Sweating in cattle. IV. Control of sweat glands secretion

1959 ◽  
Vol 52 (1) ◽  
pp. 66-71 ◽  
Author(s):  
G. C. Taneja
Keyword(s):  
Nervous System ◽  
Body Temperature ◽  
Sympathetic Nervous System ◽  
Sweat Glands ◽  
Appreciable Effect ◽  
Air Temperatures ◽  
Before And After ◽  
Sympathetic Nervous ◽  
Cutaneous Evaporation ◽  
The University

Two calves (Aberdeen Angus and American Brahman) were used exposed to different combinations of wet- and dry-bulb temperatures in a psychromatric chamber at the Physiology Department of the University of Queensland. These animals were 7–8 months old when first exposed to heat.Effect of various drugs affecting the sympathetic nervous system (adrenaline, noradrenaline, Dibenamine, Priscol, atropine and acetylcholine) on the rate of cutaneous evaporation in calves was tested. Cutaneous evaporation was measured by means of a capsule before and after the administration of these drugs.Cutaneous evaporation increased with the introduction of adrenaline and was suppressed by the administration of Dibenamine. Noradrenaline and Priscol had no appreciable effect. Acetylcholine failed to stimulate sweating and atropine did not block the sweat glands.Sweat glands of cattle were, therefore, found to be functional and their innervation adrenergic. Cattle use sweat to prevent body temperature from rising, yet the amount of sweat secreted is not large enough to allow cattle to maintain thermoneutrality at high air temperatures.

Control of the sympathetic nervous system by TRPV1 in the regulation of body temperature

Neuropeptides ◽  
2017 ◽  
Vol 65 ◽  
pp. 131-132
Author(s):  
Khadija Alawi ◽  
Aisah Aubdool ◽  
Lihuan Liang ◽  
Elena Wilde ◽  
Abhinav Vepa ◽  
...  
Keyword(s):  
Nervous System ◽  
Body Temperature ◽  
Sympathetic Nervous System ◽  
Sympathetic Nervous

scholarly journals Development of temperature regulation in newborn reindeer

Rangifer ◽  
1981 ◽  
Vol 1 (1) ◽  
pp. 29 ◽  
Author(s):  
R. Hissa ◽  
S. Saarela ◽  
M. Nieminen
Keyword(s):  
Nervous System ◽  
Body Temperature ◽  
Sympathetic Nervous System ◽  
Metabolic Rate ◽  
Heat Production ◽  
Temperature Regulation ◽  
Rangifer Tarandus ◽  
Normal Body Temperature ◽  
Newborn Calves ◽  
Sympathetic Nervous

<p>Development of temperature regulation was investigated by determining the ability of newborn reindeer calves (Rangifer tarandus tarandus) to maintain a normal body temperature when exposed to an incrementially decreasing ambient temperature. Newborn calves (1 day old) can maintain their body temperature even at -15 &deg;C. They can increase their metabolic rate five- to sixfold. Heat production is primarily stimulated by the sympathetic nervous system. The response to exogenous administration of noradrenaline and propranolol was investigated.</p><p>Poronvasan l&aring;mmons&aring;&aring;telyn syntym&aring;nj&aring;lkeinen kehittyminen.</p><p>Abstract in Finnish / Yhteenveto: Vastasyntyneiden poronvasojen kylmansietoa ja lammonsaatelya tutkittiin toukokuussa 1981 Inarin Kaamasessa Paliskuntain yhdistyksen koetarhassa. Tutkittavat vasat olivat 1-10 vuorokauden ikaisia. Vasa asetettiin j&aring;&aring;hdytett&aring;va&aring;n mittauskammioon. Sen aineenvaihdunta, lampotilat niin ihon eri kohdista kuin perasuolesta, lihasvarina ja sydanfrekvenssi rekisteroitiin jatkuvasti. Tulosten mukaan naytt&aring;a silt&aring; kuin 1 vuorokauden ikaiselle vasalle -15 &deg;C olisi ehdoton alaraja l&aring;mpotilan s&aring;&aring;telyssa. Se kykeni kohottamaan hapenkulutusta talloin 5-kertaisesti. Lihasvarinan merkitys on vahainen verrattuna kemialliseen l&aring;mmontuottoon kylmassa. Tama voitiin osoittaa injisoimalla vasaan sympaattisen hermoston valittajaainetta noradrenaliinia.</p><p>Temperaturreguleringens utvikling hos nyf&oslash;dte reinkalver.</p><p>Abstract in Norwegian / Sammendrag: Temperaturreguleringens utvikling er studert ved &aring; bestemme nyf&oslash;dte reinkalvers evne til &aring; opprettholde normal kroppstemperatur under p&aring;virkning av gradvis synkende omgivelsestemperatur. Nyf&oslash;dte kalver (1 d&oslash;gn gamle) kan opprettholde sin kroppstemperatur selv ved -15 &deg;C. De kan &oslash;ke sin omsetningshastighet fem til seks ganger. I starten er varmeproduksjonen stimulert av det sympatiske nervesystem. Virkningen av tilf&oslash;rt noradrenalin og propranolol ble studert og skjelving synes &aring; spille bare en mindre rolle umiddelbart etter f&oslash;dselen.</p>

scholarly journals Influences of Lavender Essential Oil Inhalation on Stress Responses during Short-Duration Sleep Cycles: A Pilot Study

