pituitrin and Fever

Fever is the hallmark of the stereotyped host response to microbial infection, although it is just one of a number of high-risk strategies employed by the infected host to clear itself of invading pathogens. The febrile response is accompanied by activation of multiple endogenous antipyretic systems that serve to suppress its magnitude or duration. These include neuroactive substances of neural and humoral origin, some of which (e.g., glucocorticoids, melanocortins, and IL-10) have broad-ranging anti-inflammatory actions. Glucocorticoids, vasopressin, and melanocortins appear to exert their antipyretic effects by acting on receptors within the brain, but beyond this the mechanisms involved are unknown. It is hypothesized, but not proven, that endogenous antipyretic systems protect the host against the destructive consequences of unchecked fever. Importantly, pharmacological blockade of the actions of endogenous antipyretic systems increases fevers of even low to moderate intensity. Therefore, in addition to protecting against catastrophic consequences of high fever, endogenous antipyretic systems seem to play a fundamental physiological role in determining the normal course of fever. Elucidating the neural and biochemical mechanisms involved in suppression of fever by physiological antipyretic systems will yield a rich benefit, both by advancing the basic understanding of host defense strategies, and by permitting the design of novel antipyretic and anti-inflammatory strategies for therapeutic intervention in human disease.

Topics: Adrenocorticotropic Hormone; alpha-MSH; Analgesics, Non-Narcotic; Annexin A1; Cytokines; Fever; Glucocorticoids; Humans; Neuropeptides; Vasopressins

Vasopressin administered into the ventral septum exerts a dose-related antipyresis. This site of action is similar in a number of species. The fever-reducing properties of vasopressin are both site and neuropeptide specific. Evidence supporting a role for endogenous vasopressin in fever suppression is the demonstration that the release of the peptide from the ventral septal area is altered during fever: the amount released correlates negatively with febrile changes in body temperature. In addition, changes in the concentration of vasopressin in the septum and amygdala have been demonstrated immunocytochemically during fever: an activation of vasopressinergic neurons occurs which is similar to that observed in pregnant animals at term when fever is absent. Specific antibodies directed against vasopressin or specific vasopressin antagonist analogues (e.g., d(CH2)5Tyr(Me)AVP) enhanced the febrile response to a pyrogen challenge when injected into the ventral septum. The same antagonist also can antagonize the antipyretic effect of exogenously administered vasopressin. The use of relatively specific antagonists and agonists of vasopressin, directed against the V1 and V2 subtypes of the peripheral vasopressin receptor, suggests that the central receptor responsible for the antipyretic effect of vasopressin may resemble the V1 subtype. Recent experiments using electrophysiological techniques have demonstrated the existence of thermoresponsive units in the ventral septal area whose activity may be altered by vasopressin which is possibly derived from the paraventricular nucleus and bed nucleus of the stria terminalis.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Body Temperature Regulation; Brain; Fever; Vasopressins

Primary blood coagulation and wound sealing are orchestrated by von Willebrand factor (VWF), a large multimeric glycoprotein. Upon release of arginine vasopressin (AVP), VWF containing high molecular weight multimers is secreted. By measuring copeptin, the C-terminal part of the AVP prohormone, we recently found strongly increased AVP levels in children with febrile seizures (FS) as compared to children with fever but without seizures. It is unknown if increased AVP levels in FS are of any biological function. Therefore, our a priori hypothesis was that children with FS have increased VWF parameters in parallel with higher AVP levels.. We conducted a prospective, cross-sectional study of children aged between 6 months and 5 years. Children that presented at our emergency department with fever or a recent FS (within four hours) were evaluated to be included to the study. We measured serum copeptin and VWF parameters, including analyses of VWF:Antigen (WVF:Ag), VWF:collagen binding activity (VWF:CB) and VWF multimers in children with FS, febrile infections without seizures and additionally, in a non-febrile control group.. We included 54 children in our study, 30 with FS, 10 in the febrile control group, and 14 in the non-febrile control group. Serum copeptin levels were significantly higher in children with FS (median [IQR] 24.73 pmol/l [13.65-68.65]) compared to the febrile control group (5.66 pmol/l [4.15-8.07], p = 0.002) and the non-febrile control group (4.78 pmol/l [3.33-5.3], p<0.001). VWF:CB levels were also significantly higher in children with FS (VWF:CB 2.29 U/ml [1.88-2.97]) as compared to the febrile (VWF:CB 1.41 U/ml [1.27-1.93], p = 0.048) and the non-febrile control group (VWF:CB 1.15 U/ml [0.98-1.21], p<0.001). VWF:Ag tended to be higher in children with FS compared to both control groups. Multivariate regression analysis revealed FS and copeptin as major determinants of VWF:CB.. Our results suggest that increased secretion of AVP in children with FS is associated with higher plasma levels of VWF parameters. Especially VWF:CB may serve as additional biomarker in the diagnosis of FS.

