Effect of cerebrospinal fluid hyperosmolality on sweating in the heat-stressed patas monkey

1989 ◽  
Vol 67 (1) ◽  
pp. 128-133 ◽  
Author(s):  
M. D. Owen ◽  
R. D. Matthes ◽  
C. V. Gisolfi
Keyword(s):  
Cerebrospinal Fluid ◽  
Rectal Temperature ◽  
Sweat Rate ◽  
Recovery Period ◽  
Erythrocebus Patas ◽  
Artificial Cerebrospinal Fluid ◽  
Skin Temperatures ◽  
Central Stimulation ◽  
Osmotic Stimuli

Dehydration increases the osmolality of body fluids and decreases the rate of sweating during thermal stress. By localizing osmotic stimuli to central nervous system tissues, this study assessed the role of central stimulation on sweating in a heat-stressed nonhuman primate. Lenperone-tranquilized patas monkeys (Erythrocebus patas n = 5), exposed to 41 +/- 2 degrees C, were monitored for calf sweat rate, rectal and mean skin temperatures, oxygen consumption, and heart rate during infusions (255–413 microliters) of hypertonic artificial cerebrospinal fluid (ACSF) into the third cerebral ventricle. ACSF made hypertonic with NaCl to yield osmolalities of 800 and 1,000 mosmol/kgH2O significantly decreased sweat rate compared with control ACSF (285 mosmol/kgH2O), achieving maximal reductions during infusion of 37 and 53%, respectively. Rectal temperature significantly increased during the recovery period, reaching elevations of 0.69 and 0.72 degrees C, respectively, at 20 min postinfusion. In contrast, ACSF made hypertonic with sucrose (800 mosmol/kgH2O) failed to change sweat rate or rectal temperature during infusion in three animals. Thus, intracerebroventricular infusions of hypertonic ACSF mimicked dehydration-induced effects on thermoregulation. The reduction in heat loss during infusion appeared to depend on an elevation in cerebrospinal fluid [Na+] and not osmolality per se.

Effects of CSF ANG II and AVP on sweating in the heat-stressed patas monkey

1989 ◽  
Vol 67 (1) ◽  
pp. 134-140 ◽  
Author(s):  
M. D. Owen ◽  
R. D. Matthes ◽  
C. V. Gisolfi
Keyword(s):  
Cerebrospinal Fluid ◽  
Rectal Temperature ◽  
Time Course ◽  
Potential Role ◽  
Sweat Rate ◽  
Ang Ii ◽  
Erythrocebus Patas ◽  
Patas Monkey ◽  
Artificial Cerebrospinal Fluid

Increasing cerebrospinal fluid [Na+] reduces sweat rate (msw) in the heat-stressed patas monkey (Erythrocebus patas). This study determined the potential role of two neuropeptides, angiotensin II (ANG II) and arginine vasopressin (AVP), in mediating this response. Artificial cerebrospinal fluid, containing either ANG II or AVP, was infused into the third cerebral ventricle of lenperone-tranquilized monkeys (n = 4) exposed to 41 +/- 2 degrees C. Solutions were infused at 16.5 microliters/min for 25 min (total vol approximately 413 microliters). ANG II (1.25, 2.5, 5, and 10 ng/microliters) tended to decrease .msw. However, during infusion, only the decline at 10 min associated with the 1.25-ng/microliters dose (26%) was different (P less than 0.004) from control. This dose elevated (P less than 0.004) core rectal temperature by 1.14 degrees C at 20 min postinfusion. In contrast, AVP (0.5 and 1.5 micrograms/microliters artificial cerebrospinal fluid) had no significant effect on .msw compared with control infusions. Both doses of AVP produced a slight but significant increase in rectal temperature of 0.14 and 0.22 degrees C, respectively, at 20 min postinfusion. In conclusion, the magnitude and time course of the change in .msw with central ANG II suggest that it does not act as the sole mediator of the decline in .msw observed with elevated cerebrospinal fluid [Na+]. The minimal effects produced by third ventricular AVP exclude this route as a means by which AVP could modulate .msw during dehydration.

