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Biomedical subjects

T F Lee

Publications and source records attributed to T F Lee.

70 records · Page 4Linked to original sources
PubMed1979

Effects of morphine and related drugs on core temperature of two strains of rat.

The changes in core temperature induced by low (5 mg/kg) and high (40 mg/kg) doses of morphine were compared in Wistar and Sprague-Dawley rats. In Sprague-Dawley rats the low dose caused a hyperthermia and the high dose a hypothermia but in Wistar rats both doses caused a hyperthermia. In either case the change in core temperature was antagonized by naloxone (2 mg/kg). Tolerance to the effects of the high dose of morphine developed in both strains of rat. Dextromoramide (3.75 and 15 mg/kg) also had an effect on core temperature, but in this case the responses of the strains were opposite to those seen with morphine. Laevomoramide was relatively ineffective. Naloxone (2 mg/kg) had no effect on the ability of rats of either strain to withstand heat or cold stress, providing no evidence that endogenous morphine-like substances have a physiological role in thermoregulation.

Animals↗
PubMed1979

Evidence for an endogenous dopamine-mediated hypothermia in the rat.

1 Unilateral intrahypothalamic injection of either dopamine (10 mug) or amphetamine (10 mug) caused a fall in core temperature in the rat. Pimozide (0.5 mg/kg, i.p.) significantly reduced the hypothermic response, whereas pretreatment with phentolamine (1 mg/kg, i.p.) or methysergide (5 mg/kg, i.p.) was ineffective.2 Systemic pretreatment with cocaine (20 mg/kg) abolished the hypothermic effect of amphetamine, but slightly enhanced the hypothermic response to dopamine.3 Systemic pretreatment with tranylcypromine (10 mg/kg) had no significant effect on the fall in core temperature induced by either amphetamine or dopamine.4 Intraperitoneal injection of cocaine and tranylcypromine, on their own, caused a fall in core temperature in the rat, which was significantly antagonized by either systemic or central pretreatment with pimozide. Phentolamine and methysergide failed to block the hypothermia.5 Unilateral intrahypothalamic injection of cocaine (20 mug) or tranylcypromine (10 mug) also caused a significant fall in core temperature, which was reduced by intrahypothalamic pretreatment with pimozide (0.5 mug), but not significantly changed by pretreatment with phentolamine (25 mug) or methysergide (5 mug).6 These results provide evidence for the presence of a dopaminergic system within the preoptic region, which mediates a lowering of core temperature in the rat.

Amphetamine↗
PubMed1978

Dopamine receptors in the central thermoregulatory pathways of the rat.

1. Intrahypothalamic injection of either dopamine (10 microgram) or apomorphine (10 microgram) in a dose volume of 1 microliter. caused an almost immediate rise in tail skin temperature and a concomitant fall in core temperature in the conscious rat maintained at an ambient temperature of 17 +/- 1 degrees C. 2. The location of the dopamine-sensitive site was defined more accurately by reducing the dose volume to 0.5 microliter. and injecting dopamine at different points throughout the preoptic and anterior hypothalamic region. 3. The largest mean fall in core temperature (1.13 +/- 0.22 degrees C) was obtained after injection into the preoptic region. Injections with their perimeters more than 0.4 mm rostral or caudal to this site were ineffective. 4. Rats placed 0.65 m below a 250 W infra-red lamp responded to the imposed heat load by vasodilation of the tail skin blood vessels, indicated by an increased tail skin temperature. 5. Bilateral, but not unilateral, injection of either pimozide (0.5 microgram) or haloperidol (2.5 microgram) into the preoptic region significantly reduced the increase in tail skin temperature so that the rats were less able to withstand the imposed heat load. 6. Three serial sections (0.5 mm thick) were prepared from the preoptic anterior hypothalamic region of the rat brain, one anterior, one posterior and one corresponding to the dopamine-sensitive site. 7. Tissue from the middle slice increased its rate of synthesis of 3,5-cyclic AMP in response to addition of dopamine 20 or 100 micron to the incubation medium. The posterior slice was inactive, but the anterior slice had similar activity to the middle slice. 8. The effect of dopamine on the middle slice was specifically blocked by haloperidol (0.1 micron), whereas the effects on the anterior slice were partially blocked by both haloperidol (0.1 micron) and propranolol (0.1 micron). 9. These results indicate that there is within a well defined area of the preoptic region a population of dopamine receptors, which play a part in the transmission of information from warm sensors to heat loss effectors.

Animals↗
PubMed1978

Is acetylcholine involved in a dopamine receptor mediated hypothermia in mice and rats?