Topics: Biomarkers; Child, Preschool; Cross-Sectional Studies; Female; Fever; Glycopeptides; Humans; Infant; Male; Neurophysins; Prospective Studies; Protein Precursors; Seizures, Febrile; Vasopressins; von Willebrand Diseases; von Willebrand Factor

Gitelman syndrome (GS) is a renal tubular disorder of the thiazide-sensitive sodium chloride cotransporter, which is located in the distal tubule of the loop of Henle. We present a rare case of GS complicated by severe hyponatraemia and hypophosphataemia. A 17-year-old boy was admitted to our institution with fever and lethargy. The workup revealed typical features of GS, i.e. hypokalaemia, hypomagnesaemia and metabolic alkalosis. In this report, we discuss the differential diagnoses and rationale for accepting GS as the most likely diagnosis. This case was complicated by severe hyponatraemia (115 mmol/L) and hypophosphataemia (0.32 mmol/L). We concluded that the syndrome of inappropriate secretion of antidiuretic hormones could not be ruled out and that respiratory alkalosis was the most likely aetiology of hypophosphataemia. This case report also generates an interesting discussion on water and electrolyte metabolism.

Topics: Adolescent; Alkalosis, Respiratory; Electrolytes; Fever; Gitelman Syndrome; Humans; Hyponatremia; Hypophosphatemia; Lethargy; Male; Vasopressins

Topics: Africa, Eastern; Albumins; Anemia; Child; Coma; Critical Illness; Developing Countries; Dose-Response Relationship, Drug; Drug Administration Schedule; Fever; Fluid Therapy; Humans; Meningitis, Bacterial; Pneumonia; Randomized Controlled Trials as Topic; Resuscitation; Shock; Sodium Chloride; Vasopressins

A 3-year-old girl presented with osmotic demyelination syndrome after undergoing uneventful neuroendoscopic cystostomy for a growing cystic suprasellar craniopharyngioma following microscopic subtotal resection 1 year previously. Endocrinopathy had well been controlled by hormone replacement therapy and administration of 1-amino-8-d-arginine-vasopressin with serum sodium concentration within the normal range. She presented generalized seizure and fever on postoperative day 7, with hyponatremia beginning on postoperative day 4 and deteriorating despite frequent correction. The serum sodium concentration began to fluctuate on the same day, in the range 111-164 mEq/l, which lasted for 2 weeks, refractory for intense management. Her body temperature also fluctuated between hypo- and hyperthermia not correlated with serum inflammatory markers. Her conscious disturbance progressively deteriorated with spastic paraparesis. T(2)-weighted magnetic resonance (MR) imaging taken on postoperative day 19 revealed hyperintense areas in the pons, external capsule, bilateral thalami, and basal nuclei, which had not been recognized before, suggesting osmotic demyelination syndrome causing central pontine and extrapontine myelinolysis. MR imaging taken on postoperative days 230 and 360 showed some diminished lesions but others persisted and resulted in a cavity. The patient's depressed conscious level did not improve. Suprasellar craniopharyngioma with long-standing hypothalamic dysfunction may be associated with severe osmotic demyelination syndrome even after less invasive surgery, so serum sodium derangement after surgery should be promptly corrected even if only subtle signs are present.

Topics: Brain; Child, Preschool; Consciousness Disorders; Craniopharyngioma; Disease Progression; Female; Fever; Hormone Replacement Therapy; Humans; Hyponatremia; Hypothalamus; Magnetic Resonance Imaging; Myelinolysis, Central Pontine; Nerve Fibers, Myelinated; Neurosurgical Procedures; Pons; Postoperative Complications; Vasopressins; Water-Electrolyte Balance

The objective of this study was to determine the effect of modulating the plasma concentrations of the avian antidiuretic hormone, arginine vasotocin (AVT), upon the febrile response to lipopolysaccharide (LPS) in Pekin ducks. LPS, intravenously administered into conscious control birds at a dose of 1 microg x kg(-1), caused a monophasic increase in body temperature of 0.85 +/- 0.12 degrees C associated with a Thermal Response Index of 2.5 +/- 0.6 C degrees h. Plasma AVT concentrations in the control birds also increased with the progression of the fever response, more than doubling from their basal values. Ducks in which the circulating level of AVT had either been elevated by the intravenous infusion of the peptide or dehydration, or reduced by the administration of a specific AVT antibody prior to LPS administration, produced body temperature profiles and Thermal Response Index values that did not differ significantly from those of the control birds. The lack of any direct effect of variations in plasma AVT concentrations upon the magnitude of the fever response indicates that the LPS-induced elevation in plasma AVT is not associated with modulating the rise in body temperature obtained in avian fever.

