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PubMed1979

The function of glucocorticoids in thermogenesis.

Studies both in vivo and in vitro implicate glucocorticoids in various aspects of thermogenesis and prevention of heat loss. Many or most of these effects are probably permissive. Adrenalectomized, cold-exposed rats require glucocorticoids for catecholamine-mediated mobilization of free fatty acids, for shivering responses, and for vasoconstriction and piloerection. Glucocorticoid pretreatment of hypothermic hamsters results in a physiological state more similar bioenergetically to hibernation than to hypothermia. For example, such hamsters can arouse to normothermia from a body temperature of 8 C in a 7--8 C cold room. Lipolytic, gluconeogenic, glycogenolic, and pressor actions resulting from several hormone interactions that require glucocorticoids for optimum responses may account for the enhanced thermogenic ability shown by glucocorticoid-pretreated hamsters. Glucocorticoid treatment also results in enhanced blood and liver carbohydrate levels during hypothermia, a condition similar to that occurring in naturally hibernating animals as opposed to the depleted carbohydrate reserves generally seen in hypothermic animals.

Adipose Tissue↗
PubMed1979

Behavioral and biochemical effects of para-methoxyphenylethylamine.

p-methoxyphenlethylamine (p-MPEA) induces the "serotonin syndrome" in mice which consists of lateral head weaving, Straub tail, hindlimb abduction, tremor, hyperactivity, reciprocal fore-paw treading, salivation and piloerection. These p-MPEA-induced behavioral signs were partially prevented by pretreatment with serotonin (5HT) uptake blockers (fluoxetine, chlorimipramine, Org 6582) and 5HT receptor blockers (methiothepin, methysergide, cinnanserin) but not by two depletors of brain 5HT (p-chlorophenylalanine, reserpine). p-MPEA selectively released 5HT and inhibited 5HT uptake from mouse whole brain synaptosomes. The concentrations of both 5HT and 5-hydroxyindoleacetic acid (5HIAA) in whole mouse brain were increased at 1 and 2 hours after injection of p-MPEA (50 mg/kg). The effect of p-MPEA on displacement of specific tritiated 5HT binding to membranes from mouse brain was considerably less than that of p-chlorophenylethylamine (p-CPEA), p-methoxytryptamine (pMT) and quipazine. Thus p-MPEA may induce the "serotonin syndrome" predominantly by releasing 5HT from presynaptic nerve terminals.

Animals↗
PubMedDate not supplied

Effect of hypothermia on lipolytic processes in blood and adipose tissue of rat.

Short-lasting hypothermia raises the FFA level in the blood and this rise is associated with increased lipid-mobilizing activity and higher lipolytic activity of the serum. Raised FFA level and increased lipid-mobilizing activity of the serum persist even when the degree of general anaesthesia is sufficient for preventing thermogenesis signs (shivering and piloerection) caused by falling body temperature. Beta-adrenergic blockade fails to abolish the effect of lipolysis activation caused by hypothermia. These observations suggest that during hypothermia in the blood of the animals appear factors stimulating lipolysis in the adipose tissue. One of these factors may stimulate tissue lipolysis independently of beta-adrenergic receptors. Insulin blocks significantly lipolytic processes in the adipose tissue of hypothermic animals, but its administration is connected with the danger of hypoglycaemia development.

Adipose Tissue↗
PubMed1983

Toxicological studies on bestatin. I. Acute toxicity test in mice, rats and dogs.

Studies on acute toxicities of bestatin (NK421) were carried out in both sexes of mice and rats, and male dogs. NK421 was administered subcutaneously, intraperitoneally and orally in mice and rats, and orally in dogs respectively. Mice and rats were observed for 14 days after treatment and LD50 values were calculated by the probit method. NK421 showed very low toxicity and no death occurred in any species following the oral administration of the maximum dose capable of dosing such as 4 g/kg for mice, 2 g/kg for rats and 1.2 g/kg for dog. General toxic signs seen in mice and rats following subcutaneous and intraperitonial injections were as follows; depression, suppressed movement, piloerection, inhibition of spontaneous movement, anorexia and emaciation. Death occurred within 5 days after administration. The toxic target organs of NK421 were found to be kidney, lymphoid tissue and liver based on histopathological examination of dead animals.

