MAINTENANCE OF BODY TEMPERATURE OF RESTRAINED ADRENALECTOMIZED RATS EXPOSED TO COLD: EFFECT OF ADRENAL CORTICAL HORMONES

1956 ◽  
Vol 34 (1) ◽  
pp. 721-729 ◽  
Author(s):  
P. F. Iampietro ◽  
M. J. Fregly ◽  
E. R. Buskirk

Experiments were performed to determine the role of the adrenal glands in the maintenance of colonic temperature of rats which were restrained and exposed to air at 5 °C. Colonic temperature decreased linearly with time in the cold air; hence, colonic cooling rate (CCR) was adopted as a measure of response to cold. Bilateral adrenalectomy increased CCR. Administration of cortisone acetate, adrenal cortical extract (ACE) or desoxycorticosterone acetate to adrenalectomized rats decreased CCR. Maximal decrease occurred with administration of 1.00 mgm. cortisone/rat/day or 0.25 ml. ACE/rat/day; higher doses of each hormone were less and less effective in returning CCR toward that of sham-operated rats. An adrenalectomized rat could not be rendered normal with respect to CCR no matter what dose of either ACE or cortisone was administered. In contrast, only the highest dose of DOCA administered (4.0 mgm./rat/day) significantly reduced CCR to that of sham-operated rats. The cooling test is similar to the standard growth test in that the response to administration of cortisone and ACE passes through a maximum and then declines with increasing dosage. The lower colonic temperature of adrenalectomized rats in air at 25 °C. was returned to that of sham-operated rats when cortisone (1.00 mgm. or more) or ACE (0.25 ml. or more) was administered; however, colonic temperature did not appear either to increase incrementally or to pass through a maximum with increasing doses of either hormone. DOCA had no effect on initial colonic temperature. Untreated adrenalectomized rats rarely survived lowering of colonic temperature to 22.5 °C; hence, the minimum colonic temperature to which adrenalectomized rats can be cooled and subsequently survive is considerably above that for normal rats (LD50 15.3 °C). Administration of any of the above hormones increased survival even in those doses which did not affect CCR.

1956 ◽  
Vol 34 (4) ◽  
pp. 721-729
Author(s):  
P. F. Iampietro ◽  
M. J. Fregly ◽  
E. R. Buskirk

Experiments were performed to determine the role of the adrenal glands in the maintenance of colonic temperature of rats which were restrained and exposed to air at 5 °C. Colonic temperature decreased linearly with time in the cold air; hence, colonic cooling rate (CCR) was adopted as a measure of response to cold. Bilateral adrenalectomy increased CCR. Administration of cortisone acetate, adrenal cortical extract (ACE) or desoxycorticosterone acetate to adrenalectomized rats decreased CCR. Maximal decrease occurred with administration of 1.00 mgm. cortisone/rat/day or 0.25 ml. ACE/rat/day; higher doses of each hormone were less and less effective in returning CCR toward that of sham-operated rats. An adrenalectomized rat could not be rendered normal with respect to CCR no matter what dose of either ACE or cortisone was administered. In contrast, only the highest dose of DOCA administered (4.0 mgm./rat/day) significantly reduced CCR to that of sham-operated rats. The cooling test is similar to the standard growth test in that the response to administration of cortisone and ACE passes through a maximum and then declines with increasing dosage. The lower colonic temperature of adrenalectomized rats in air at 25 °C. was returned to that of sham-operated rats when cortisone (1.00 mgm. or more) or ACE (0.25 ml. or more) was administered; however, colonic temperature did not appear either to increase incrementally or to pass through a maximum with increasing doses of either hormone. DOCA had no effect on initial colonic temperature. Untreated adrenalectomized rats rarely survived lowering of colonic temperature to 22.5 °C; hence, the minimum colonic temperature to which adrenalectomized rats can be cooled and subsequently survive is considerably above that for normal rats (LD50 15.3 °C). Administration of any of the above hormones increased survival even in those doses which did not affect CCR.


1993 ◽  
Vol 265 (5) ◽  
pp. R1179-R1183 ◽  
Author(s):  
R. H. Derijk ◽  
P. J. Strijbos ◽  
N. van Rooijen ◽  
N. J. Rothwell ◽  
F. Berkenbosch