Topics: Animals; Arginine Vasopressin; Body Temperature Regulation; Dehydration; Ducks; Female; Fever; Lipopolysaccharides; Male; Vasopressins

Fevers are known to be suppressed near term in the mother, but the mechanism responsible for this phenomenon is not understood. We tested the hypothesis that the suppression of fever at term is a result of enhanced vasopressin-induced antipyresis. Effects of intracerebroventricular prostaglandin E(2) (PGE(2)) were examined in rats at gestational days 16-17 and 19-20 (near term) and days 1-2 postpartum. PGE(2) (50 ng) elevated body and interscapular brown adipose tissue (iBAT) temperatures and increased sympathetic nerve activity to the iBAT. PGE(2)-induced changes in iBAT temperature and nerve activity, as well as in rectal temperature, were reduced or eliminated near term, and responses were recovered in the postpartum period. Blood pressure and heart rate changes induced by central PGE(2) were also decreased at near term. Coinfusion of Manning compound, a V(1) vasopressin receptor antagonist, with PGE(2) throughout the peripartum period did not reverse the suppressed iBAT temperature and nerve activity or body temperature responses to PGE(2). Microdialysis experiments revealed unchanged terminal release of vasopressin in the ventral septal area after PGE(2) infusion in either pregnant or parturient rats. These results suggest that fever reduction at near term is not associated with enhanced vasopressin antipyresis, but may be a result of reduced sympathetic tone and in particular a reduced sympathetic drive to the iBAT. This finding may reflect a generalized reduction in autonomic output around the time of parturition.

Topics: Adipose Tissue, Brown; Animals; Antidiuretic Hormone Receptor Antagonists; Body Temperature; Body Temperature Regulation; Cardiovascular System; Delivery, Obstetric; Dinoprostone; Female; Fever; Nervous System; Postpartum Period; Pregnancy; Pregnancy Complications; Pregnancy, Animal; Rats; Rats, Sprague-Dawley; Rectum; Vasopressins

1. The objective of this study was to determine the changes in plasma concentrations of the hormones arginine vasotocin (AVT) and angiotensin II (AII) associated with lipopolysaccharide (LPS)-induced fever in Pekin ducks. 2. LPS, intravenously administered into conscious birds at doses of 1, 10 and 100 microgram kg-1, caused dose-dependent and monophasic increases in body temperature, with fever index values of 3.5, 7.0 and 10.6, respectively. 3. Plasma AVT concentrations also increased with the progression of the fever, with the largest elevation (from 8.4 +/- 1. 6 to 25.2 +/- 3.2 pg ml-1; means +/- s.e.m., n = 7) being caused by the highest dose of LPS. 4. Plasma AII concentrations did not significantly change from basal values (mean of 45.5 +/- 6.3 pg ml-1 for all groups) during the acute phase of the fever response. 5. The osmotic status of the birds, as indicated by plasma osmolality and electrolyte values, did not significantly change in any of the experimental animals. 6. The elevation of AVT in avian fever leads to speculation about a possible antipyretic action of this hormone, which would have particular relevance to understanding the evolution of fever.

Topics: Angiotensin II; Animals; Body Temperature; Ducks; Female; Fever; Lipopolysaccharides; Male; Osmolar Concentration; Potassium; Sodium; Vasopressins; Water-Electrolyte Balance

Neuropeptide and cyclooxygenase (Cox) gene expression was examined in the brains of catheterized pigs killed 30 or 120 min after intravenous injection of a low (20 microg) dose of lipopolysaccharide endotoxin (LPS), previously demonstrated to induce fever in this species. In the paraventricular hypothalamic nucleus (PVN), corticotrophin releasing hormone (CRH) mRNA was shown to be present in the pars parvocellularis but was not upregulated 30 or 120 min after 20 microg LPS, or 90 min after 60 microg LPS; there was also no change in proopiomelanocortin (POMC) message in the anterior pituitary (AP). Similarly, expression of mRNAs for lysine vasopressin (LVP) or oxytocin (OT) did not change in the PVN after LPS (20 microg), although LVP message was increased (p<0.05) at 30 min in the hypothalamic supraoptic nucleus (SON). Expression of Cox-1 and Cox-2 genes was quantified in the organum vasculosum lamina terminalis (OVLT) and choroid plexus (CP) in an attempt to determine whether altered expression of prostaglandin (PG) synthetic enzymes in brain vasculature is involved in LPS fever. Although vascular endothelial cells in both structures expressed Cox-1 and Cox-2 mRNAs, neither increased in the OVLT following LPS. However, in the CP, Cox-1 mRNA was enhanced (p<0.05) at 30 and 120 min after LPS injection and Cox-2 showed a similar (NS) change. These results provide the first description of CRH and Cox gene expression in the porcine brain. They also suggest that LPS may influence the activity of genes controlling LVP synthesis in the hypothalamus and PG production by the brain vasculature.

