Exposure to psychological stress increases body temperature (Tb). This stress fever may be immunologically beneficial in some patient populations but detrimental in others (e.g., HIV-infected individuals). For this reason, it is desirable to determine pharmacological methods of preventing stress fever. In rats, stress fever is modeled by exposure to a novel environment or 'open field.' The beta-adrenergic antagonists, nadolol and propranolol, block this stress fever. Neither of these beta-antagonists discriminates between subtypes of beta-receptors. The purpose of this study was to determine the relative contribution of the different beta-receptor types to stress fever using beta1-, beta2-, and beta3-receptor subtype selective antagonists (atenolol [beta1], ICI-118551 [beta2], and SR 59230A [beta3]) and agonists (dobutamine [beta1], salbutamol [beta2], and BRL 37344 [beta3]) on the Tb of rats. Tb was measured with a biotelemetry system. Our data suggest that central nervous system beta-receptor blockade with subtype-selective antagonists prevents the stress-induced rise in Tb; however, the beta3-antagonist was effective only at doses that produced hypothermia in a non-stressed control group. The stress-induced fever was mimicked by central nervous system administration of the selective beta2-agonist, salbutamol, and the beta3-agonist, BRL 37344. We hypothesize that the blockade of stress-induced fever by beta-blockers may be due to the sedative actions of these drugs.

Adrenergic beta-Agonists↗

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Cytokines and fever.

Fever is an excellent example of neuroimmunomodulation in that mediators of immunity initiate a pathway to raise the thermoregulatory set-point, resulting in behavioral and physiological responses that increase body temperature. This rise in temperature is thought to be adaptive, facilitating host defenses. Many cytokines are endogenous mediators of fever (i.e. endogenous pyrogens), including interleukin (IL)-, 1 beta, IL-6 and others. Tumor necrosis factor-alpha may be both an endogenous pyrogen and an endogenous antipyretic or cryogen, depending on the nature of the inflammatory stimuli. Although there is evidence that cytokines within the hypothalamus initiate fever, recent findings indicate that the signal to increase these brain cytokines may be neural (i.e. from peripheral nerves), rather than humoral (i.e. circulating endogenous pyrogen).

Animals↗

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Hemorrhage suppresses fever, interleukin-6, and tumor necrosis factor-alpha responses to lipopolysaccharide in rats.

The purpose of this study was to test the hypothesis that attenuation of the fever response to lipopolysaccharide (LPS) following hemorrhage is accompanied by changes in serum glucocorticoid levels and a decreased bioactivity of TNF-alpha and IL-6 in plasma. Hemorrhage was induced in rats by the withdrawal of 20% of estimated total blood volume. LPS (50 microg/kg) or saline were injected intraperitoneally immediately after the hemorrhage. Blood samples were taken 1.5 h for TNF-alpha bioactivity and corticosterone measurements and 5 h after treatment for IL-6 bioactivity. Body temperature (Tb) was measured by biotelemetry. The 20% hemorrhage led to a significant reduction in hematocrit measured at 1.5 and 5 h after treatment. Furthermore, 20% hemorrhage caused a substantial elevation in serum corticosterone measured by radioimmunoassay at 1.5 h after treatment. This high concentration of corticosterone was not further potentiated by injection of LPS. Hemorrhaged rats treated with LPS responded with a markedly attenuated fever. Both TNF-alpha and IL-6 rises in the circulation due to LPS injection were significantly smaller in hemorrhaged rats compared to nonhemorrhaged LPS-injected rats. However, this degree of hemorrhage did not alter the T(b) or plasma TNF-alpha and IL-6 activity in hemorrhaged rats injected with saline. These results show that the inhibitory effect of hemorrhage on LPS-induced fever may be related to the decreased TNF-alpha and IL-6 activity in plasma. Hemorrhage-induced high level of corticosterone might contribute to the attenuation of fever, perhaps via the suppression of pyrogenic cytokines.