Administration, Oral↗
PubMed1983

Experimental induction of benzodiazepine tolerance and physical dependence.

To initiate studies of benzodiazepine tolerance and physical dependence, a reproducible animal model has been developed utilizing chlordiazepoxide in rats. Based on the "chronically equivalent" dosing principle, a regimen has been devised to maintain rats in a state of quantifiable intoxication for 5 weeks. Chlordiazepoxide was delivered intragastrically on a b.i.d. basis in doses individually adjusted day-to-day and animal-to-animal to produce an equivalent impairment of motor function evaluated by a gross neurological screen. Quantitative analysis of central nervous system depression ratings during the time of peak effect (4 hr postdose) confirmed that the criterion of chronic equivalence was indeed met. Over the 5-week period of repeated dosing, tolerance was reflected in a 5-fold increase in maintenance dose, from 163.3 mg/kg on day 2 to 839.3 mg/kg on day 35. Tolerance developed more rapidly during the first 9 to 10 days, but continued to develop thereafter more slowly without apparent ceiling. Upon abrupt withdrawal, a syndrome of hyperexcitation developed. Signs included twitches, tremors, muscle hypertonus, arched back, piloerection, myoclonic jerks, augmented struggle and vocalization upon handling, increased startle response, tail erection, teeth chatter, blanched ears and weight loss. No spontaneous convulsions occurred. Latency to onset of withdrawal ranged from 2 to 5 days, and signs peaked in intensity in 8 days and disappeared by 14 days posttreatment. This animal model appears to provide a useful tool for the study of specific mechanisms underlying benzodiazepine tolerance and physical dependence.

Animals↗
PubMed1980

[Subacute toxicity of aclacinomycin A in rats (author's transl)].

Wistar rats, both male and female, were treated with aclacinomycin A at 4 dosage levels (0.375, 0.75, 1.5 and 3.0 mg/kg/day) by daily intraperitoneal injection for 30 days. Several rats died in the two higher dose groups (1.5 mg/kg/day: male 2/8 and 3.0 mg/kg: male 8/8, female 8/8. Piloerection, anorexia, depression of spontaneous activity, diarrhea and slight incontinence were observed in rats in 3.0 mg/kg/day dose group. Body weight gain decreased after day 3 in rats receiving 1.5 and 3.0 mg/kg/day. A significant decrease in the total WBC count and a slight decrease in RBC count were observed in animals of 1.5 mg/kg/day dose group which were survived for 30 days. Autopsy findings demonstrated atrophy of the thymus and spleen, and hyperemia and hemorrhage in the intestine. The atrophy of the thymus and decreased hematopoiesis in the bone marrow were histologically noted in the two highest dose groups. No cardiotoxicity was observed.

Aclarubicin↗
PubMed1980

[Effects of guanfacine on the central nervous system (author's transl)].

Effects of guanfacine, a new centrally acting antihypertensive drug, on the central nervous system were studied in mice and rats, and findings compared with those of clonidine. In mice, guanfacine caused slight hypersensitivity and marked piloerection at 4 or 16 mg/kg, p.o. Clonidine exhibited the same symptoms as guanfacine, but at a higher dose elicited severe central excitation such as clonic convulsion. Such central depressive effects as hyposensitivity and catalepsy were, however, observed following administration of both drugs, at the same dose levels, to rats. Clonidine showed a tendency o prolong hexobarbital sleeping time in mice, but such was not observed with guanfacine. Both drugs markedly suppressed responses to nociceptive stimuli in mice. The spontaneous cortex and hippocampus electroencephalograms were respectively changed to high amplitude-slow waves and desynchronized waves by administration of either guanfacine or clonidine at 2 mg/kg, i.v. in curarized rats. Spontaneous motor activity was reduced by both drugs. Both drugs, especially clonidine, caused a fall in body temperature. Both drugs failed to inhibit convulsions induced by electric shock and by intraperitoneally administered pentylenetetrazol. From these results it was concluded that the central effects of guanfacine, while resembling those of clonidine, were generally weaker than those of clonidine.