Topics: Animals; Autoradiography; Corticotropin-Releasing Hormone; Cyclooxygenase 1; Cyclooxygenase 2; Endothelium, Vascular; Fever; Gene Expression; Hypothalamus, Anterior; Isoenzymes; Lipopolysaccharides; Lypressin; Oxytocin; Paraventricular Hypothalamic Nucleus; Pituitary Gland, Anterior; Pro-Opiomelanocortin; Prosencephalon; Prostaglandin-Endoperoxide Synthases; RNA, Messenger; Supraoptic Nucleus; Swine; Vasopressins

Vasopressin has been reported to be an endogenous antipyretic peptide. The present study assessed whether this peptide has similar effects on stress-induced hyperthermia. Infusion of 3 ng of vasopressin into the lateral ventricle prior to a 40-min restraint stress reduced significantly the hyperthermic response of rats to this stress, compared to saline-injected controls. Half of the vasopressin-injected animals showed an immediate hypothermic response, with a significant reduction in body temperature of 0.34 degree C or more within 10 min; however, the effect of vasopressin on stress-induced hyperthermia remained significant after exclusion of these animals from the analysis. Administration of a V1 receptor antagonist prior to the stress did not affect the hyperthermic response, which may suggest that the hyperthermic response had reached maximal (ceiling) levels. Administration of vasopressin, or of the V1 receptor antagonist immediately after the stress, did not affect defervescence, suggesting that vasopressinergic systems are not implicated in the defervescence process. Thus, the results show that ICV administration of vasopressin reduces stress-induced hyperthermia. The mechanisms underlying the effects remain to be elucidated.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Body Temperature; Brain Chemistry; Fever; Injections, Intraventricular; Male; Rats; Restraint, Physical; Stress, Psychological; Vasoconstrictor Agents; Vasopressins

Vasopressin (VP), given intracerebrally to rats, can induce antipyresis, motor disturbances, and increases in arterial blood pressure. The possibility that the VP-binding sites in the fundus striati (FStr) could participate in these effects was investigated. After a bilateral injection of 100 pmol of VP into the FStr, the fever induced by an injection of the lipopolysaccharide of Escherichia coli (50 micrograms/kg ip) was not affected. Bilateral injections of 100 pmol of VP did not induce motor disturbances or alterations in body temperature after either of two successive injections. In contrast, bilateral injections of VP into urethan-anesthetized rats induced dose-dependent increases in arterial pressure without affecting heart rate. This increase was blocked by a V1 antagonist; oxytocin and a V2 agonist were ineffective. In keeping with this preliminary pharmacological analysis, radio-ligand-binding studies of the FStr revealed binding sites in the FStr exhibiting a binding profile typical of the V1 subtype. This study suggests that the V1 receptors in the FStr could participate in the central regulation of the blood pressure.

Topics: Animals; Autoradiography; Binding Sites; Blood Pressure; Body Temperature Regulation; Corpus Striatum; Fever; Heart Rate; Male; Motor Activity; Rats; Rats, Sprague-Dawley; Rats, Wistar; Receptors, Vasopressin; Vasopressins

