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Biomedical subjects

L Janský

Publications and source records attributed to L Janský.

At least 19 recordsLinked to original sources
PubMed1992

A discrete mode of the antipyretic action of AVP, alpha-MSH and ACTH.

The antipyretic effect of AVP, alpha-MSH and ACTH consists in lowering the thermoregulatory threshold and in shortening the time span of the fever. Thus, neuropeptides influence activity of hypothalamic neurones regulating body temperature. This was confirmed by recent experiments of Moravec (this volume) which indicate that spontaneous activity and thermosensitivity of neurones in hypothalamic slices can be influenced, by AVP. Why neuropeptides of different chemical structure such as AVT, on one hand, and alpha-MSH and ACTH, on the other hand, induce the same effect on thermoregulation remains to be elucidated.

Adrenocorticotropic Hormone↗
PubMed1992

The effect of PGE2 on activity and thermosensitivity of hypothalamic neurones in rat brain slices.

Using brain slices the effect of prostaglandin E2 (PGE2) on neurones from different locations of the rat hypothalamus was analysed. PGE2 (150 ng), when injected into the perfusion chamber, influences all hypothalamic neurones studied. The pattern of firing rate changes after PGE2 is variable, but the depressive effect predominates--72% of neurones decrease their firing rate in long-term experiments. PGE2 also lowers the thermosensitivity of warm sensitive neurones and increases the thermosensitivity of temperature insensitive neurones.

Animals↗
PubMed1989

Short days induce changes in specific melatonin binding in hamster median eminence and anterior pituitary.

Autoradiography of 125I-melatonin binding to hamster brain sections revealed a competitive 125I-melatonin binding in median eminence only. Saturation studies on crude membrane fraction revealed high-affinity melatonin binding sites in median eminence (Kd = 59 pM) and anterior pituitary (Kd = 97 pM). In the hamsters maintained on LD 14:10, the concentration of the binding sites was 10.4 and 6.0 fmol/mg protein in median eminence and anterior pituitary respectively; long-term exposure to LD 8:16 decreased the concentration to less than a half.

Animals↗
PubMed1989

The role of dopaminergic pathways in thermoregulation in the rabbit.

Dopamine, when injected into the anterior hypothalamus of the rabbit, induced a slight hyperthermia due to an upward shift of the threshold central temperature for induction of cold thermogenesis, panting and vasodilation. A slightly reduced thermosensitivity of the controller regulating vasodilation may also contribute to the hyperthermic effect of dopamine. Intrahypothalamic injections of the dopamine agonist, apomorphine, induced a similar effect to that of dopamine, with the exception that the thermosensitivity of the controller regulating vasodilation was not changed. Intraperitoneal injections of a dopamine antagonist, haloperidol, induced a marked hypothermia, due to a downward shift of the threshold central temperature for induction of cold thermogenesis, panting and vasodilation. A slightly reduced thermosensitivity of the controller regulating vasodilation was also observed. Intrahypothalamic injections of haloperidol did not induce an antagonist effect to dopamine, but rather tended to induce hyperthermia. Thermoregulatory responses, occurring after administration of dopamine or apomorphine, partially resembled those seen after administration of neurotensin or prostaglandins.

Animals↗
PubMed1988

Mode of ACTH antipyretic action.

The method of intestinal cooling was used to analyze the effect of centrally administered ACTH in microgram quantities on hypothalamic centers regulating activity of thermoregulatory outputs (cold thermogenesis--CT, peripheral vasomotor tone--PVMT, respiratory evaporative heat loss--REHL). ACTH, when injected into the supraoptic area of the anterior hypothalamus of normal rabbits, had no significant effect on body temperature control. Intrahypothalamic administration of ACTH during the early phase of the fever, induced by intravenous injection of exogenous pyrogen, evoked dissociation of temperature thresholds for cold and warm defence, shifting the threshold for induction of cold thermogenesis to lower central temperatures. The thermosensitivity of centers controlling cold thermogenesis was lowered and the maximal values of cold thermogenesis were depressed to about 30% of those in control rabbits. Central administration of ACTH in the late phase of the fever (120 min after IV injection of endotoxin) induced a smaller effect than in the early phase of the fever--the downward shift of the temperature threshold for cold thermogenesis was less evident and the thermosensitivity of the controller remained unchanged. The changes in activity of thermoregulatory centers that occurred after ACTH in febrile rabbits correspond to those observed in the late phase of the fever in ACTH-untreated rabbits. It is suggested therefore, that the presumed increase in ACTH production during fever might represent a negative feed-back mechanism contributing to the termination of the febrile state.

