLUSIONS: Aminophylline infusion increases ischemic threshold and prolongs exercise duration in patients with syndrome X. It is hypothesized that aminophylline acts by inhibiting the coronary steal phenomenon through adenosine receptor blockade. It does not improve the deterioration in left ventricular function at peak exercise or the delayed response in ejection fraction in the recovery period, presumably because the beneficial effects of aminophylline that result from the redistribution of coronary blood flow are limited.

Aminophylline

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Aminophylline