Analgesics↗
PubMed1981

Carbachol-induced agonistic behavior in cats: aggressive or defensive response.

The effects of intrahypothalamic carbachol microinjections were investigated in unprovoked cats. The carbachol evoked mydriasis, attention, vocalization, and piloerection, i.e. features of a typical defense were usually concomitant in evoked response, while the clear-cut aggressive or escape patterns appeared only once. No basic differences were observed in the set of manifestations induced by low (1-2.5 micrograms) and high (20-40 micrograms) doses of carbachol, and from left and right hypothalamus as well as from medial and lateral portion of the hypothalamus. It is concluded that carbachol-induced response does not represent an aggressive pattern but corresponds to the cat’s defense and threat behavior.

Aggression↗
PubMed1995

Prevention of anti-T-cell receptor alpha beta monoclonal antibody-induced side-effects by treatment with cyclosporin A without interference of monoclonal antibody-induced immunosuppression in mice.

Anti-T-cell receptor (TCR)alpha beta monoclonal antibody (mAb; H57-597) injection in mice caused cytokine (tumour necrosis factor and interferon-gamma) release and clinical side-effects such as piloerection and body weight loss similar to anti-CD3 mAb (145-2C11) injection. Treatment with cyclosporin A (CsA) for 3 days, from day -2 to day 0, prior to anti-TCR alpha beta mAb injection almost completely abolished the mAb-induced cytokine release, and completely inhibited the mAb-induced body weight loss. Furthermore, treatment with CsA from day -2 to day 0 did not inhibit the mAb-induced in vivo immunosuppressive effects, i.e. prolongation of skin allograft and T-cell depletion in the periphery. These results indicate that CsA treatment prior to mAb treatment could effectively inhibit the mAb-induced side-effects without interference of the mAb-induced in vivo immunosuppression. From these results, we propose that CsA treatment prior to injection of anti-TCR alpha beta mAb may be recommended to reduce mAb-induced side-effects.

Animals↗
PubMed1993

Precipitated withdrawal by pentazocine in methadone-maintained volunteers.

Pentazocine is a partial mu agonist opioid with one-half to one-sixth the parenteral analgesic potency of morphine. The purpose of this study was to characterize the effects of pentazocine in comparison to naloxone (an opioid antagonist), hydromorphone (an opioid mu agonist) and saline in methadone-dependent volunteers by using the same experimental methods used previously in the study of the opioid analgesics buprenorphine, butorphanol and nalbuphine. In a residential laboratory, five volunteer male opioid abusers, maintained on 30 mg p.o. of methadone daily, underwent pharmacological challenges 2 to 3 times per week. Pharmacological challenges consisted of a double-blind i.m. injection of: pentazocine (dose range 7.5-120 mg), hydromorphone (5 and 10 mg), naloxone (0.1 and 0.2 mg) or saline. Injections were given 20 hr after the last dose of methadone. Measures included physiological indices and self-reports and observer ratings of drug effects. Naloxone and hydromorphone produced characteristic antagonist-like and agonist-like effects, respectively, on subjective, observer and physiological indices. Pentazocine produced primarily antagonist-like effects, with higher doses (> = 60 mg) producing significant elevations of visual analog scale ratings of Drug Effects, Bad Effects and Sick; of observer ratings of piloerection, restlessness and adjective scores of opioid withdrawal; as well as increases in blood pressure, heart rate and pupil diameter and decreases in skin temperature. Similar to the previous study of butorphanol, the specific profile of effects produced by pentazocine differed from that produced by naloxone, suggesting non-mu effects may modulate the mu effects of pentazocine.

Adult↗
PubMed1995

The combination of tizanidine markedly improves the treatment with dextromethorphan of heroin addicted outpatients.

