Thermoregulatory effects of monoamine potentiators and inhibitors in the rat

1976 ◽  
Vol 231 (1) ◽  
pp. 148-152 ◽  
Author(s):  
R Francesconi ◽  
M Mager
Keyword(s):  
Ambient Temperature ◽  
Total Dose ◽  
Temperature Regulation ◽  
Nerve Terminals ◽  
Intraventricular Administration ◽  
Central Administration ◽  
Thermoregulatory Responses ◽  
Dose Dependent

Exogenously administered monoamines may elicit variable thermoregulatory responses dependent on dosage, species, site of administration, ambient temperature, etc. In an attempt to reconcile several inconsistencies, we have undertaken a series of studies related to monoaminergic control of temperature regulation. Thus, intraventricular administration of serotonin (2.64-26.4 mug) and norepinephrine (3.3-32.8 mug) in rats evoked acute (15-60 min) dose-dependent hypothermic responses (delta Tre = 2 degrees C) that were gradually superseded by significant, more persistent hyperthermia (delta Tre = 1 degreee C). Administration of chlorimipramine or imipramine (total dose 40 mug), even in monoamine-depleted animals, caused long-lasting hyperthermic responses, presumably by the prevention of reuptake of serotonin and norepinephrine at nerve terminals involved in thermoregulation. Pretreatment with the serotonin inhibitor cyproheptadine (4o mug) attenuated the hyperthermia achieved by central administration of chlorimipramine alone. We conclude that both monoamines can act as thermogenic agents under the conditions of these experiments.

Thermoregulatory responses to lipopolysaccharide in the mouse: dependence on the dose and ambient temperature

2005 ◽  
Vol 289 (5) ◽  
pp. R1244-R1252 ◽  
Author(s):  
Alla Y. Rudaya ◽  
Alexandre A. Steiner ◽  
Jared R. Robbins ◽  
Alexander S. Dragic ◽  
Andrej A. Romanovsky
Keyword(s):  
Ambient Temperature ◽  
Dose Range ◽  
Dose Dependence ◽  
Experimental Conditions ◽  
Thermoregulatory Responses ◽  
Hypothermic Response ◽  
High Doses ◽  
The Relationship ◽  
Dose Dependent ◽  
Higher Doses

Most published studies of thermoregulatory responses of mice to LPS involved a stressful injection of LPS, were run at a poorly controlled and often subneutral ambient temperature (Ta), and paid little attention to the dependence of the response on the LPS dose. These pitfalls have been overcome in the present study. Male C57BL/6 mice implanted with jugular vein catheters were kept in an environmental chamber at a tightly controlled Ta. The relationship between the Tas used and the thermoneutral zone of the mice was verified by measuring tail skin temperature, either by infrared thermography or thermocouple thermometry. Escherichia coli LPS in a wide dose range (100-104μg/kg) was administered through an extension of the jugular catheter from outside the chamber. The responses observed were dose dependent. At a neutral Ta, low (just suprathreshold) doses of LPS (100-101μg/kg) caused a monophasic fever. To a slightly higher dose (101.5μg/kg), the mice responded with a biphasic fever. To even higher doses (101.75-104μg/kg), they responded with a polyphasic fever, of which three distinct phases were identified. The dose dependence and dynamics of LPS fever in the mouse appeared to be remarkably similar to those seen in the rat. However, the thermoregulatory response of mice to LPS in a subthermoneutral environment is remarkably different from that of rats. Although very high doses of LPS (104μg/kg) did cause a late (latency, ∼3 h) hypothermic response in mice, the typical early (latency, 10–30 min) hypothermic response seen in rats did not occur. The present investigation identifies experimental conditions to study LPS-induced mono-, bi-, and polyphasic fevers and late hypothermia in mice and provides detailed characteristics of these responses.

EFFECT OF INTRAVENTRICULAR ADMINISTRATION OF NORADRENALINE ON WATER DIURESIS IN GOATS

1975 ◽  
Vol 66 (3) ◽  
pp. 375-383 ◽  
Author(s):  
G. VANDEPUTTE-VAN MESSOM ◽  
G. PEETERS
Keyword(s):  
Intraventricular Administration ◽  
Excretion Ratio ◽  
Dose Response Relationship ◽  
Water Diuresis ◽  
3Rd Ventricle ◽  
Dependent Inhibition ◽  
Dose Dependent Inhibition ◽  
High Doses ◽  
Excretion Rates ◽  
Dose Dependent

SUMMARY During water diuresis in conscious goats, noradrenaline (NA), its antagonists phentolamine, phenoxybenzamine and propranolol and also atropine were administered into the 3rd ventricle. The subsequent effects on water diuresis and on the excretion rates of Na+, K+ and Cl− were investigated. Infusion of NA into the 3rd ventricle induced a strong and significant antidiuretic response and a decrease in the Na+: K+ excretion ratio; these effects were dose-dependent. High doses of NA produced a significant increase in urinary K+ excretion. Similar results were observed after i.v. administration of arginine-vasopressin. Pretreatment with phentolamine injected into the 3rd ventricle produced a dose-dependent inhibition of the NA-induced antidiuretic effects. Phenoxybenzamine also blocked the response to NA but a dose-response relationship was not apparent. Atropine and propranolol did not block the response to NA.