1. The actions of peripheral arginine vasopressin (AVP) on the febrile responses of conscious rabbits induced by peripherally administered polyinosinic:polycytidylic acid (poly(I).poly(C)) have been studied using an AVP V1 receptor antagonist ([deamino-Pen1, O-Me-Tyr2, Arg8]-vasopressin). 2. Temperature responses were monitored continuously using rectal thermistor probes. Test substances were administered intravenously (i.v.). Blood samples were taken at timed intervals from a marginal ear vein and plasma PGE2 and PGF2 alpha levels determined by radioimmunoassay. 3. Poly(I).poly(C) (2.5 micrograms/kg) stimulated a reproducible biphasic rise in body temperature with a lag phase of 45-60 min and peaks at 90 and 225 min. The febrile response was accompanied by a 5-fold rise in circulating immunoreactive (ir) PGE2, which peaked after 90 min and remained elevated up to 300 min. Poly(I).poly(C) also stimulated a 2.5-fold rise in circulating irPGF2 alpha, which peaked after 150 min and was followed by a return to basal levels after 300 min. 4. The overall magnitude of the febrile response to poly(I).poly(C) (2.5 micrograms/kg, i.v.) was significantly antagonized by the AVP V1 receptor antagonist (250 micrograms/kg, i.v.) administered 5 min prior to the pyrogen. 5. The irPGE2 response to poly(I).poly(C) (2.5 micrograms/kg, i.v.) was significantly antagonized by the AVP V1 receptor antagonist (250 micrograms/kg, i.v.) administered 5 min prior to the pyrogen. The irPGF2 alpha response was only reduced at the peak 150 min time point measurement. 6. In conclusion, these results show a modulatory role for a peripherally administered AVP V1 antagonist in the febrile responses to poly(I).poly(C), suggesting a possible propyretic role for endogenous peripheral AVP. This modulatory role appears to be mediated via actions on prostaglandin E2.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Arginine Vasopressin; Body Temperature; Dinoprost; Dinoprostone; Fever; Interferon Inducers; Male; Poly I-C; Rabbits; Vasopressins

Previous investigations on the antipyretic properties of arginine vasopressin have used bacterial endotoxins or pyrogens to induce fever. Because these experimental models of fever fail to mimic all aspects of the responses to infection, we felt it was important to examine the role of endogenously released vasopressin as a neuromodulator in febrile thermoregulation during infection. Therefore the present study examines the effects of chronic infusion of a V1-receptor antagonist or saline (via osmotic minipumps into the ventral septal area of the brain) on a fever induced by injection of live bacteria. Telemetry was used for continuous measurement of body temperature in the awake unhandled rat. Animals infused with the V1-antagonist exhibited fevers that were greater in duration compared with those of saline-infused animals. These results support the hypothesis that vasopressin functions as an antipyretic agent or fever-reducing agent in brain. Importantly, they suggest that endogenously released vasopressin may play a role as a neuromodulator in natural fever.

Topics: Animals; Arginine Vasopressin; Body Temperature Regulation; Brain; Drinking; Eating; Escherichia coli Infections; Fever; Infusion Pumps; Male; Rats; Rats, Sprague-Dawley; Vasopressins

Experiments were undertaken to characterize a possible receptor mediating antipyretic action of arginine vasopressin (AVP) within the medial amygdaloid nucleus (meA) in the conscious rat. Additional experiments were directed at determining whether the action of endogenously released AVP can be revealed in the meA during fever in the conscious rat. These objectives were achieved using vasopressin analogues directed against vasopressor (V1a) and antidiuretic (V2) receptors. Bilateral injection of AVP (40 pmol) into the meA of conscious rats suppressed fever evoked by intracerebroventricular (icv) administration of prostaglandin E1 (PGE1, 50 ng). The V2 receptor agonist 1-desamino-8-D-AVP (40 pmol) injected into the meA evoked only moderate antipyresis compared with AVP, possibly because of interaction of this agonist with V1a receptors. The antipyretic effect of AVP was blocked when injection of the peptide was preceded by a bilateral injection of the V1a antagonist 1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)-2-(O-methyl)tyrosine AVP [d(CH2)5Tyr(Me)AVP, 400 pmol] into the meA. Injection of d(CH2)5Tyr(Me)AVP alone into the meA was without significant effect on afebrile core temperature. Injection of d(CH2)5Tyr(Me)AVP or 1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid)-2-D-valine,4-valine AVP (a V2 antagonist) alone into the meA before icv PGE1 resulted in fevers that were not significantly different from artificial cerebrospinal fluid controls. These data are consistent with the possibility that AVP might act within the meA to evoke antipyresis via receptors that resemble V1a (vasopressor) receptors. However, the action of AVP endogenously released into the meA does not appear to be an absolute requisite in the normal modulation of PGE1 fever.

Topics: Alprostadil; Amygdala; Angiotensin Receptor Antagonists; Animals; Anti-Inflammatory Agents, Non-Steroidal; Arginine Vasopressin; Deamino Arginine Vasopressin; Fever; Injections, Intraventricular; Male; Rats; Receptors, Angiotensin; Receptors, Vasopressin; Vasopressins

Topics: Adrenocorticotropic Hormone; Animals; Arachidonic Acid; Body Temperature Regulation; Brain; Cytokines; Fever; Humans; Hypothalamus; Melanocyte-Stimulating Hormones; Neurons; Pyrogens; Vasopressins

Topics: Animals; Cerebral Ventricles; Colchicine; Endotoxins; Escherichia coli; Fever; Guinea Pigs; Injections, Intraventricular; Male; Median Eminence; Neurons; Vasopressins