Adrenocorticotropic Hormone↗
PubMed1987

Thermoregulation of the rabbit during the late phase of endotoxin fever.

In the late phase of the fever occurring 120 or more min after i.v. injection of endotoxin (1 microgram/kg) to female rabbits, marked shifts of thresholds for respiratory evaporative heat loss and for peripheral vasodilatation to higher body core temperatures were observed. In contrast, the threshold body core temperature for cold thermogenesis was shifted downwards. As a result, the interthreshold zone was widened. Within the body temperature range of 37.4 to 39.9 degrees C neither heat production or heat loss mechanisms were operant and the body temperature was determined mainly by passive heat transfer between the body and the environment. Outside this zone, the sensitivities of the heat and cold defence activities to changes in body core temperature appeared to be unchanged.

Animals↗
PubMed1987

Effect of bombesin on thermoregulation of the rabbit.

Injections of bombesin (BOM, 125, 250 and 500 ng) into the preoptic/anterior hypothalamus caused dose-related decreases of threshold temperatures for metabolic cold defence, cutaneous vasomotor tone and respiratory rate, combined with a reduced sensitivity of these thermoregulatory effectors in response to core temperature changes induced at thermoneutral or warm ambient conditions. Intracisternal (i.c.) injections of BOM (250 ng) produced qualitatively identical thermoregulatory effector changes in response to core temperature changes. Injections of BOM into the posterior hypothalamus did not affect body temperature control. Increased locomotor behavior, licking and grooming was elicited, however, from all injection sites. The results explain the prevailing hypothermic effect of BOM as the consequence of the concerted decrease in threshold temperatures and "gains" of all autonomic thermoregulatory effectors and suggest the activation of warm inputs, relative to cold inputs, at the hypothalamic level as the underlying mechanism. Direct or indirect inhibition of the intrinsic hypothalamic system involving thyrotropin-releasing hormone (TRH) and consequent deactivation of central noradrenergic pathways known to generate the entire autonomic pattern of cold defence might be involved in the neuro-humoral changes resulting in hypothermic effects of centrally applicated BOM.

Animals↗
PubMed1986

Hyperthermic effect of neurotensin in the rabbit.

Neurotensin injected into the anterior hypothalamus of the rabbit induces a consistent upward shift of the threshold core temperatures for inducing cold thermogenesis, peripheral vasomotor tone and respiratory evaporative heat loss, while leaving the efficiency and the intensity of these thermoregulatory outputs unchanged. Neurotensin injections into the PH are without effect on body temperature control. The effect of neurotensin is interpreted as a selective inhibition of activity of warm sensors in the anterior hypothalamus. The possible mediating role of dopaminergic pathways in the neurotensin action is discussed.

Animals↗
PubMed1986

Effect of external factors on gonadal activity and body mass of male golden hamsters (Mesocricetus auratus).

Effects of photoperiod, temperature and food and water availability on body and testicular mass of golden hamsters were investigated. Lack of water or food inhibited body growth. Short photoperiod (LD 8:16) enhanced body growth in males fed 'poor diet' but it had no effect in animals on 'high quality diet'. Cold exposure diminished body growth in animals with access to water but not in those deprived of water. It is suggested that lowered motor activity is mainly responsible for body mass gain of animals kept under the short photoperiod. All stressful factors (water deprivation, 'poor diet' or cold) induced involution of testes. The time course of testicular involution was similar to that induced by short photoperiod. Testicular involution was, after several weeks, followed by spontaneous recrudescence. Combination of stressful external cues speeded up testicular involution. Since the testicular involution induced by water deprivation, "poor diet" and cold also occurred in animals kept in constant light or under long photoperiod (which are known to produce functional pinealectomy) it is concluded that the inhibitory effects of stressful external factors on testes are not mediated by the pineal. The decrease in testosterone production induced by external cues precedes changes in testicular mass. In individuals kept in the cold, testosterone production remains low, in spite of spontaneous recrudescence of the testes. No simple relationship between testosterone concentration in the blood and testicular mass was observed. The mass of the interscapular brown adipose tissue (ISBAT) changes strikingly during the hibernation cycle. Immediately after exposure to cold it decreases and stays at the low level for 40 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Nutritional Physiological Phenomena↗
PubMed1985

Arrest of the circadian pacemaker driving the pineal melatonin rhythm in hibernating golden hamsters, Mesocricetus auratus.