PVN lesions prevent the endothelin 1-induced increase in arterial pressure and vasopressin

2001 ◽  
Vol 280 (2) ◽  
pp. E349-E356 ◽  
Author(s):  
Noreen F. Rossi ◽  
Haiping Chen
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Arterial Pressure ◽  
Paraventricular Nuclei ◽  
Artificial Cerebrospinal Fluid ◽  
Electrolytic Lesions ◽  
The Central Nervous System ◽  
Baseline Values ◽  
Long Evans

Endothelin (ET) acts within the central nervous system to increase arterial pressure and arginine vasopressin (AVP) secretion. This study assessed the role of the paraventricular nuclei (PVN) in these actions. Intracerebroventricular ET-1 (10 pmol) or the ETA antagonist BQ-123 (40 nmol) was administered in conscious intact or sinoaortic-denervated (SAD) Long-Evans rats with sham or bilateral electrolytic lesions of the magnocellular region of the PVN. Baseline values did not differ among groups, and artificial cerebrospinal fluid (CSF) induced no significant changes. In sham-lesioned rats, ET-1 increased mean arterial pressure (MAP) 15.9 ± 1.3 mmHg in intact and 22.3 ± 2.7 mmHg in SAD ( P < 0.001 ET-1 vs. CSF) rats. PVN lesions abolished the rise in MAP: −0.1 ± 2.8 mmHg in intact and 0.0 ± 2.9 mmHg in SAD. AVP increased in only in the sham-lesioned SAD group 8.6 ± 3.5 pg/ml ( P < 0.001 ET-1 vs. CSF). BQ-123 blocked the responses. Thus the integrity of the PVN is required for intracerebroventricularly administered ET-1 to exert pressor and AVP secretory effects.

Role of skin and of core temperatures in man's temperature regulation

1965 ◽  
Vol 20 (1) ◽  
pp. 31-36 ◽  
Author(s):  
C. H. Wyndham
Keyword(s):  
Skin Temperature ◽  
Rectal Temperature ◽  
Temperature Regulation ◽  
Passive Control ◽  
Sweat Rate ◽  
Heat Conductance ◽  
Response Characteristics ◽  
Highly Nonlinear ◽  
The Right ◽  
Skin Temperatures

The response characteristics have been studied of the curves relating heat conductance and sweat rate to change in rectal temperature at different levels of skin temperature, and vice versa. The increase in these responses with deviation in rectal temperature from the “neutral” setting is highly nonlinear; the neutral point and the curve shift to the right and the slope decreases with lowering of skin temperature and vice versa when it is raised. With further deviation of rectal temperature these responses reach maximum values, i.e., become “saturated.” All of these features are analogous to servomechanisms with negative feedback, giving sensitive and stable control. Control of these responses by skin temperature is more linear, characterizing passive control systems which are insensitive and less stable. Quantitatively, the effect at skin temperature of 26 C of 1 C rise in rectal temperature on heat conductance and sweat rate is 10 times greater than the same rise in skin temperature; at a neutral skin temperature of 33–34 C, a rise of 1 C in rectal temperature is 6–7 times greater; at a high skin temperature of 36 C, a rise in rectal temperature of 1 C is 4–5 times greater. relationship between heat conductance and a change in either rectal or skin temperatures; relationship between sweat rate and a change in either rectal or skin temperatures; response characteristics of curves relating heat conductance to change in either rectal or skin temperatures; response characteristics of curves relating sweat rate to change in either rectal or skin temperatures; assessment of the contribution of skin and rectal temperatures to man's temperature regulation Submitted on October 22, 1963

scholarly journals TRH microdialysis into the RTN of the conscious rat increases breathing, metabolism, and temperature

1999 ◽  
Vol 87 (2) ◽  
pp. 673-682 ◽  
Author(s):  
Carlos Cream ◽  
Eugene Nattie ◽  
Aihua Li
Keyword(s):  
Cerebrospinal Fluid ◽  
Rectal Temperature ◽  
Random Order ◽  
Conscious Rat ◽  
Tissue Volume ◽  
Retrotrapezoid Nucleus ◽  
Sustained Effects ◽  
Artificial Cerebrospinal Fluid ◽  
E 32 ◽  
Stimulation Of

Thyrotropin-releasing hormone (TRH) injected into the retrotrapezoid nucleus (RTN) of anesthetized rats produces a large, prolonged stimulation of ventilatory output (C. L. Cream, A. Li, and E. E. Nattie. J. Appl. Physiol. 83: 792–799, 1997). Here we inject or dialyze TRH into the RTN of conscious rats. In 6 of 17 injections (200 nl, 3.1 ± 1.7 mM), ventilation (V˙e) increased 31% by 10 min, with recovery by 60 min. With dialysis, each animal of one group ( n = 5) received, in random order, 10 mM TRH, 10 mM TRHOH (a metabolite of TRH), and artificial cerebrospinal fluid (aCSF); each animal of a second group ( n = 5) received aCSF and 1 mM TRH. TRHOH and aCSF had no sustained effects. TRH (1 mM) increasedV˙e (32%, P < 0.02, by 10 min, with recovery by 60 min), O2 consumption (V˙o 2; 19%, P < 0.03), and body (rectal) temperature (Tre; 0.5°C, P < 0.09). TRH (10 mM) increasedV˙e (78%, P < 0.01, by 10 min, with no recovery at 60 min), V˙o 2(48%, P < 0.01), and Tre (1.0°C, P < 0.01). TRH also induced arousal. The tissue volume affected in dialysis, estimated by spread of dialyzed fluorescein (332.3 mol wt, mol wt of TRH = 362.4), was 1,580 ± 256 nl for 10 mM ( n = 5) and 590 ± 128 nl for 1 mM ( n = 5). We conclude that 1) the RTN is involved in the integration ofV˙e,V˙o 2, Tre, and arousal and 2) TRH may establish the responsiveness of RTN neurons.