Healthcare ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 909
Author(s):  
Wakako Yogi ◽  
Mana Tsukada ◽  
Yosuke Sato ◽  
Takuji Izuno ◽  
Tatsuki Inoue ◽  
...  
Keyword(s):  
Nervous System ◽  
Essential Oil ◽  
Sympathetic Nervous System ◽  
Short Duration ◽  
Stress Responses ◽  
Japanese Version ◽  
Sleep Cycle ◽  
System Response ◽  
Before And After ◽  
Sympathetic Nervous

Lavender essential oil (LEO) was reported to improve sleep quality. We investigated the influence of aromatherapy by testing the effects of LEO on stress responses during a short-duration sleep in a single-blind, randomized, crossover trial. The subjects were twelve healthy adults who were nonsmokers without any known disease and who were not prescribed medications, and nine of these completed the study. After the subjects had fallen asleep, they were sprayed with LEO using an aroma diffuser. Before and after 90 min of sleep, α-amylase, chromogranin A (CgA), and cortisol levels in saliva were measured as objective stress indicators, and the Japanese version of the UWIST Mood Adjective Checklist was used as a subjective indicator. A comparison of changes before and after sleep, with and without LEO, revealed that the cortisol level did not significantly change; however, α-amylase (p < 0.05) and CgA (p < 0.01) levels significantly decreased after LEO inhalation. A mood test indicated no change in mood before and after sleep, with or without LEO. Since α-amylase and CgA reflect the sympathetic nervous system response, these results indicate that LEO aromatherapy during a short-duration sleep cycle suppresses the stress response, especially that of the sympathetic nervous system.

scholarly journals Haematohidrosis with headache- a rare phenomenon of sweating blood: A case report

2019 ◽  
Vol 45 (3) ◽  
pp. 205-207
Author(s):  
Amit Roy Chowdhury ◽  
Mohammed Rafiqul Islam ◽  
Hasan Zahidur Rahman ◽  
Maftahul Jannat ◽  
Md. Habibur Rahman
Keyword(s):  
Nervous System ◽  
Case Report ◽  
Family History ◽  
Sympathetic Nervous System ◽  
Blood Vessels ◽  
Clinical Condition ◽  
Patient Experiences ◽  
Sweat Glands ◽  
Sympathetic Nervous ◽  
Medical University

Background: Haematohidrosis is an extremely rare clinical condition in which the patient experiences sweat mixed with blood. Till date only a few cases of haematohidrosis have been reported in national and international medical journals. Pathogenesis of the condition is not yet established but rupture of the blood vessels of sweat glands due to activation of sympathetic nervous system from stress, anxiety or any other reason have been proposed as the cause of bleeding. Objective: It was aimed to present the case who presented with episodes of sweat mixed with blood from different sites of her body. Methods: A case of haematohidrosis who experiences bloody sweat which comes with episodes of headache, was studied during in Bangabandhu Sheikh Mujib Medical University, Dhaka. Results: Interestingly, it was to be found that a child of the patient, who is a 4 year old boy and a nephew of her, are suffering from the same condition. No family history was found in any of the previous cases. All other history and the investigations were insignificant. It was to be diagnosed the headache as migraine. Conclusion: The patient was treated with propranolol and paracetamol. Her bloody sweat decreased significantly in both severity and frequency with the treatment.

Propofol-induced Increase in Vascular Capacitance Is Due to Inhibition of Sympathetic Vasoconstrictive Activity 

1998 ◽  
Vol 89 (6) ◽  
pp. 1495-1500 ◽  
Author(s):  
Sumio Hoka ◽  
Ken Yamaura ◽  
Tomoaki Takenaka ◽  
Shosuke Takahashi
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Circulatory Arrest ◽  
Bolus Administration ◽  
Block Group ◽  
Intact Group ◽  
Vascular Capacitance ◽  
Before And After ◽  
Sympathetic Nervous ◽  
The Right