Pineal melatonin rhythm in golden hamsters was abolished during hibernation. After arousal in darkness, pineal melatonin increased rapidly regardless of whether the arousal was induced during the day or at night. Rapid increase of pineal melatonin after arousal was markedly diminished in animals exposed to light. In hamsters aroused at midnight, the melatonin rhythm in constant darkness ran with the reversed phase relative to hamsters aroused at noon. Since after arousal the melatonin rhythm obviously starts anew from the same phase, we conclude that the circadian pacemaker driving the rhythm might be arrested during hibernation at the day-time phase.

Animals↗
PubMed1985

Thyroid hormones in rats during long-term cold exposure and hypometabolic effect of reverse triiodothyronine on adrenaline induced thermogenesis.

One-day cold exposure to 5 degrees C induced temporal increase of reverse-triiodothyronine (rT3), triiodothyronine (T3) and thyroxine (T4) concentrations in the blood of rats (by 151%, 91% and 107%, respectively). The levels of all thyroid hormones remain elevated for at least 10 days of cold exposure. The injection of rT3 (330 micrograms kg-1 s.c.) inhibited the resting and adrenaline stimulated metabolism 1-3 days after application independently from the thyroid status of the animals. Since the hypothermic effect of rT3 occurred in thyroidectomized rats, it was concluded that rT3 acted primarily on peripheral, tissues, rather than on the thyroid.

Animals↗
PubMed1976

Effect of different environmental temperatures on the serotonin concentration and turnover in the brain stem of a hibernator.

The serotonin (5-HT) and 5-hydroxyindoleacttic acid (5-HIAA) levels and 5-HT turnover were studies in the brain stem of warm- (+30 degrees C) and cold- (+6 degrees C) acclimated golden hamsters, exposed for 3 hours to temperatures of +6 degrees C, +30 degrees C and +37 degrees C, respectively. In war-acclimated hamsters kept under conditions the 5-HT level in the brain did not change significantly during the year. The 5-HIAA level was slightly higher in the winter. The 5-HT turnover varied within limits of 0.071 to 0.180 mug/g/hour-1. Three hours' exposure of warm-acclimated golden hamsters to cold (6 degrees C) increased the concentrations of 5-HT and 5-HIAA and the 5-HT turnover in the brain. After long-term adaptation to cold (6 degrees C) the 5-HT level, and the 5-HT turnover returned to the original level. Three hours' exposure of golden hamsters to higher environmental temperatures (warm-acclimated individuals to 37 degrees C and cold-acclimated individuals to 30 degrees C) also increased the 5-HT turnover. The concentrations of 5-HT and 5-HIAA increased in cold-acclimated golden hamsters exposed to 30 degrees C and was not changed in warm-acclimated ones, exposed to 37 degrees C. Although the elevated temperatures induce greater changes in serotonin metabolism than lowered temperatures, the serotonin pathways in the brain do not seem to be affected by short-term temperature changes specifically. The findings are rather indicative that changes in 5-HT turnover may be the primary reaction to stressful conditions.

Animals↗
PubMed1976

Substitution of calorigenic effects of noradrenaline and adrenaline and differences in their inhibition by propranolol.

The calorigenic effect of infused adrenaline and noradrenaline was measured in cold-acclimated rats. The slopes of the dose-response curves for the two catecholamines and the maxima of the curves were the same. The adrenaline dose-response curve showed a shift to the right, towards higher infusion doses, compared with the noradrenaline curve. Thermogenesis due to the two catecholamines was not additive throughout the whole range of doses used. In interaction with noradrenaline, propranolol caused a parallel shift of the dose-response curve to the right, whereas in interaction with adrenaline it depressed the maximum. The concept that the two catecholamines act via different regulation sites on a common thermogenetic effector is discussed.

Acclimatization↗