Amitriptyline and imipramine inhibit the release of acetylcholine from parasympathetic nerve terminals in the rat iris

1984 ◽  
Vol 62 (7) ◽  
pp. 857-859 ◽  
Author(s):  
J. S. Richardson ◽  
T. G. Mattio ◽  
E. Giacobini
Keyword(s):  
Nerve Terminals ◽  
Dependent Manner ◽  
Parasympathetic Nerve ◽  
Drug Concentrations ◽  
Release Of Acetylcholine ◽  
Rat Iris ◽  
Anticholinergic Side Effects ◽  
Dose Dependent ◽  
Drug Free

The electrically stimulated release of [3H]acetylcholine from the parasympathetic nerve terminals of the rat iris in vitro is increased in a dose-dependent manner by scopolamine but is decreased by the tricyclic antidepressants amitriptyline and imipramine. The increased release in the presence of scopolamine seems to be due to the blockade of a presynaptic muscarinic autoreceptor that, in the drug-free state, inhibits the release of acetylcholine. However, at drug concentrations that should have comparable antimuscarinic potency, the antidepressants inhibit the release of acetylcholine. This suggests that the anticholinergic side effects of the antidepressants may be due to the reduced release of acetylcholine from parasympathetic nerve terminals as well as a possible direct postsynaptic muscarinic receptor blocking action. Whatever the mechanism of this action, the antidepressants do not have the same effect as scopolamine at the presynaptic muscarinic autoreceptor in the rat iris.

scholarly journals Comparative Drug Disposition, Urinary Pharmacokinetics, and Renal Effects of Multilamellar Liposomal Nystatin and Amphotericin B Deoxycholate in Rabbits

2003 ◽  
Vol 47 (12) ◽  
pp. 3917-3925 ◽  
Author(s):  
Andreas H. Groll ◽  
Diana Mickiene ◽  
Vidmantas Petraitis ◽  
Ruta Petraitiene ◽  
Raul M. Alfaro ◽  
...  
Keyword(s):  
Total Dose ◽  
Amphotericin B ◽  
Drug Disposition ◽  
Fungal Infections ◽  
Standard Dose ◽  
Concentration Data ◽  
Drug Concentrations ◽  
Amphotericin B Deoxycholate ◽  
Dose Dependent Decrease ◽  
Dose Dependent

ABSTRACT The comparative drug dispositions, urinary pharmacokinetics, and effects on renal function of multilamellar liposomal nystatin (LNYS; Nyotran) and amphotericin B deoxycholate (DAMB; Fungizone) were studied in rabbits. Drug concentrations were determined by high-performance liquid chromatography as total concentrations of LNYS and DAMB. In comparison to a standard dose of 1 mg of DAMB/kg of body weight, therapeutic dosages of LNYS, i.e., 2, 4, and 6 mg/kg, resulted in escalating maximum concentrations (C max) (17 to 56μ g/ml for LNYS versus 3.36 μg/ml for DAMB; P< 0.001) and values for the area under the concentration-time curve from 0 to 24 h (AUC0-24) (17 to 77μ g · h/ml for LNYS versus 12μ g · h/ml for DAMB; P < 0.001) in plasma but a significantly faster total clearance from plasma (0.117 to 0.080 liter/h/kg for LNYS versus 0.055 liter/h/kg for DAMB; P = 0.013) and a ≤8-fold-smaller volume of distribution at steady state (P = 0.002). Urinary drug concentration data revealed a ≥10-fold-higher C max (16 to 10 μg/ml for LNYS versus 0.96μ g/ml for DAMB; P = 0.015) and a 4- to 7-fold-greater AUC0-24 (63 to 35μ g · h/ml for LNYS versus 8.9μ g · h/ml for DAMB; P = 0.015) following the administration of LNYS, with a dose-dependent decrease in the dose-normalized AUC0-24 in urine (P= 0.001) and a trend toward a dose-dependent decrease in renal clearance. Except for the kidneys, the mean concentrations of LNYS in liver, spleen, and lung 24 h after dosing were severalfold lower than those after administration of DAMB (P,<0.002 to <0.001). Less than 1% each of the total dose of LNYS was recovered from the kidneys, liver, spleen, and lungs; in contrast, a quarter of the total dose was recovered from the livers of DAMB-treated animals. LNYS had dose-dependent effects on glomerular filtration and distal, but not proximal, renal tubular function which did not exceed those of DAMB at the highest investigated dosage of 6 mg/kg. The results of this experimental study demonstrate fundamental differences in the dispositions of LNYS and DAMB. Based on its enhanced urinary exposure, LNYS may offer a therapeutic advantage in systemic fungal infections involving the upper and lower urinary tracts that require therapy with antifungal polyenes.