Repeated daily intravenous injections of bacterial endotoxin induce a refractory state to their usual pyrogenic effects. The neuropeptide arginine vasopressin (AVP) has been implicated in natural fever suppression and may be involved in the process of pyrogenic tolerance to intravenous endotoxin. This study was conducted to test this hypothesis. Tolerance was induced by two successive daily intravenous injections of Escherichia coli endotoxin (50 micrograms/kg) into conscious unrestrained rats. This tolerance was maintained, unaltered, after a third or fourth subsequent injection. However, bilateral administration of an AVP V1-receptor antagonist (0.43-4.3 nmol) into the ventral septal area (VSA) of the rat brain markedly enhanced the thermoregulatory response to a third or fourth endotoxin challenge compared with saline controls. The effect of the V1 antagonist was dose related. In contrast, an AVP V2 antagonist (0.43 nmol) bilaterally injected into the VSA did not affect the tolerant reaction to endotoxin. Furthermore, neither saline nor the V1 antagonist significantly affected core temperature when administered within the VSA without subsequent endotoxin. These results are consistent with the hypothesis that AVP acts as an endogenous antipyretic within the VSA during fever. Moreover, the data suggest a possible role for centrally acting vasopressin during pyrogenic tolerance to E. coli endotoxin.

Topics: Animals; Arginine Vasopressin; Body Temperature Regulation; Drug Tolerance; Endotoxins; Escherichia coli; Fever; Male; Rats; Rats, Inbred Strains; Septum Pellucidum; Vasopressins

The authors discuss about five cases of diabetes insipidus observed in patients affected by traumatic cervical spine fractures and/or dislocations, without either evident lesions of the cerebral structures at CT scan examination, or important craniocerebral trauma. In all patients polyuria and hyperthermia arose some days after the traumatic accident and regressed spontaneously or after exogeneous vasopressin administration. Vasopressin urinary levels confirmed the presence of a true diabetes insipidus, the origin of which is in largely obscure. A central medullary vasopressin mediated pathway, demonstrated only in experimental animals, may be responsible for such a finding.

Topics: Adolescent; Adult; Cervical Vertebrae; Diabetes Insipidus; Female; Fever; Fractures, Bone; Humans; Hypothalamo-Hypophyseal System; Joint Dislocations; Male; Polyuria; Radiography; Spinal Cord Injuries; Syndrome; Vasopressins

It has been found recently that N alpha-acetyl-[Arg8]vasopressin (Ac-VP) is present in the brain of rats. The physiological significance of this peptide is as yet unknown. Therefore, the central nervous system effects of this peptide were investigated, namely, its effects on passive avoidance behavior, exploratory behavior and body temperature. The interaction of Ac-VP with the central nervous system effects of vasopressin (VP) was also studied. Ac-VP had a slight agonistic effect on passive avoidance behavior, i.e. it facilitated passive avoidance behavior at a dose 100 times higher than that of VP. Relatively low doses (3-10 ng) of Ac-VP attenuated passive avoidance behavior, which suggests that Ac-VP interfered with an endogenous compound involved in the control of passive avoidance responding. Ac-VP was also able, albeit in higher doses (30 ng), to competitively antagonize the effect of [Cyt6]VP-(5-9), a highly potent, putative endogenous metabolite of vasopressin in the rat brain. This antagonism could be due to an interaction of Ac-VP with sites other than the V1 vasopressin receptor. Ac-VP had no significant influence on other central nervous system effects of the hormonally active nonapeptide VP, such as exploratory behavior and body temperature. These effects were readily antagonized by the V1 vasopressin receptor antagonist d(CH2)5Tyr(Me)VP. Ac-VP may be competitive antagonist of behaviorally active vasopressin metabolite(s) in the brain.

Topics: Animals; Arginine Vasopressin; Avoidance Learning; Behavior, Animal; Body Temperature; Dose-Response Relationship, Drug; Endotoxins; Fever; Injections, Intraventricular; Male; Peptide Fragments; Rats; Rats, Inbred Strains; Time Factors; Vasopressins

Bioelectrochemical potentials of the rabbit hypothalamic supraoptic, paraventricular, suprachiasmatic nuclei, and medial preoptic area changed in a similar way in fever induced with i.v. administration of leucocytic pyrogen/interleukin I in all the structures due, probably, to their compact localization. The dynamics of bioelectrochemical activity coincided with that of rectal temperature derivative. The alterations of bioelectrochemical activity seem to reflect hypothalamic metabolic changes closely associated with effector mechanisms of thermoregulation in fever rather than with the temperature itself. The differences in the reaction patterns of neurosecretory nuclei are compared with changes in their vasopressin-synthetizing function during fever.