Increases in thermogenesis and body temperature (fever) frequently accompany infection or injury and are thought to be mediated by endogenous pyrogens (e.g. cytokines), which are released from activated immune cells such as macrophages. Therefore, we have investigated the effect of selective elimination of peripheral macrophages on the changes in oxygen consumption (VO2) and colonic temperature in response to bacterial lipopolysaccharide (LPS) in the rat. Peripheral macrophages were depleted by intravenous injection of liposomes containing the drug dichloromethylene diphosphonate (Cl2MDP). Resting oxygen consumption and colonic temperatures were not affected by macrophage elimination. In intact rats, peripheral injection of LPS (0.1-0.5 mg/kg) elicited an increase in colonic temperature and in oxygen consumption that declined at higher doses (2.5 mg/kg). The pyrogenic and thermogenic responses to LPS were significantly attenuated in rats in which peripheral macrophages were eliminated. Previously, we have reported that elimination of macrophages blunts the plasma interleukin-1 (IL-1) response to LPS. Here we show that elimination of macrophages does not affect the increase in plasma IL-6 concentrations in response to LPS. These data indicate that the pyrogenic and thermogenic responses to LPS are at least in part dependent on mechanisms involving peripheral macrophages, and that peripherally produced IL-1 rather than IL-6 may be an important mediator of the changes in oxygen consumption and colonic temperature in response to LPS.


1960 ◽  
Vol 199 (3) ◽  
pp. 437-444 ◽  
Author(s):  
Melvin J. Fregly

The effects of cortisone acetate and thyroxine, administered separately or in combination, on colonic cooling rate (CCR) have been studied in restrained, adrenalectomized rats subjected to air at 5°C. Thyroxine alone at 5.0 µg/day reduced the rapid CCR of adrenalectomized rats but failed to return it to that of sham-operated rats. Cortisone acetate alone at 1.0 mg/day reduced CCR but also failed to restore it to normal. A higher dose (2.0 mg/day) was even less effective. Administration of 5.0 µg/day thyroxine simultaneously with 2.0–2.5 mg cortisone acetate returned CCR to that of sham-operated rats. Simultaneous administration of cortisone acetate with graded doses of thyroid stimulating hormone (TSH) to adrenalectomized rats resulted in greater reduction of CCR than with either treatment alone. Cortisone acetate did not appear to interfere either with tissue utilization of thyroxine or with thyroid gland response to TSH administration. The cooling test has also proved a useful tool for comparing potencies of a synthetic (dexamethasone) and a naturally occurring steroid (progesterone) with that of cortisone acetate. Dexamethasone is estimated to have a potency 700 times that of cortisone acetate, while progesterone is only one-third as potent.


1969 ◽  
Vol 47 (2) ◽  
pp. 179-184 ◽  
Author(s):  
M. Oravec ◽  
T. L. Sourkes

AMTP (α-methyl-DL-tryptophan) stimulates the incorporation of (labeled) alanine, glutamate, leucine, isoleucine, histidine, threonine, tryptophan, pyruvate, and acetate into hepatic glycogen. Accompanying this phenomenon is an enhanced rate of oxidation of these substances to carbon dioxide, except for acetate whose oxidation is not influenced by AMTP. AMTP also causes an increased excretion of urea and a rise in body temperature. Presence of the adrenal glands is necessary for the stimulatory action of AMTP on the oxidation of alanine, glutamate, isoleucine, and pyruvate. AMTP-stimulated oxidation of leucine and threonine is only partially dependent upon the adrenal gland. The oxidation of histidine is increased to the same extent by AMTP in both intact and adrenalectomized rats. The ability of AMTP to increase the level of tryptophan pyrrolase activity and, thereby, to create an imbalance of the proportion of amino acids in the rat is implicated in the mechanism responsible for its glyconeogenic property and ability to increase catabolism of amino acids.


2021 ◽  
pp. jeb.234344
Author(s):  
Caroline Cristina-Silva ◽  
Luciane H. Gargaglioni ◽  
Kênia Cardoso Bícego

The brainstem region medullary raphe modulates non-shivering and shivering thermogenesis and cutaneous vasomotion in rodents. Whether the same scenario occurs in the other endothermic group, i.e. birds, is still unknown. Therefore, we hypothesised that the medullary raphe modulates heat gain and loss thermoeffectors in birds. We investigated the effect of glutamatergic and GABAergic inhibitions in this specific region on body temperature (Tb), oxygen consumption (thermogenesis), ventilation (O2 supply in cold, thermal tachypnea in heat) and heat loss index (cutaneous vasomotion) in one-week-old chicken exposed to neutral (31°C), cold (26°C) and heat (36°C) conditions. Intra-medullary raphe antagonism of NMDA glutamate (AP5; 0.5, 5 mM) and GABAA (bicuculline; 0.05, 0.5 mM) receptors reduced Tb of chicks at 31°C and 26oC, due mainly to an O2 consumption decrease. AP5 transiently increased breathing frequency during cold exposure. At 31°C, heat loss index was higher in the bicuculline and AP5 groups (higher doses) than vehicle at the beginning of the Tb reduction. No treatment affected any variable tested at 36oC. The results suggest that glutamatergic and GABAergic excitatory influences on the medullary raphe of chicks modulate thermogenesis and glutamatergic stimulation prevents tachypnea, without having any role in warmth-defence responses. A double excitation influence on the medullary raphe may provide a protective neural mechanism for supporting thermogenesis during early life, when energy expenditure to support growth and homeothermy is high. This novel demonstration of a thermoregulatory role for the raphe in birds suggests a convergent brainstem neurochemical regulation of body temperature in endotherms.