Intracerebroventricular injection of prostaglandin E2 increases splenic sympathetic nerve activity in rats

1995 ◽  
Vol 269 (3) ◽  
pp. R662-R668 ◽  
Author(s):  
T. Ando ◽  
T. Ichijo ◽  
T. Katafuchi ◽  
T. Hori
Keyword(s):  
Prostaglandin E2 ◽  
Sympathetic Nerve ◽  
Time Course ◽  
Sympathetic Nerve Activity ◽  
Dependent Manner ◽  
Central Administration ◽  
Nerve Activity ◽  
High Doses ◽  
Alpha Chloralose ◽  
Dose Dependent

The effects of central administration of prostaglandin E2 (PGE2) and its selective agonists on splenic sympathetic nerve activity (SNA) were investigated in urethan- and alpha-chloralose-anesthetized rats. An intra-third-cerebroventricular (13V) injection of PGE2 (0.1-10 nmol/kg) increased splenic SNA in a dose-dependent manner. An I3V injection of an EP1 agonist, 17-phenyl-omega-trinor PGE2 (1-30 nmol/kg), also resulted in a dose-dependent increase in splenic SNA, with a time course similar to that of PGE2-induced responses. In contrast, EP2 agonists, butaprost (10-100 nmol/kg I3V) and 11-deoxy-PGE1 (10-100 nmol/kg I3V), had no effect on splenic SNA. An I3V injection of M & B-28767 (an EP3/EP1 agonist, EP3 >> EP1) increased splenic SNA only at high doses (10-100 nmol/kg). Pretreatment with an EP1 antagonist, SC-19220 (200 and 500 nmol/kg), completely blocked the responses of splenic SNA to PGE2 (0.1 nmol/kg) and M & B-28767 (10 nmol/kg), respectively. These findings indicate that brain PGE2 increases splenic SNA through its action on EP1 receptors.

Biophysics and Physiology of Temperature Regulation in Thermogenic Flowers

2001 ◽  
Vol 21 (2) ◽  
pp. 223-236 ◽  
Author(s):  
Roger S. Seymour
Keyword(s):  
Ambient Temperature ◽  
Heat Production ◽  
Temperature Regulation ◽  
Alternative Oxidase ◽  
Thermal Balance ◽  
Seed Plants ◽  
Large Drop

The flowers or inflorescences of certain primitive seed plants are able to regulate their temperature during blooming by modulating the rate of heat production to remain much warmer than the surroundings. A large drop in ambient temperature causes a smaller drop in flower temperature which causes an increase in the rate of heat production by futile involvement of the cytochrome and alternative oxidase respiratory pathways. The result is that the rate of heat production is inversely related to ambient temperature and flower temperature remains high and relatively independent of ambient temperature. While the biophysics of thermal balance in the whole flowers is better understood, the regulation of the biochemical heat-generating pathways is not known.

Seasonal variation of temperature regulation: do thermoregulatory responses “spring” forward and “fall” back?

2020 ◽  
Vol 64 (7) ◽  
pp. 1221-1231 ◽  
Author(s):  
Urša Ciuha ◽  
Stylianos Kounalakis ◽  
Adam C. McDonnell ◽  
Igor B. Mekjavic
Keyword(s):  
Seasonal Variation ◽  
Temperature Regulation ◽  
Thermoregulatory Responses

Hypothalamic control of body temperature: insights from the past

2004 ◽  
Vol 97 (5) ◽  
pp. 1593-1594 ◽  
Author(s):  
Gary W. Mack
Keyword(s):  
Body Temperature ◽  
Temperature Regulation ◽  
Proportional Control ◽  
Set Point ◽  
Historical Significance ◽  
The Past ◽  
Thermoregulatory Responses ◽  
Hypothalamic Control ◽  
Classic Papers

This essay looks at the historical significance of three APS classic papers that are freely available online: Hammel HT, Hardy JD, and Fusco MM. Thermoregulatory responses to hypothalamic cooling in unanesthetized dogs. Am J Physiol 198: 481—486, 1960 ( http://ajplegacy.physiology.org/cgi/reprint/198/3/481 ). Hammel HT, Jackson DC, Stolwijk JAJ, Hardy JD, and Strømme SB. Temperature regulation by hypothalamic proportional control with an adjustable set point. J Appl Physiol 18: 1146—1154, 1963 ( http://jap.physiology.org/cgi/reprint/18/6/1146 ). Hellstrøm B and Hammel HT. Some characteristics of temperature regulation in the unanesthetized dog. Am J Physiol 213: 547—556, 1967 ( http://ajplegacy.physiology.org/cgi/reprint/213/2/547 ).

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