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Biomedical subjects

B Hine

Publications and source records attributed to B Hine.

At least 19 recordsLinked to original sources
PubMed1998

Linking public health education and practice: the Australian experience.

The public health workforce in Australia is highly skilled, multifunctional, and drawn from a variety of backgrounds, including clinical practice and non-health areas. A wide range of activities is needed to meet the educational and training requirements of this workforce, including on the job inservice training, context specific continuing education programs and short courses, distance and self-directed learning packages, and postgraduate University level courses. The core components of public health today include: a social and political commitment to health, a shared responsibility between government and the public, and a multidisciplinary field of action. The challenge for those providing education and training for the public health workforce is to ensure graduates have the broad range of knowledge and skills needed in this climate. A system-wide approach to learning, where knowledge and skill development is related to the practices and settings of service and program delivery, will ensure strong links between education and practice.

Australia↗
PubMed1995

Differential open field reactivity in HAS and LAS rats.

To identify potential differences in emotional reactivity in high (HAS) and low (LAS) alcohol-sensitive rats in open field tests, 20 ethanol naive, 19th generation HAS and 20 LAS rats from the University of Colorado's Alcohol Research Center each received three consecutive daily 20-min exposures to a 1-sq m open field. The results of repeated-measures ANOVA and Keuls tests, performed on each of five concurrently recorded behaviors, indicated that, compared to HAS rats, LAS animals exhibited significantly greater latencies to begin ambulation, elevated ambulation, and rearing scores that failed to habituate over 3 days, and an increasing intersession bolus count. In addition, significant positive correlations occurred between days 2 + 3 (but not day 1) ambulation and bolus counts in LAS but not HAS rats, and between day 1 ambulation and (i) rearings and (ii) center square entries in HAS but not LAS rats. Together with other cited data, these results provide support for a hypothesis of relatively greater emotional reactivity in LAS rats and illustrate the need for multiple measures and sessions in evaluating open field behavior.

Animals↗
PubMed1990

Acute morphine lowers brain stimulation reward thresholds in rats with depressed or elevated response rates.

The positively-reinforcing effect of acute morphine sulfate (MS) administration was assessed by concurrent rate-dependent and rate-independent measures of brain stimulation reward in male rats. An acute 4 mg/kg MS injection produced a rapid, statistically-significant decrease in reward threshold of 28.5%, when compared with saline control values, 45 min after injection. Response rates for brain stimulation delivery decreased by 60.6%, when compared with saline values during the period of maximum threshold change. Other animals, injected with an acute 1 mg/kg MS dose, exhibited significant threshold decreases (21.5%), relative to changes in saline values that occurred in a prior session, and response-rate increases of 23.1%, relative to saline-session changes, when the data were recorded 40 min after injection. The findings reported here demonstrate that the decreases in reward threshold produced by acute morphine administration are independent of the response-rate changes that occur and also support the idea that morphine's rewarding effect may be independent of the behavioral inhibition or activation that can result from the effects of different morphine doses.

Animals↗
PubMed1985

Morphine and delta 9-tetrahydrocannabinol: two-way cross tolerance for antinociceptive and heart-rate responses in the rat.

Tail-flick analgesic responses and heart-rate changes were measured in male Sprague-Dawley rats challenged with an acute IP morphine sulfate (MS) or delta 9-THC injection after receiving daily injections of delta 9-THC or morphine, respectively. Degree of tolerance development to each agent was determined before the cross-tolerance challenge was administered. Cross tolerance occurred to analgesic and bradycardic effects of a 10 mg/kg THC challenge in rats receiving 50 mg/kg MS injections over a 23-day period. Cross tolerance to the bradycardic effects of a 20 mg/kg MS challenge occurred in rats receiving seven daily 10 mg/kg delta 9-THC injections and to MS tail-flick analgesia after 14 days. Although rapid tolerance occurred during administration of both agents, cross tolerance to THC bradycardia occurred only in groups exhibiting complete tolerance to MS injections; cross tolerance to MS bradycardia was observed in animals that were only partially tolerant to THC injections. The data extend earlier cross tolerance data in the mouse to the rat, and provide new information using heart rate, a response that may mirror aversive internal states induced by drugs.

Analgesia↗
PubMed1980

Opiate receptor function may be modulated through an oxidation-reduction mechanism.

Cupric ion, a thiol oxidant, caused naloxone-reversible analgesia when injected intracerebroventricularly in mice; its potency was close to that of morphine. Dithiothreitol, a thiol reductant, reversed the analgesia induced by cupric ion and antagonized analgesia induced by morphine. Oxidized dithiothreitol had no effect. These findings, together with evidence for redox modification of opiate receptor binding in vitro, suggest that a mechanism of oxidation-reduction of thiols may modulate opiate receptor function.

Animals↗
PubMed1979

Thioridazine and EKG anomalies.

Acute i.v. infusion but not daily oral administration of thioridazine-HCl in the dog produced EKG anomalies similar to those reported in psychiatric patients taking this drug. Lack of EKG effects after thioridazine-5-sulfoxide infusion and presence of anomalies after thioridazine at equivalent doses suggests further evaluation of the relationship between reported plasma levels of thioridazine and its ring-sulfoxide in association with EKG changes.