1960 ◽  
Vol 198 (4) ◽  
pp. 718-720 ◽  
Author(s):  
R. J. Girerd ◽  
C. L. Rassaert ◽  
G. DiPasquale ◽  
R. L. Kroc

In the adrenalectomized rat placed on a regular diet, neither ammoniated glycyrrhizin nor licorice was able to prolong survival time beyond that of the controls while desoxycorticosterone acetate (DCA) was very effective. When adrenalectomized rats were maintained on saline, it was observed that only DCA caused significant polydipsia, arterial hypertension and cardiovascular lesions; ammoniated glycyrrhizin and licorice were practically inactive, in contrast to their previously reported activity in the normal rat. The presence of the adrenal glands appears necessary to the renal cardiovascular effects of these extracts and it seems that the observed activity is mediated through these glands and that neither ammoniated glycyrrhizin nor licorice possesses direct DCA-like or mineralocorticoid properties.


1973 ◽  
Vol 52 (6) ◽  
pp. 1265-1267 ◽  
Author(s):  
Halina M. Curbelo ◽  
Alberto B. Houssay ◽  
Carlos H. Gamper ◽  
Ofelia Sancho

Adrenalectomy decreased sialic acid content in the submaxillary and retrolingual glands of normal male rats. The administration of cortisol acetate to adrenalectomized rats increased submaxillary and retrolingual sialic acid content; administration of desoxycorticosterone acetate decreased the submaxillary gland content but not the retrolingual gland content.


1973 ◽  
Vol 74 (3) ◽  
pp. 449-460 ◽  
Author(s):  
Patrick C. Walsh ◽  
Ronald S. Swerdloff ◽  
William D. Odell

ABSTRACT Serum follicle stimulating hormone (FSH) and luteinizing hormone (LH) were measured by radioimmunoassay in a group of elderly men following castration and oestrogen therapy. Prior to orchiectomy, mean serum concentrations of LH and FSH were within the normal range. Two days following castration, serum LH concentrations increased in all eight patients; higher levels of LH were subsequently measured in all but one patient after periods of time ranging from 49 to 210 days. Serum FSH levels, measured in three patients following castration, increased in a pattern parallel to LH changes. Ethinyl oestradiol (EOe) in doses ranging from 5 to 300 μg/day was administered to ten men who had been castrated 3 to 72 months earlier. Oestrogen treatment suppressed both LH and FSH in a parellel manner in nine of ten patients. LH was first suppressed to intact levels in one of eight patients treated with 20 μg/day of EOe, in two of six patients treated with 50 μg/day, and in one patient by 80 μg/day. FSH was not suppressed to precastration levels until 50 μg/day of EOe was administered; this dose suppressed three of six patients. Higher doses of EOe (150–300 μg/day) suppressed both LH and FSH to levels below the sensitivity of the assay. These data fail to demonstrate any differential effect of oestrogen on LH and FSH release.


Author(s):  
Lucas Ravkov ◽  
Bradley Diak ◽  
Mark Gallerneault ◽  
Peter Clark ◽  
Giuseppe Marzano
Keyword(s):  

1998 ◽  
Vol 275 (5) ◽  
pp. R1461-R1467 ◽  
Author(s):  
Tetsuya Ando ◽  
Jean Rivier ◽  
Hitoshi Yanaihara ◽  
Akira Arimura

We previously reported the elevation of plasma interleukin (IL)-6 activity in response to immobilization stress in rats. To investigate the role of peripheral corticotropin-releasing factor (CRF) in this response, we examined the effects of CRF antagonists on immobilization-induced IL-6 response. Intravenous pretreatment with either [d-Phe12,Nle21,38,CαMeLeu37]-anti-human rat (h/r) CRF12—41(1.5 mg/kg) or cyclo(30—33)[d-Phe12, Nle21,38,Glu30,Lys33]-h/rCRF12—41(Astressin, 0.5 mg/kg) attenuated the IL-6 response to immobilization, which confirmed our previous finding that systemic administration of an antiserum against CRF blocked this response. In addition, an intraperitoneal injection of h/rCRF (100 μg/kg) or rat urocortin (10 and 100 μg/kg) increased the plasma IL-6 activity, mimicking the response to immobilization. An intravenous injection of h/rCRF (100 μg/kg) also elevated plasma IL-6 in adrenalectomized rats. These findings suggest that peripheral CRF mediates the plasma IL-6 elevation in response to immobilization.


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