According to the hypothesis implying that the main mechanism underlying opiate addiction is the blockade by opiates of NMDA receptor functions and subsequent upregulation and supersensitivity of the receptors, noncompetitive NMDA receptor blocker dextromethorphan (DM) has been successfully used in the heroin addict treatment. As the stimulation of NMDA receptors modulates the release of neurotransmitters and hormones such as NE, D, ACh, GH, LH, LSH, ACTH etc., all of which have been found responsible for the manifestation of abstinence syndrome signs including craving and neuronal death by excessive stimulation of NMDA receptors, the incomplete blockade of the NMDA receptors minimizes the intensity of the abstinence syndrome and provides the downregulation of the receptors. In the present study, tizanidine (TIZ), which inhibits the release of endogenous excitatory aminoacids by the agonistic activity on alpha 2-adrenoreceptors, was combined with DM to obtain further benefits. Forty-four male and three female heroin addicts were the subjects of the study. Their daily mean heroin intake was about 2.28 g street heroin. The main duration of heroin use was approximately 3.4 years. Two to three hours after abrupt withdrawal, the outpatients were given 15 mg DM every hour, 25 or 50 mg chlorpromazine (CPZ) + 4 mg TIZ every six hours and 10 mg diazepam + 10 mg hyoscine N-butyl Br + 250 mg dipyrone every six hours three hours following CPZ. The addicts were controlled twice a day. Yawning, rhinorrhea, perspiration, piloerection, restlessness, insomnia, emesis, diarrhea, craving, rejection of smoking and pupils were observed and/or questioned. Two of the 47 outpatients took heroin on the first days.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

The ontogeny of mu opiate tolerance and dependence in the rat: antinociceptive and biochemical studies.

The ontogeny of tolerance to mu opiate antinociception and the behavioral and endocrine profiles of the opiate withdrawal syndrome were studied in rats. Animals were treated with saline or an increasing dose regimen of morphine for 5 days (5-25 mg/kg b.i.d. s.c.) and were tested 36 hr later for morphine or sufentanil antinociception in the hot-plate paw-lift test, or withdrawal was precipitated with 5 mg/kg of naloxone 12 hr after the last chronic morphine dose. Twenty-seven-, 20- and 15-day-old rats all developed tolerance as indicated by a rightward shift of the dose-response curve after chronic morphine. Animals treated on days 4 to 8 and tested on day 10 did not develop tolerance to the same chronic dose regimen used in older animals. In contrast to the observed developmental difference in tolerance, both neonatal and weanling rats developed physical dependence after morphine treatment, as evidenced by the presence of withdrawal symptoms after naloxone administration. Withdrawal in weanling rats was characterized by ptosis, piloerection, abnormal posture, forepaw treading, vocalization on touch and mastication. In addition, both serum corticosterone and adrenocorticotropic hormone secretion were increased during passive withdrawal. The behaviors constituting the withdrawal syndrome precipitated in neonates were distinct from those in weanling rats. Spontaneous vocalization, wall climbing, tremor, mouthing and increased locomotion were all observed. As in the older animals, both serum corticosterone and adrenocorticotropic hormone secretion were elevated during passive withdrawal. Tremor also was induced in opiate naive neonates when naloxone (5 mg/kg) was administered 2 hr after a single 25-mg/kg morphine injection. Brain and serum morphine levels and the time course of antinociception were not altered by chronic morphine treatment at any age. Saturation binding assays in brain homogenates indicated that chronic morphine did not produce changes in receptor number or affinity for the antagonist. The shift induced by the guanine nucleotide Gpp(NH)p (10 microM) from high to low affinity on days 27 and 10, respectively, was not altered by chronic morphine treatment. These data indicate that 10-day-old rats are refractory to developing tolerance relative to older animals, and that changes in receptor number or coupling to guanine nucleotide proteins do not accompany tolerance to this regimen.

Animals↗
PubMedDate not supplied

Antihypertensive effects of a new transdermal delivery system for clonidine (M-5041T) in spontaneously hypertensive rats.