1 Apomorphine and oxotremorine caused a dose-related fall in core temperature in the mouse and a fall in core temperature preceded by an increase in tail-skin temperature in the rat.2 In both species the slope of the dose-response curve was greater for oxotremorine (8.2 +/- 0.6 mice, 0.9 +/- 0.1 rats) than it was for apomorphine (1.7 +/- 0.3 mice, 0.5 +/- 0.07 rats).3 The mouse was more sensitive than the rat to the effects of both agonists.4 Atropine (0.625 to 5 mg/kg) and hyoscine (0.5 and 1 mg/kg) caused a dose-related rightward shift of the dose-response curve to oxotremorine in mice, but pimozide (0.25 to 1 mg/kg) was ineffective. Similar results were obtained in the rat.5 Pimozide (0.125 to 1 mg/kg) caused a dose-related rightward shift of the dose-response curve to apomorphine in mice, but atropine (1.25 to 1 mg/kg) and hyoscine (0.5 and 1 mg/kg) were ineffective. Similar results were obtained in the rat.6 Intrahypothalamic injection of apomorphine (10 mug) and oxotremorine (1.25 mug) caused a fall in core temperature in rats. Pimozide (0.5 mg/kg i.p.) caused reversal of the effect of apomorphine but did not significantly change the response to oxotremorine. Atropine (2.5 mg/kg i.p.) blocked the effect of oxotremorine, but not that of apomorphine.7 These results suggest that there are both central dopamine and central muscarinic acetylcholine receptors which mediate a fall in core temperature in rodents, but do not support the hypothesis that any connection exists between these two receptor populations.

Acetylcholine↗
PubMed1977

Do central dopamine receptors have a physiological role in thermoregulation?

1 Core and tail skin temperature was measured in rats which had guide cannulae implanted into their brains to allow drug injections directly into the preoptic anterior hypothalamus. 2 Apomorphine and dopamine (10 microgram in 1 microliter) injected into the area of the preoptic anterior hypothalamus caused a fall in core temperature which was preceded by a rise in tail skin temperature. 3 The decrease in core temperature following central injection of either apomorphine or dopamine was significantly reduced by pretreating rats for 2 h with pikozide 0.5 mg/kg i.p.). 4 Bilateral intrahypothalamic injection of pimozide (0.5 microgram in 1 microliter) significantly reduced the hypothermic effect of systemic apomorphine (1.25 mg/kg i.p.). 5 Control rats placed 65 cm below a 250 W infrared lamp responded with vasodilation of tail skin blood vessels as indicated by an increase in tail skin temperature. Pimozide pretreatment (0.5 mg/kg i.p.) significantly reduced this response. 6 These results suggest that the preoptic anterior hypothalamus contains dopamine receptors which mediate hypothermia in rodents and raise the possibility that endogenous dopamine has a physiological role in thermoregulation.

Animals↗
PubMedDate not supplied

In vivo release of dopamine during perfusion of neurotensin in substantia nigra of the unrestrained rat.

The functional effect of neurotensin on the kinetics of dopamine (DA) release in the substantia nigra of the freely moving rat was investigated. After guide tubes for push-pull perfusion were implanted stereotaxically just above the substantia nigra, endogenous stores of DA in this structure were labelled by micro-injection of 0.02-0.05 microCi of [14C]-DA. Then an artificial cerebrospinal fluid (CSF) was perfused within the site at a rate of 20 microliters/min at successive 5 min intervals. Neurotensin added to the CSF perfusate in concentrations of 0.05-0.1 microgram/microliter evoked an immediate, Ca++ dependent release of DA from sites directly within the substantia nigra or a delayed efflux when the peptide was perfused at the edge of this structure. Neurotensin failed to affect the pattern of release of this monoamine at sites which were not within the substantia nigra. Further, the body temperature of the rat also was not altered by neurotensin at any of the sites of perfusions. A relatively inactive analogue of the peptide, [D-Arg]9 neurotensin, was essentially without effect on DA activity. In double isotope experiments in which the substantia nigra of the rat was labelled with both [3H]-5-HT and [14C]-DA, the perfusion with neurotensin failed to affect 5-HT efflux while the release of DA was enhanced. Chromatographic analysis of the metabolites of DA in samples of push-pull perfusates revealed that neurotensin enhanced significantly the level of DOPAC and HVA. Overall, these results demonstrate that in the unrestrained rat neurotensin acts selectively within the substantia nigra to alter the presynaptic, Ca++ dependent release of DA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Is neurotensin in the brain involved in thermoregulation of the monkey?

Cannulae for intracerebroventricular (ICV) infusion were implanted stereotaxically in monkeys (Macaca fascicularis) maintained post-operatively in a primate restraint chair. During each experiment, a series of physiological measures was recorded simultaneously on a polygraph which included colonic temperature, vasomotor tone, heart rate, respiratory rate, and basal metabolism as reflected by O2 uptake. The ICV infusion in a volume of 0.5 ml of neurotensin (NT) in doses ranging from 3-150 micrograms produced neither a statistically significant nor consistent change in body temperature or vasomotor response. Although the highest dose of 450 micrograms NT infused ICV caused an immediate bradycardia and a concomitant decline in metabolic and respiratory rates, an average decline in core temperature of 0.6 degrees C and the accompanying cutaneous vasodilation often had a latency as long as 1.0 hr. In contrast to the typical hypothermia in this species following an ICV infusion of catecholamines, implicated in the central pathways underlying thermoregulation, NT failed to elicit a coordinated set of physiological responses for heat dissipation in the monkey. Therefore, it is unlikely that this tridecapeptide plays a role in the central mechanisms mediating the control of body temperature of this primate species.

Animals↗
PubMedDate not supplied

Sentinel surveillance for enterovirus 71, Taiwan, 1998.

Outbreaks of enterovirus 71 have been reported around the world since 1969. The most recent outbreak occurred in Taiwan during April-July 1998. This hand, foot, and mouth disease epidemic was detected by a sentinel surveillance system in April at the beginning of the outbreak, and the public was alerted.

Disease Outbreaks↗