Animals↗
PubMed1977

Cardiovascular effects of delta9-tetrahydrocannabinol in conscious and anaesthetized dogs.

1. Temporal effects of delta9-tetrahydrocannabinol (THC) on heart rate and blood pressure in conscious dogs were compared to those in anaesthetized dogs. 2. In conscious dogs, THC in doses of 0.25 and 0.1 mg/kg resulted in maximal heart rate reductions of 48 and 41%, respectively, and in no significant change in blood pressure. 3. In anaesthetized animals THC in doses of 0.5 and 0.25 mg/kg caused a peak reduction in heart rate of 38 and 34%, and of blood pressure of 24 and 8%, respectively. 4. The results demonstrate that the bradycardia in response to THC in dogs is independent of the concomitant anaesthesia. 5. We conclude that the discrepancy between heart rate response to THC in dogs and in man is due to a species difference.

Anesthesia↗
PubMed1977

Analgesic, heart rate, and temperature effects of delta8-THC during acute and chronic administration to conscious rats.

Acute and chronic effects of delta8-THC on tail-flick, heart rate, and rectal temperature responses in conscious, unrestrained male rats were studied. In the acute experiment unidirectional dose-dependent analgesic, hypothermic, and negative chronotropic cardiac effects were observed within the dose range employed. Of the three variables, heart-rate decreases were most sensitive to the effects of THC, reaching significance at 2 mg/kg. Rapid development of tolerance occurred for all three measures, with complete tolerance developing within 13 days only to the heart-rate decreases. The results discussed in the context of previous data.

Analgesics, Opioid↗
PubMed1975

Involvement of biogenic amines in drug-induced aggressive pecking in chicks.

Pairs of neonate chicks were administered psychoactive agents and pecks against each other were recorded during 4-hr test sessions. The first experiment assessed where drug-induced aggressive pecking could serve as a useful anti-depressant screening model. Although pecking was induced by tricyclics, d-amphetamine, and L-Dopa, ineffective agents included a MAO inhibitor (pargline) and a tricyclic indole antidepressant (iprindole). These data cast doubt on the validity of the chick pecking model as a specific antidepressant tests. A second experiment attempted to determine where different amines were involved in pecking induced by an antidepressant and a CNS stimulant. Pairs of chicks were pretreated with various doses of amine antagonists, and a standard dose of imipramine (IMI) or d-amphetamine (AMP) was administered. Haloperidol completely antagonized AMP but not IMI pecking, while phentolamine and propranolol did not modify AMP pecking, suggesting involvement of dopamine. Pecking induced by IMI was partially antagonized by a dose of methysergide ineffective in modifying AMP pecking. Neither phentolamine nor propranolol blocked IMI pecking. Serotonin was further implicated in IMI pecking in a third experiment, whether chronic PCPA pretreatment significantly decreased IMI, but not AMP pecking. These data suggest that aggressive pecking induced by AMP and IMI may be mediated by different amine systems.

Aggression↗
PubMed1975

Morphine-dependent rats: blockade of precipitated abstinence by tetrahydrocannabinol.

Male rats were implanted subcutaneously with a pellet containg 75 milligrams of morphine base or placebo, and naloxone hydrochloride (4 milligrams per kilogram of body weight) was administered 72 hours later. Treatment with delta-9-tetrahydrocannabinol (2, 5, or 10 milligrams per kilogram) 1 hour before maloxone administration significantly reduced the intensity of abstinence; the two higher doses blocked the appearance of wet shakes and escapes, diarrhea, and increased defecation. delta-9-Tetrahydrocannabinol did not induce abstinence itself, and prior treatment with cannabidiol was ineffective in reducing naloxoneprecipitated abstinence in animals with morphine pellets. These data suggest that delta-9-tetrahydrocannabinol may be of value in facilitating narcotic detoxification.

Animals↗
PubMed1975

Differential effect of cannabinol and cannabidiol on THC-induced responses during abstinence in morphine-dependent rats.

The same dose of cannabinol (CBN) or cannabidiol (CBD) further increased the attenuation of precipitated abstinence signs observed in morphine-dependent rats that also received an acute dose of delta 9-THC. By contrast, rotational behavior (turning), which is observed concomitantly in THC-treated rats during morphine abstinence, was not increased by CBN, but was potentiated by CBD. These data illustrate differences between psychoinactive cannabinoids in their interaction with delta 9-THC that might be relevant to possible clinical use of Cannabis in narcotic detoxification.

Animals↗
PubMed1975

Attenuation of precipitated abstinence in methadone-dependent rats by delta 9-THC.

Racemic methadone hydrochloride was administered to male rats in daily subcutaneous injections of 10-30 mg/kg. Dependence, when assessed by naloxone challenge after 26 days, was quantitatively and qualitatively similar to that previously reported by us for rats implanted with a 75 mg morphine pellet for 72 hours. Abstinence scores in animals pretreated acutely with 10 mg/kg delta 9-THC one hour before naloxone were significantly less than those of a vehicle control group, and wet shakes and gastrointestinal signs of abstinence were blocked. These results extend previous observations of morphine abstinence attenuating properties of delta 9-THC to effects on animals dependent on methadone.

Animals↗