The antihypertensive effects of a new transdermal delivery system for clonidine (clonidine tape; M-5041T) were investigated in spontaneously hypertensive rats and normotensive Wistar-Kyoto rats. In spontaneously hypertensive rats, M-5041T, at doses of 0.5-4.5 mg/kg (1.25-11.25 cm2/kg), produced a dose-dependent decrease of both systolic blood pressure and heart rate for 24 hr during transdermal application. These significant hypotensive effects lasted for 24 hr following the patching of M-5041T on the back of the animals at a dose of 4.5 mg/kg. In normotensive Wistar-Kyoto rats, the hypotensive and bradycardic effects of M-5041T were weak compared with those in spontaneously hypertensive rats. In both rat strains, M-5041T (4.5 mg/kg) caused behavioral changes such as sedation, piloerection and exophthalmos, accompanied by hypotensive effects. Both M-5041T (1.5 mg/kg) and clonidine (50 micrograms/kg, subcutaneously and 100 micrograms/kg, orally) induced similar hypotensive effects, accompanied by sedation. The hypotensive effects following transdermal M-5041T or systemic clonidine administrations were correlated with the time courses of the plasma clonidine concentration. In contrast to clonidine administered subcutaneously or orally, M-5041T produced a gradual increase in the plasma clonidine concentration, which persisted at a consistent level for at least 12 hr thereafter. Significant hypotensive effects lasted for 12 and 24 hr following M-5041T patching at 1.5 and 4.5 mg/kg, respectively. The present findings suggest that M-5041T can serve as an efficient and useful antihypertensive transdermal delivery system to achieve persistent blood pressure control.

Administration, Cutaneous↗
PubMed1994

[Essential hypertension: psychosomatic aspects].

Essential hypertension is a heterogenous disease made up of several still unspecified subgroups. According to the dual theory of hypertension, acquired and genetic factors can lead to vascular muscle defects and increased sympathetic drive, which, either both or each alone, can lead to an increased vascular resistance. Acquired factors can either help a predisposition to become a manifest disease, act by itself to cause a disease or prevent a genetic trait from becoming manifest. Among the acquired factors, we differentiate those lying inside the personality, which means they are early acquired in life and those lying outside of the individual such as job-stress, noise exposure etc. How the external stressors are perceived depends upon the personality make up and the social support system. Within the presented model the Greek word 'crisis' plays an important role, since it characterizes a state in which a decision has to be made. In a situation in which a decision cannot be made in reality or tried out in fantasy life, the organism will activate the autonomic nervous system in a planless fashion, alternating very rapidly between its two branches, with concomitant symptoms of trembling, piloerection, salivation, vomiting, urination, defecation etc. In case this persists for a longer period of time the reciprocity between the two systems may break down, the organism seems to be psychologically immobilized. In the beginning of stress exposure, increased sympathetic nervous system activity is seen as an adaptive response, thereby enabling the individual to cope, but if the attempts to cope meet with constant failure, the stress becomes unbearable. The attitude of giving up which then develops is accompanied by a low level functioning of the sympathetic nervous system. This goes along with an adaptation for the baroreceptor depressor mechanism. As a consequence, any kind of additional stress would not lead to a relieving counterregulation. This might be a small stone within the mosaic of essential hypertension.

Adaptation, Psychological↗
PubMedDate not supplied

[A method for the quantitative assessment of the withdrawal syndrome in morphine-dependent rats].

The evaluation of strength of morphine withdrawal syndrome in rats after the 17th day i. p. morphine administration is proposed as calculation of individual indexes in "open field" test. It is found, that injection 1, 5 or 10 mg/kg of morphine 30 min before testing, decreases the withdrawal syndrome in dose dependent manner. Disappearance of particular withdrawal signs took place in different doses of morphine pretreatment. According to this effect all the signs were divided into four groups and signs of each group were given by the specificity coefficient (from 0 to 3). The total individual index of the withdrawal syndrome was calculated as a sum of particular signs, multiplied by the particular coefficient. Specificity of significant signs decrease according to the order: "wet dog" shakes, diarrhea, writhings, dyspnea, paw shakes, ptosis, piloerection and teeth chattering.

Animals↗
PubMed1995

Electrical and chemical stimulation of the same hypothalamic loci in relation to agressive behaviour in cats: a comparison study.