Animals↗

PubMedDate not supplied

Inappropriate counter-regulatory hormone levels in insulin treated diabetes.

The data herein presented describe, identify, and quantitate interrelationships among blood glucose and serum insulin, growth hormone, cortisol, and glucagon levels of hospitalized insulin-treated diabetic patients. The findings indicate that conventional diet and insulin therapy of diabetes mellitus is almost always accompanied by inappropriate counter-regulation by growth hormone, cortisol, and glucagon. The data are consonant with the hypothesis that a shortage of insulin is only one of the multihormonal defects of diabetes.

Blood Glucose↗

PubMedDate not supplied

Inappropriate counter-regulatory hormone levels in insulin treated diabetes.

Blood Glucose↗

PubMedDate not supplied

[Effect of exertion on serum growth hormone concentration in healthy, obese and diabetic subjects].

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Adult↗

PubMedDate not supplied

[Blood serum testosterone in men with acne vulgaris].

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Acne Vulgaris↗

PubMedDate not supplied

Enhanced apomorphine-induced fighting in rats after prolonged oral treatment with drugs altering noradrenergic transmission.

Male Wistar rats were given orally for seven days water, clonidine (0.125 or 0.25 mg/kg bid) or S3341, a new clonidine-like drug (2.5 or 5.0 mg/kg bid) and afterwards pairs of rats were injected ip with 2.5 mg/kg of apomorphine (APO). Water-treated animals did not behave aggressively. Clonidine and S3341 both induced clear aggression when combined with a subthreshold dose of APO. Some degree of hyperirritability developed in these two groups during drug treatment when observed in the home-cage. No significant changes in aggressive behavior were noted upon acute administration of both drugs, though some tendency to augment aggressivity could be observed after clonidine (0.25 mg/kg po). It is suggested that noradrenergic neurons play an inhibitory role in APO-induced fighting.

Aggression↗

PubMedDate not supplied

Basomedial amygdaloid lesions and p-CPA induced muricidal aggression.

Bilateral lesions of basomedial amygdaloid nuclei are capable of significantly inhibiting muricidal aggression induced by oral p-chlorophenylalanine (p-CPA) in male rats. Rats lesioned in extra-amygdaloid structures or sham-lesioned show the usual p-CPA-induced muricidal activity, which ranges from 70 to 80% of treated animals. The results obtained indicate that basomedial amygdaloid nuclei play an important role in regulating p-CPA-induced muricidal aggression, even though the effect lasts for a relatively limited period of time. This fact is probably due to the intervention of still unidentified compensatory mechanisms.

Amygdala↗

PubMedDate not supplied

On the role of noradrenergic neurotransmission in the action of desipramine and amitriptyline in animal models of depression.

Three weeks of treatment with desipramine (DMI) and amitriptyline (AMI) reduced the hypothermic action of clonidine in rats. Both electrolytic and 6-hydroxydopamine lesions of the locus coeruleus (LC) and administration of DSP-4 counteracted the reduction of clonidine hypothermia produced by antidepressants. Lesions of the LC and DSP-4 administration also antagonized the anti-immobility action of single doses of DMI but failed to modulate the action of AMI in the forced swim test. Chronic DMI action on the rat immobility was reduced by 6-hydroxydopamine lesions of the LC: other lesions (electrolytic, DSP-4) were ineffective. Electrical stimulation of the LC increased the rat activity in the forced swim paradigm, producing an effect similar to that of antidepressants. The anti-immobility effect of DMI as well as LC stimulation were antagonized by drugs blocking alpha-adrenoceptors (phenoxybenzamine, prazosin) but not by propranolol, a non-selective antagonist of beta-adrenoceptors. On the other hand, the anti-immobility action of AMI was unchanged by all adrenolytics used in that study. The results indicate that the LC system and alpha 1-adrenoceptors play an important role in the antidepressive action of DMI, but not AMI, in the forced swim test.

Amitriptyline↗