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H Cappell

Publications and source records attributed to H Cappell.

At least 37 records · Page 2Linked to original sources
PubMed1983

A placebo-controlled double-blind comparative clinical study of the disulfiram- and calcium carbimide-acetaldehyde mediated ethanol reactions in social drinkers.

Treatment for 2 days with disulfiram (3.5 mg/kg once daily) and calcium carbimide (0.7 mg/kg twice daily) in social drinkers produced, as compared to controls, similar blood ethanol values, 2- to 3-fold increases in blood acetaldehyde, respectively, and increased heart rate, pulse pressure, skin temperature, and flushing following 0.15 g/kg of ethanol taken 12 hr after the last drug administration. Peak blood acetaldehyde concentration was greater for calcium carbimide compared to disulfiram (p less than 0.05) and subjects treated with calcium carbimide experienced greater discomfort compared to disulfiram due to palpitations and shortness of breath, and they reported less intention to drink during the reaction. However, neither drug produced sufficient aversion to curtail further drinking totally. With repeated drinks, there was an overall reduction of blood acetaldehyde concentration for calcium carbimide of 85% and for disulfiram of 35%. These data may provide a biochemical basis for the claims of certain alcoholics that they can drink to "burn off" the effects of these drugs.

Acetaldehyde↗
PubMed1982

Effects of pentobarbital and cocaine in rats expecting pentobarbital.

Rats received extensive exposure to pentobarbital in a distinctive environment, and were subsequently tested for tolerance to the sedative effects of pentobarbital either in the distinctive environment or in an environment previously associated only with saline. Rats tested when expecting pentobarbital (i.e., in the usual drug environment) were tolerant, but rats tested when not expecting the drug (i.e., in the saline environment) were not tolerant. These results extend demonstrations of conditional tolerance to the general behavioral arousal effects of a sedative hypnotic. Subsequently, the same rats were administered cocaine either when expecting pentobarbital or when not expecting pentobarbital. Rats administered cocaine when expecting pentobarbital exhibited more intense forms of cocaine-induced behavior than rats administered cocaine but not expecting pentobarbital. These results establish the phenomenon of conditional cross-potentiation between conditional drug states and unconditional drug-effects.

Animals↗
PubMed1981

Pavlovian control of cross-tolerance between pentobarbital and ethanol.

Tolerance to several effects of a number of drugs has been shown to depend on Pavlovian conditioning processes. Experiment I extended the compensatory conditioning model (Siegel 1975) to tolerance to the hypothermic effect of pentobarbital (30 mg/kg). In Experiment I, rats that acquired hypothermic tolerance in one environment did not display tolerance when tested in an environment not previously associated with drug administration. In Experiment II, rats were made tolerant to the hypothermic effect of pentobarbital (30 mg/kg) and tested for cross-tolerance to ethanol (2.5 g/kg). Cross-tolerance was observed, but it was significantly reduced if the test was in an environment different from the one in which tolerance to pentobarbital was originally acquired. Thus, the compensatory conditioning model accounts for at least part of the tolerance and cross-tolerance to the thermic effects of alcohol and pentobarbital. The physiological processes in the CNS underlying tolerance and cross-tolerance for these drugs, therefore, are controlled by associative processes.

Animals↗
PubMed1981

Homeostatic regulation and Pavlovian conditioning in tolerance to amphetamine-induced anorexia.

A series of experiments on the role of Pavlovian processes in tolerance to amphetamine-induced anorexia in rats was conducted. In Experiment 1A, tolerance to the suppressant effect of d-amphetamine (4.0 mg/kg) on milk consumption was substantially diminished in an environment not previously associated with drug administration. Experiment 1B supported the interpretation that Pavlovian compensatory conditioning rather than a nonassociative mechanism mediated this phenomenon. Experiment 2 examined the hypothesis that "contingent tolerance" results from an inadvertent manipulation of Pavlovian cues. As in previous research, tolerance was contingent in that it did not develop if the rats were not exposed to food under the influence of the drug. Tolerance developed only if access to food occurred under the influence of amphetamine, but as in Experiment 1A, it was substantially diminished in an environment not previously associated with drug administration. Thus, tolerance to amphetamine-induced anorexia was shown to be both contingent on previous experience with food in the drugged state and subject to Pavlovian control. No current explanation for the occurrence of contingent tolerance or for the control of tolerance by Pavlovian processes can at once account for both of these findings. Experiment 3 confirmed the hypothesis that interaction with the food stimulus would be necessary to extinguish tolerance. This finding is also problematic for any current behavioral theory of tolerance. It is proposed that interaction with food is necessary for the homeostatic regulation of disturbances in eating caused by amphetamine. When activated, this regulatory process operates by means of Pavlovian conditional compensatory processes.

Animals↗
PubMed1979

Conditioned tolerance to the hypothermic effect of ethyl alcohol.

Results from experiments with rats support the proposition that tolerance to the hypothermic effect of alcohol involves the Pavlovian conditioning of compensatory responses. Tolerance was substantially reduced when alcohol was administered in an environment that had not been associated with alcohol. Direct evidence of a conditioned hyperthermic compensatory response was found.

Animals↗
PubMed1979

An associative analysis of pretreatment effects in gustatory conditioning by amphetamine.

