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Biomedical subjects

J Madden

Publications and source records attributed to J Madden.

At least 73 records · Page 4Linked to original sources
PubMed1982

Dissociation of long-term analgesia and the shuttle box escape deficit caused by inescapable shock.

Inescapably shocked rats perform poorly on a two-way shuttle box escape task 24 hr after the shock. Because inescapably shocked rats become analgesic upon reexposure to a small amount of shock 24 hr after inescapable shock, they are likely to be analgesic during the shuttle box escape task. Subjects receiving an equivalent amount of escapable shock display neither the escape dificit nor the analgesia. Both the analgesia and the escape deficit respond in a similar fashion to the manipulation of a variety of other variables. These findings have led to the suggestion that the analgesia ("long-term analgesia") may cause the inescapable-shock-produced escape deficit. However, the present experiments demonstrated that two pituitary manipulations that completely eliminate the analgesia have no effect on the escape deficit. Both hypophysectomy and dexamethasone administration blocked the analgesic consequences of inescapable shock but did not reduce the magnitude of the escape deficit. Therefore, the long-term analgesia produced by inescapable shock does not cause the deficit in shuttle box escape performance displayed by inescapably shocked rats. Furthermore, these results indicate that the pituitary is not essential in the production of this escape deficit.

Analgesia↗
PubMed1981

Cross tolerance between morphine and the long-term analgesic reaction to inescapable shock.

Animals exposed to a variety of stressors display a temporary analgesic reaction. This short-term analgesia has been shown to be reversible by opiate antagonists and cross-tolerant with morphine following some stress conditions, but not following others. It has recently been shown that inescapable shock parameters which produce behavioral '"learned helplessness" effects also produce a short-term analgesic reaction, and that this reaction can be re-aroused by a brief exposure to shock 24 hours later. Further, both the immediate and long-term antinociceptive reaction which follow shocks of this type have been shown to be reversible by opiate antagonists. Here it is shown that the long-term analgesic reaction is completely cross tolerant with morphine. Implications of these results for opioid mediation of learned helplessness and opioid versus nonopioid mediation of stress-induced analgesia are discussed.

Animals↗
PubMed1981

Management of the brown recluse spider bite.

A model to study the dermonecrotic effects of a crude fraction of venom from the brown recluse spider (Loxosceles reclusa) was developed using female New Zealand white rabbits. In the rabbit model, surgical excision of the sites of intradermally injected crude venom did not always prevent subsequent necrosis or wound dehiscence despite the use of fluorescein to determine the surgical margin. Heparin and steroids did not prevent the venom-induced necrosis and were much less effective than surgical excision or injecting a specific antivenom. When given within 24 hours, the specific antivenom raised against the brown recluse spider venom blocked or markedly attenuated the toxic effects of the venom in the rabbit model system.

Animals↗
PubMed1980

Opiate antagonists and long-term analgesic reaction induced by inescapable shock in rats.

Five experiments examined the influence of opiate antagonists on both the short-term analgesic reaction resulting 30 min after exposure to inescapable shock and the long-term analgesic reaction resulting after reexposure to shock 24 hr after inescapable shock exposure. Experiment 1 showed that the long-term analgesic reaction could be reduced by administration of naltrexone prior to exposure to inescapable tail shock. Experiment 2 showed that the reduction in the long-term analgesic reaction produced by naltrexone was dose-dependent. Experiment 3 showed that the long-term analgesic reaction could also be reduced by administration of naltrexone prior to reexposure to shock. Experiment 4 showed that the long-term analgesic reaction could be reduced by administration of large dose of naloxone prior to reexposure to shock. Experiment 5 showed that the short-term analgesic reaction was reduced by naltrexone administered prior to inescapable shock. Some implications of these results for the biochemical substrates of both learned helplessness and stress-induced analgesia are discussed.

Animals↗
PubMed1978

Regulation of gonadotropin secretion in Turner's syndrome.

To determine the role of body fat in regulating secretion of luteinizing hormone and follicle-stimulating hormone, we measured both at 20-minute intervals for 24 hours in eight children with Turner's syndrome. The 24-hour mean luteinizing hormone levels varied from 20.2 to 70.5 mlU per milliliter. Total body weight, total body fat and percentage of body fat showed a significant negative correlation with the 24-hour mean luteinizing hormone concentrations (P less than 0.01). The 24-hour mean follicle-stimulating hormone concentrations ranged from 60.4 to 229 mlU per milliliter, with a significant negative correlation between total body fat and percentage body fat and the 24-hour mean concentrations (P less than 0.05). These negative correlations were not mediated by estrogens or androgens.

Adipose Tissue↗
PubMed1978

Luteinizing hormone and follicle-stimulating hormone secretory dynamics in Turner's syndrome.

In eight teenage patients with Turner's syndrome, LH and FSH were measured at 20-min intervals for 24 h. The 24-h mean LH and FSH levels ranged from 20.2-70.5 mIU/ml and 60.4-229 mIU/ml, respectively. There was a significant positive correlation between the individual LH and FSH levels in the eight patients; the common correlation coefficient was 0.449 (P less than 0.001). The 24-h mean estradiol level was measurable in only two of the patients and the 24-h mean testosterone level for the eight patients was 0.10 ng/ml. The mean LH concentration during sleep was significantly higher (P less than .01) than during waking. The mean FSH concentration during sleep was also significantly higher (P less than 0.05) than during waking. The LH and FSH peak levels after LRH were significantly correlated with the 24-h mean LH (r = 0.918; P less than 0.01) and FSH concentrations (r = 0.754; P less than 0.05), respectively.

Adolescent↗
PubMed1975

Fetal stress from methadone withdrawal.

A pregnant patient in the midtrimester of pregnancy was begun on a methadone detoxification program. The fetal neurobiologic response was monitored by serial amniotic fluid amines (epinephrine and norepinephrine). The detoxification program showed a marked fetal response of the adrenal gland (E) and sympathetic nervous system (NE) that was blunted when the methadone dose was increased. Detoxification during pregnancy is not recommended unless the fetus can be biochemically monitored.

Adrenal Glands↗
PubMed1975

The interaction of hemicholinium-3 (HC-3) with cholinomimetics and atropine.

In either spontaneously beating or electrically driven atrial preparations of the guinea pig HC-3 (0.01-1 mM) inhibited negative inotropic responses to acetylcholine or carbachol. Although there was a parallel rightwards shift of the log concentration--response curves for acetylcholine or carbachol and no depression of the maximal response the type of antagonism was not competitive as the relationship between dose ratio -- 1) and concentration of HC-3 was not linear over the whole range investigated. A lesser degree of antagonism than expected for a competitive antagonist was observed with higher concentrations of HC-3. HC-3 was a more effective antagonist of responses to carbachol than to acetylcholine and pretreatment of animals with dyflos did not modify this difference. In addition, HC-3 was found to antagonize the inhibitory action of atropine on responses to acetylcholine and to a lesser extent carbachol. The results can be explained in terms of the interaction of HC-3 at a regulatory site distinct from the binding sites for cholinomimetics and atropinics. Interaction of HC-3 at the postulated site produces a noncompetitive antagonism of both agonists and competitive antagonists by modifying the affinities of the compounds for their respective binding sites.

Animals↗