Observations on the effect of salicylate in fever and the regulation of body temperature against cold

1976 ◽  
Vol 54 (2) ◽  
pp. 101-106 ◽  
Author(s):  
Q. J. Pittman ◽  
W. L. Veale ◽  
K. E. Cooper
Keyword(s):  
Body Temperature ◽  
Skin Temperature ◽  
Rectal Temperature ◽  
Heat Production ◽  
Intravenous Infusion ◽  
Sodium Salicylate ◽  
Single Injection ◽  
Continuous Intravenous Infusion ◽  
Skin Temperatures

Prostaglandins appear to be mediators, within the hypothalamus, of heat production and conservation during fever. We have investigated a possible role of prostaglandins in the nonfebrile rabbit during thermoregulation in the cold. Shorn rabbits were placed in an environment of 20 °C, and rectal and ear skin temperatures, shivering and respiratory rates were measured. A continuous intravenous infusion of leucocyte pyrogen was given to establish a constant fever of approximately 1 °C, and after observation of a stable febrile temperature for 90 min, a single injection of 300 mg of sodium salicylate, followed by a 1.5 mg/min infusion was then given. After the salicylate infusion was begun, rectal temperature began to fall, and reached nonfebrile levels within 90 min. Shivering activity ceased, respiratory rates increased, and in two animals, ear skin temperature increased. When these same rabbits were placed in an environment of 10 °C, at a time they were not febrile, and an identical amount of salicylate was given, rectal and ear skin temperatures, shivering and respiratory rates did not change. These results indicate that prostaglandins do not appear to be involved in heat production and conservation in the nonfebrile rabbit.

scholarly journals Noradrenergic control of central oxytocin release during lactation in rats

1998 ◽  
Vol 274 (3) ◽  
pp. E453-E458 ◽  
Author(s):  
Steven L. Bealer ◽  
William R. Crowley
Keyword(s):  
Cerebrospinal Fluid ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Additional Experiment ◽  
Adrenergic Agonist ◽  
Magnocellular Nuclei ◽  
Artificial Cerebrospinal Fluid ◽  
Oxytocin Release ◽  
Stimulation Of

Noradrenergic systems regulate the systemic release of oxytocin (OT) in lactating rats. However, a role for norepinephrine (NE) in release of OT within the magnocellular nuclei during suckling has not been established. These studies were designed to determine 1) if suckling induces NE release in the supraoptic (SON) and paraventricular (PVN) nuclei of conscious rats and 2) the role of NE in the central, intranuclear release of OT within these nuclei. Female Holtzman rats were implanted with microdialysis probes adjacent to the PVN or SON on lactation days 8- 12. The following day, the pups were isolated from the dams for 4 h. Microdialysis probes were perfused with artificial cerebrospinal fluid (ACSF) or with ACSF containing an α- or a β-adrenergic receptor antagonist. Dialysate was collected before, during, and after suckling and analyzed for NE or OT. In an additional experiment, an α- or β-adrenergic agonist was administered via the microdialysis probes into the PVN in nonsuckled, lactating rats. Extracellular NE increased in the PVN during suckling but was not detectable in the SON. OT concentrations in dialysates from the PVN and SON significantly increased during suckling. Blockade of either α- (in both PVN and SON) or β- (PVN) adrenergic receptors prevented the suckling-induced increase in central OT release. OT release was increased in nonsuckled, lactating rats by central application of either an α- or β-adrenergic agonist. These data demonstrate that intranuclear NE release is increased in the PVN by suckling and that subsequent stimulation of both α- and β-noradrenergic receptors mediates intranuclear OT release.