Various attempts have been made to account for the fact that pertreatment with some pharmacological agents reduces the ability of such agents to induce conditioned aversion to a flavor. One explanation, based on the concept of tolerance, suggests that pretreatment is effective because it renders the animal less sensitive to direct effects of a given dose of the agent. A second explanation emphasizes the possibility that procedural consequences of pretreatment interfere with associability of flavor and drug effect during conditioning. The second explanation was tested in two experiments. In experiment I nonreinforced presentations of drug administration cues completely reversed the attenuating effects of amphetamine pretreatment on gustatory conditioning by amphetamine. This finding was replicated and extended in the second experiment which was also designed to eliminate an alternative nonassociative explanation for the results. The principle of associative blocking may explain the effect of pretreatment on subsequent gustatory conditioning by drugs.

Animals↗
PubMed1979

Associative factors in drug pretreatment effects on gustatory conditioning: cross-drug effects.

The pretreatment effect (PE) in gustatory avoidance conditioning refers to the fact that pretreatment with a variety of pharmacological agents subsequently reduces the ability of the same agents to induce gustatory aversion. Explanations of this phenomenon emphasize either tolerance or associative interference. Any explanation of the phenomenon must also account for the present findings which demonstrate the PE when agents of pretreatment and conditioning were pharmacologically dissimilar. Rats were pretreated with d-amphetamine and tested for acquisition of an aversion to saccharin conditioned by amphetamine or morphine. The PE was obtained regardless of the drug used in conditioning. An associative manipulation involving nonreinforced presentation of the drug administration cues (i.e., injections followed by saline instead of drug), that attenuated the PE when pretreatment and conditioning were with amphetamine, was also effective when the pretreatment agent was amphetamine and the conditioning agent was morphine. The findings were interpreted within a framework of compensatory conditioning of a general physiological mechanism common to all gustatory avoidance.

Animals↗
PubMed1977

Parametric investigations of the effects of prior exposure to amphetamine and morphine on conditioned gustatory aversion.

Pretreatment by a psychoactive drug can greatly attenuate the conditioning of gustatory avoidance by that drug. Although such findings have been interpreted in terms of tolerance, alternative explanations are possible. In a series of experiments, it was found that pretreatments with morphine or amphetamine massed at 24-h intervals were no more effective in attenuating conditioning than pretreatments spaced at 120-h intervals, but pretreatment with morphine provided more persistent protection against subsequent conditioning by itself than did amphetamine in a comparable previous experiment. The similarity of massed and spaced pretreatment effects can be interpreted without appealing to tolerance as a factor, but the greater persistence of morphine pretreatment implicates tolerance as a mechanism.

Animals↗
PubMed1977

Drinking, driving, and the attribution of responsibility.

Among 112 students asked to attribute responsibility in 8 hypothetical traffic accident stuations, the state of alcohol intoxication affected both the degree of responsibility and the magnitude of financial sanctions assessed a potentially responsible driver involved in a road accident.

Accidents, Traffic↗
PubMed1976

Effects of amygdala lesions on taste aversions produced by amphetamine and LiCl.

Rats which sustained bilateral damage to the amygdala were treated with one of two diversely acting agents (either d-amphetamine sulphate 4 mg/kg, or lithium chloride 0.24 M) in a taste aversion paradigm. Both groups of animals showed an attenuation of the aversion on the first test day after the initial pairing with the drug thus demonstrating that this effect of the lesion was not UCS specific. The implication of these findings for the hypothesis concerning the role of the amygdala in taste aversion conditioning is discussed.

Amygdala↗
PubMed1975

Conditioned aversion by amphetamine: rates of acquisition and loss of the attenuating effects of prior exposure.

Chronic prior treatment with amphetamine greatly attenuates the conditined aversion to saccharin that may be produced by amphetamine. Two experiments were designed to determine some of the limiting conditions of this phenomenon. In Experiment 1, chronic treatment with 7.5 mg/kg of amphetamine was administered for 0, 1, 5, or 20 days prior to pairing saccharin with an injection of 1.0 mg/kg of d-amphetamine sulphate. The results indicate that between 5 and 20 days of treatment were necessary for the treatment to be effective in attenuating conditioned aversion. In Experiment 2, rats were withdrawn from treatment with 20 mg/kg of amphetamine for 1, 7, or 14 days prior to conditioning trials with 1.0 mg/kg of amphetamine. The prior treatment lost it effectiveness in attenuating conditioned aversion between 7 and 14 days after withdrawal. Although alternative explanations are possible, the time intervals required for acquisition and loss of the effectiveness of prior treatment are consistent with the hypothesis that tolerance is the mechanism underlying the observed effects.

Animals↗
PubMed1975

Modification of the punishing effects of psychoactive drugs in rats by previous drug experience.

In Experiment 1, it was shown that chronic prior exposure to amphetamine attenuated the conditioned avoidance of saccharin that was produced by both amphetamine and morphine during gustatory conditioning trials; the relationship between morphine and amphetamine was somewhat anomalous because of their pharmacological dissimilarity. The relationship was also asymmetrical, since in Experiment 2, chronic prior exposure to morphine failed to mitigate avoidance conditioning by amphetamine but was effective in attenuating conditioning by morphine itself. In a third experiment, it was found that prior treatment with chlordiazepoxide attenuated saccharin avoidance conditioned by chlordiazepoxide but not by amphetamine or morphine. The findings were related to Parker, Failor, and Weidman's hypothesis, based on findings with morphine, concerning the development of conditioned preferences for substances associated with the repletion of artificially induced biological needs. It was suggested that the findings were best interpreted as a reflection of drug tolerance rather than conditioned preference.

Animals↗