Chemitrodes which permit electrical and chemical stimulation of the same hypothalamic loci were implanted in anterior hypothalamic and preoptic regions. These sites were stimulated electrically using biphasic square wave pulse (1 ms, 60 Hz) at a current strength ranging from 150-800 microA to evoke an aggressive response. At lower current strength of 150-200 micro A, defence response, a sort of non-specific response can be elicited from these regions. Increasing the current strength to 400 microA led to the recruitment of affective and somatic components and changed the response pattern either to affective attack or flight. The loci producing affective attack response were localized more laterally and ventrally while the loci producing flight response were located in the dorsomedial regions of the hypothalamus. In this response the animal made a goal-directed attempt to escape through an escape route. Increasing the current strength to 500 microA in the dorsomedial regions changed the flight response to violent flight, which involved vigorous running with unsheathed claws and attacking objects if obstructed. Similar increase in current strength at loci producing affective attack only led to a decrease in the latency of response and made the attack more vigorous. Microinfusion of carbachol in graded doses of 2-15 microgram at all these loci produced a profound affective display. At lower doses of 2 and 5 microgram, only some components of affective display like alertness, pupillary dilation and ear flatness were exhibited. Increasing the dose to 10 micrograms and 15 micrograms led to the recruitment of other affective components like piloerection, salivation, hissing and baring of teeth. Microinfusion of carbachol at all loci producing affective attack on electrical stimulation produced a prononced affective display while microinfusion of carbachol at loci producing flight response led to the development of defence posture. At six loci a typical flight response was obtained while violent flight was never exhibited at any of these sites. Microinfusion of atropine (10 microgram in 1.0 microliter saline) at these loci completely blocked the carbachol induced response. Both somatomotor and affective components were completely inhibited. However, the responses obtained on electrical stimulation were not totally blocked following atropine infusion and some of the somatomotor and affective components could be elicited with higher current strength. These studies indicate the involvement of cholinoceptive mechanisms in the elicitation of hypothalamically induced aggresive behaviour. Microinfustion of hexamethonium bromide, a nicotinic blocker in 50 micrograms doses did not affect the aggressive response.

Aggression↗
PubMed1995

Altered behavioral responses in 2,4-dichlorophenoxyacetic acid treated and amphetamine challenged rats.

Although the mechanism of 2,4-D neurotoxicity remains unknown the serotonergic system appears to mediate some of the effects of 2,4-D in rats as reported in our previous studies. In the present study we examine the concept that a challenge to a system may overcome compensatory mechanisms and thereby reveal otherwise hidden neurotoxicant-induced damage. We report the behavioral results of 50 or 100 mg/kg 2,4-Dichlorophenoxyacetic acid (2,4-D) acute exposure plus amphetamine challenge of rats. The "Serotonin Syndrome" (SS) involving prominently head movement, piloerection, moist fur, backing, hunching, Straub tail, fore paw tapping of the nose and pivoting, was exhibited by these rats, being females more affected than males. Immobility, social apathy and asymmetry were also observed. All behaviors were not seen in the 2,4-D treated rats. Stereotyped behaviors were observed earlier and were more prolonged in 2,4-D treated and amphetamine challenged rats than in rats treated only with 5 or 10 mg/kg amphetamine. Spiperone blocked all the SS behaviors. In addition, in these rats, rearing and rotation behaviors were showed and were also sex dependent. We also demonstrate that haloperidol, in a non cataleptic dose, induced catelepsy in 2,4-D treated rats. 2,4-D appears to act through serotonergic and dopaminergic mechanisms. The intensity of the response is sex dependent. Our study demonstrates that 2,4-D plus amphetamine induces a Serotonergic Syndrome plus additional Dopaminergic modulation.

2,4-Dichlorophenoxyacetic Acid↗
PubMed1996

[Autonomous hyperreflexia and labor].

Autonomic hyperreflexia is a serious complication for tetraplegic patients, especially during labour and delivery. The symptoms are piloerection, facial flushing, anxiety, headache, serious blood pressure crises and cerebrovascular accidents. A 30 year-old woman who was tetraplegic following a high cervical spinal cord lesion, showed signs of autonomic hyperreflexia. In early labour epidural analgesia was established and the vaginal delivery was successful without associated fluctuation of the blood pressure or other signs of autonomic hyperreflexia.

Adult↗