Microinjection of a cyclooxygenase inhibitor into the anteroventral preoptic region attenuates LPS fever

1998 ◽  
Vol 274 (3) ◽  
pp. R783-R789 ◽  
Author(s):  
Thomas E. Scammell ◽  
John D. Griffin ◽  
Joel K. Elmquist ◽  
Clifford B. Saper
Keyword(s):  
Cerebrospinal Fluid ◽  
Body Temperature ◽  
Preoptic Area ◽  
Prostaglandin Synthesis ◽  
Cyclooxygenase Inhibitor ◽  
Preoptic Region ◽  
Considerable Evidence ◽  
Artificial Cerebrospinal Fluid ◽  
Intravenous Ketorolac

Considerable evidence supports the role of prostaglandins in fever production, but the neuroanatomic sites of prostaglandin synthesis that produce fever remain unknown. With the use of a novel microinjection technique, we injected the cyclooxygenase inhibitor ketorolac into the preoptic area (POA) to determine which preoptic regions produce the prostaglandins required for fever. Initial experiments demonstrated that intravenous ketorolac blocked the fever normally produced by lipopolysaccharide (LPS) 5 μg/kg iv. Microinjection of ketorolac into the POA had no effect on body temperature, and injection of artificial cerebrospinal fluid into the POA did not alter LPS fever. Injection of ketorolac into the anteroventral POA markedly decreased the fever produced by LPS, compared with injections into more rostral, caudal, or dorsal locations. These observations indicate that prostaglandin synthesis in the anteroventral preoptic region is necessary for the production of fever.

Effects of salicylate on acclimatization to work in the heat

1965 ◽  
Vol 20 (1) ◽  
pp. 70-72 ◽  
Author(s):  
David E. Bass ◽  
Eugene D. Jacobson
Keyword(s):  
Rectal Temperature ◽  
Sodium Salicylate ◽  
Sweat Rate ◽  
Drug Regimen ◽  
Control Group ◽  
Heat Acclimatization ◽  
Acute Response ◽  
Hot Environments ◽  
Qualitative Responses ◽  
Skin Temperatures

Some effects of daily large doses of sodium salicylate were studied on the pattern of acclimatization to work in the heat. Acclimatization was induced by daily walks of 100 min on a level treadmill at 3.5 mph at 120/80 F (dry bulb/wet bulb). Two matched groups of six men each were acclimatized in this manner and one group received 5.9–7.8 g of sodium salicylate daily over a period of 10 days. Men treated with salicylate exhibited the same qualitative responses as the control group in terms of the acclimatization process, i.e., their rectal temperatures, skin temperatures, and pulse rates during work in the heat were lower on the later days. Quantitatively, the degree of acclimatization (as measured by rectal temperature) was less in the men receiving salicylate than in the control group. This difference was more apparent than real, however, in that when the salicylate group were taken off the drug regimen, they exhibited the same degree of acclimatization in terms of rectal temperature as did the control group. The acclimatization process did not abolish the acute response to salicylate. body temperature regulation; exercise; simulated desert environment; simulated jungle environment; hyperthermia; rectal temperature, skin temperature, sweat rate, and pulse rate in hot environments; antipyretics Submitted on June 15, 1964

Febrile nonresponsiveness of vagotomized animals: is it due to endotoxin translocation from the gut and tolerance?

1998 ◽  
Vol 275 (3) ◽  
pp. R933-R935 ◽  
Author(s):  
Andrej A. Romanovsky
Keyword(s):  
Cerebrospinal Fluid ◽  
Preoptic Area ◽  
Prostaglandin Synthesis ◽  
Cyclooxygenase Inhibitor ◽  
Preoptic Region ◽  
Considerable Evidence ◽  
Artificial Cerebrospinal Fluid ◽  
Endotoxin Translocation ◽  
Intravenous Ketorolac

The following is the abstract of the article discussed in the subsequent letter: Scammell, Thomas E., John D. Griffin, Joel K. Elmquist, and Clifford B. Saper. Microinjection of a cyclooxygenase inhibitor into the anteroventral preoptic region attenuates LPS fever. Am. J. Physiol.274 ( Regulatory Integrative Comp. Physiol. 43): R933–R935, 1998.—Considerable evidence supports the role of prostaglandins in fever production, but the neuroanatomic sites of prostaglandin synthesis that produce fever remain unknown. With the use of a novel microinjection technique, we injected the cyclooxygenase inhibitor ketorolac into the preoptic area (POA) to determine which preoptic regions produce the prostaglandins required for fever. Initial experiments demonstrated that intravenous ketorolac blocked the fever normally produced by lipopolysaccharide (LPS) 5 μg/kg iv. Microinjection of ketorolac into the POA had no effect on body temperature, and injection of artificial cerebrospinal fluid into the POA did not alter LPS fever. Injection of ketorolac into the anteroventral POA markedly decreased the fever produced by LPS, compared with injections into more rostral, caudal, or dorsal locations. These observations indicate that prostaglandin synthesis in the anteroventral preoptic region is necessary for the production of fever.

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