Topics: Animals; Body Temperature; Body Temperature Regulation; Fever; Hypothalamus; Interleukin-1; Male; Membrane Potentials; Neurosecretory Systems; Pyrogens; Rabbits; Rectum; Vasopressins

1. Infusion of human purified interleukin-1 into a lateral cerebral ventricle of the rat evoked a rise in core temperature which was abolished by heating the interleukin-1. 2. When the intracerebroventricular infusion of interleukin-1 was preceded by a bilateral injection of saline into the ventral septal area, the resulting febrile response was not different from that induced by interleukin-1 alone. However, when the vasopressin V1 antagonist, d(CH2)5Tyr(Me)AVP, was injected into the ventral septal area prior to interleukin-1, a fever was evoked which was significantly greater in magnitude and duration. This enhancement of fever by the V1 antagonist was dose related. 3. Injection of either saline or the V1 antagonist into the ventral septal area, in the absence of interleukin-1, did not evoke any consistent alteration in the core temperature of the rats. 4. The vasopressin V2 antagonist, d(CH2)5-D-ValVAVP, was injected into the ventral septal area to determine the effect of another vasopressin analogue on the fever evoked by interleukin-1. The V2 antagonist did not alter the time course of interleukin-1-induced fever or alter core temperature in the afebrile rat. 5. These data are consistent with the hypothesis that endogenous vasopressin, released in the ventral septal area, may be involved in limiting fever. In addition, these results indicate that the central receptor mediating the antipyretic action of vasopressin may resemble the V1 subtype of peripheral vasopressin receptor.

Topics: Animals; Arginine Vasopressin; Body Temperature; Fever; Interleukin-2; Male; Rats; Time Factors; Vasopressins

Topics: Child, Preschool; Fever; Humans; Vasopressins

Topics: Adult; Drinking; Fever; Humans; Male; Psychophysiologic Disorders; Rhabdomyolysis; Vasopressins; Water Intoxication

When pyrogenic substances are injected intravenously into experimental animals, a sequence of events is set in motion which involves the hypothalamus and perhaps other portions of the diencephalon to produce a febrile response. We now present evidence that the brain produces its own endogenous antipyretic which may serve as a means of controlling the extent of the fever. When arginine vasopressin is perfused through the lateral septal area of the hypothalamus of the sheep, fever is suppressed. Vasopressin alone does not lower normal body temperature when perfused through this region of the brain. In addition, evidence is provided to indicate that vasopressin is released within the lateral septal area during the febrile response. It is concluded that, in fever, arginine vasopressin may be released in the lateral septal area of the brain and serve as an endogenous antipyretic. Results indicate that, following an initial application of vasopressin into the brain itself, a subsequent similar administration of vasopressin produces seizure-like activity. Therefore, it is suggested that this release of arginine vasopressin may contribute to the production of febrile convulsion.

Topics: Animals; Animals, Newborn; Arginine Vasopressin; Body Temperature Regulation; Female; Fever; Guinea Pigs; Hypothalamus; Pregnancy; Pyrogens; Rats; Seizures, Febrile; Septum Pellucidum; Sheep; Vasopressins

The purpose of this investigation was to examine the changes in brain vasopressin (AVP) concentrations induced by endotoxin in the rat. Thirteen areas of the brain and the plasma were extracted and assayed for AVP under control conditions and at two times after endotoxin, 60 min (hypothermic phase) and 330 min (hyperthermic phase). There were no changes in AVP concentrations in the neurohypophysis, median eminence, supraoptic nucleus, paraventricular nucleus, suprachiasmatic nucleus, hippocampus or brainstem (nucleus of solitary tract). Decreased concentrations occurred at 330 min post-endotoxin in the lateral septum, medial septum, amygdala and caudate whereas increases occurred in the preoptic/anterior hypothalamus and cerebellum. Plasma levels increased by 60 min post-endotoxin and were still elevated by 330 min post-endotoxin. Endotoxin induces changes in AVP concentrations in several areas of brain, which may reflect alterations in turnover, perhaps related to the febrile rise in body temperature.

Topics: Animals; Antibodies; Body Temperature Regulation; Brain; Endotoxins; Escherichia coli; Fever; Male; Rats; Rats, Sprague-Dawley; Vasopressins

The effects of direct administration of vasopressin into the preoptic anterior hypothalamus on thermoregulatory functions were assessed in conscious rats at various ambient temperatures. Intrahypothalamic administration of vasopressin caused fever, increased metabolic heat production and decreased heat loss (cutaneous vasoconstriction) in rats. There was no changes in respiratory evaporative heat loss in response to administration of these drugs. Furthermore, it was found that the fever reactions induced by intrahypothalamic vasopressin was antagonized by pretreatment of animals with an intrahypothalamic dose of either yohimbine (an alpha-adrenergic receptor antagonist), propranolol (a beta-adrenergic receptor antagonist), or sodium acetylsalicylate (a prostaglandin synthetase inhibitor). The data indicate that a prostaglandin-adrenergic link occurs in the hypothalamic pathways which mediate the vasopressin-induced fever in rats.

Topics: Animals; Aspirin; Body Temperature Regulation; Fever; Hypothalamus; Male; Neural Pathways; Prostaglandins; Rats; Rats, Inbred Strains; Sympathetic Nervous System; Sympatholytics; Vasopressins

Diabetes insipidus was diagnosed in a 6-year-old Holstein-Friesian cow with a history of recurrent fever, ketosis, lymphadenopathy, and inappetence. The diagnosis was based on the clinical findings, response to exogenous vasopressin, and lack of urine concentration in a water deprivation test. The disease gradually regressed over a period of 1 year and did not recur.

Topics: Animals; Cattle; Cattle Diseases; Diabetes Insipidus; Female; Fever; Urinary Catheterization; Vasopressins; Water Deprivation

Plasma concentrations of arginine vasopressin were determined by radioimmunoassay in 13 normal children, 21 patients with febrile illnesses (not bacterial meningitis), and 17 patients with bacterial meningitis. The mean +/- 1 SD concentrations of AVP in the normal children and patients with various febrile illnesses were 0.7 +/- 0.6 and 1.0 +/- 1.2 muU/ml, respectively. The mean +/- 1 SD concentration of AVP in patients with bacterial meningitis was 3.3 +/- 2.3 muU/ml. The concentrations of AVP in the patients with bacterial meningitis were significantly greater (P less than 0.001) than those noted in the normal children or children with other febrile diseases.

Topics: Adolescent; Arginine Vasopressin; Child; Child, Preschool; Fever; Humans; Infant; Meningitis; Radioimmunoassay; Syndrome; Vasopressins

The role of hyperthermia in the absence of infection has been investigated in the pregnant baboon. Twenty-three near term animals were used. Catheters were placed in maternal and fetal arteries and thermocouples implanted in maternal colon and fetal esophagus. Maternal temperature was raised to between 41 and 42 degrees Centigrade (C.), by applying external heat. The temperature gradient between fetus and mother (delta T F-M) was 0.47 degree C. under steady-state conditions with maternal temperature at 38 degrees C. and rose to 0.75 degree C. at 42 degrees C. Hyperthermia caused a twofold increase in uterine activity; a metabolic acidosis developed in the mother and a profound acidosis and hypoxia developed in the fetus. There was also a marked fall in blood pressure and an increase in heart rate in both mother and fetus; late deceleration of the fetal heart rate occurred at a higher oxygen level and pHa than has been observed under normothermic conditions.

Topics: Acidosis; Animals; Arrhythmias, Cardiac; Body Temperature; Female; Fetal Death; Fetal Diseases; Fetal Heart; Fever; Haplorhini; Heart Rate; Hypotension; Hypoxia; Labor, Obstetric; Oxytocin; Papio; Pregnancy; Pregnancy Complications; Vasopressins

Topics: Adrenal Glands; Animals; Catecholamines; Corticosterone; Fever; Fibrinolysis; Male; Pituitary Gland, Posterior; Rats; Vasopressins

Topics: Aldosterone; Animals; Fever; Gastric Juice; Pepsin A; Potassium; Rats; Sodium; Vasopressins

Topics: Adolescent; Adult; Aged; Aldosterone; Blood Glucose; Fasting; Fever; Glomerular Filtration Rate; Glucose; Humans; Hyponatremia; Insulin; Middle Aged; Natriuresis; Neoplasms; Osmolar Concentration; Sodium; Tuberculosis; Vasopressins

Topics: Acromegaly; Adrenal Glands; Adult; Aged; Cushing Syndrome; Female; Fever; Glucocorticoids; Growth Hormone; Humans; Hypothalamus; Insulin; Male; Metyrapone; Middle Aged; Pituitary Diseases; Pituitary Gland; Pituitary-Adrenal Function Tests; Vasopressins

Topics: Acid Phosphatase; Body Temperature Regulation; Diuresis; Endotoxins; Fever; Glucuronidase; Humans; Hydrocortisone; Sweating; Vasopressins

Topics: Child; Child Behavior Disorders; Diabetes Insipidus; Fever; Humans; Hypernatremia; Infant; Mental Disorders; Povidone; Vasopressins