Background Venodilation is thought to be one of the mechanisms underlying propofol-induced hypotension. The purpose of this study is to test two hypotheses: (1) propofol increases systemic vascular capacitance, and (2) the capacitance change produced by propofol is a result of an inhibition of sympathetic vasoconstrictor activity. Methods In 33 Wistar rats previously anesthetized with urethane and ketamine, vascular capacitance was examined before and after propofol infusion by measuring mean circulatory filling pressure (Pmcf). The Pmcf was measured during a brief period of circulatory arrest produced by inflating an indwelling balloon in the right atrium. Rats were assigned into four groups: an intact group, a sympathetic nervous system (SNS)-block group produced by hexamethonium infusion, a SNS-block + noradrenaline (NA) group, and a hypovolemic group. The Pmcf was measured at a control state and 2 min after a bolus administration of 2, 10, and 20 mg/kg of propofol. Results The mean arterial pressure (MAP) was decreased by propofol dose-dependently in intact, hypovolemic, and SNS-block groups, but the decrease in MAP was less in the SNS-block group (-25%) than in the intact (-50%) and hypovolemic (-61%) groups. In the SNS-block + NA group, MAP decreased only at 20 mg/kg of propofol (-18%). The Pmcf decreased in intact and hypovolemic groups in a dose-dependent fashion but was unchanged in the SNS-block and SNS-block + NA groups. Conclusions The results have provided two principal findings: (1) propofol decreases Pmcf dose-dependently, and (2) the decrease in Pmcf by propofol is elicited only when the sympathetic nervous system is intact, suggesting that propofol increases systemic vascular capacitance as a result of an inhibition of sympathetic nervous system.

scholarly journals Catecholamines are key modulators of ventricular repolarization patterns in the ball python (Python regius)

2021 ◽  
Vol 154 (2) ◽  
Author(s):  
Bastiaan J.D. Boukens ◽  
William Joyce ◽  
Ditte Lind Kristensen ◽  
Ingeborg Hooijkaas ◽  
Aldo Jongejan ◽  
...  
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Body Temperature ◽  
Sympathetic Nervous System ◽  
Ventricular Repolarization ◽  
Perfused Heart ◽  
Python Regius ◽  
T Wave ◽  
Wave Inversion ◽  
Sympathetic Nervous

Ectothermic vertebrates experience daily changes in body temperature, and anecdotal observations suggest these changes affect ventricular repolarization such that the T-wave in the ECG changes polarity. Mammals, in contrast, can maintain stable body temperatures, and their ventricular repolarization is strongly modulated by changes in heart rate and by sympathetic nervous system activity. The aim of this study was to assess the role of body temperature, heart rate, and circulating catecholamines on local repolarization gradients in the ectothermic ball python (Python regius). We recorded body-surface electrocardiograms and performed open-chest high-resolution epicardial mapping while increasing body temperature in five pythons, in all of which there was a change in T-wave polarity. However, the vector of repolarization differed between individuals, and only a subset of leads revealed T-wave polarity change. RNA sequencing revealed regional differences related to adrenergic signaling. In one denervated and Ringer’s solution–perfused heart, heating and elevated heart rates did not induce change in T-wave polarity, whereas noradrenaline did. Accordingly, electrocardiograms in eight awake pythons receiving intra-arterial infusion of the β-adrenergic receptor agonists adrenaline and isoproterenol revealed T-wave inversion in most individuals. Conversely, blocking the β-adrenergic receptors using propranolol prevented T-wave change during heating. Our findings indicate that changes in ventricular repolarization in ball pythons are caused by increased tone of the sympathetic nervous system, not by changes in temperature. Therefore, ventricular repolarization in both pythons and mammals is modulated by evolutionary conserved mechanisms involving catecholaminergic stimulation.

Increased brown adipose tissue thermogenesis in obese (ob/ob) mice fed a palatable diet

1986 ◽  
Vol 250 (3) ◽  
pp. E274-E281 ◽  
Author(s):  
J. Himms-Hagen ◽  
S. Hogan ◽  
G. Zaror-Behrens
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Body Temperature ◽  
Sympathetic Nervous System ◽  
Brown Adipose Tissue ◽  
Cafeteria Diet ◽  
Sympathetic Nervous System Activity ◽  
Nervous System Activity ◽  
Brown Adipose ◽  
Sympathetic Nervous

Feeding female genetically obese (ob/ob) mice a palatable "cafeteria" diet results in increased sympathetic nervous system activity in brown adipose tissue and hypertrophy and increased thermogenesis of this tissue. There is an associated increase in the capacity of the ob/ob mouse to respond thermogenically to noradrenaline, prolongation of its survival in the cold, and an increase in body temperature at all times of day. Thus the cafeteria diet overcomes the usual refractoriness of brown adipose tissue of the ob/ob mouse to noradrenaline and to sympathetic stimulation, increases the low capacity for a thermogenic response to noradrenaline, almost normalizes resistance to cold, and increases the "set point" at which the ob/ob mouse regulates its body temperature. It is concluded that the repetitive sympathetic nervous stimulation engendered by the high-fat cafeteria diet has a trophic action on brown adipose tissue that improves its atrophied functional state and that the low sympathetic nervous system activity usually seen in brown adipose tissue of ob/ob mice eating chow under animal house conditions results in secondary atrophy of the tissue. The results point to a central location for the defect in the ob/ob mouse, perhaps in the control of the sympathetic nervous system in relation to diet availability and composition and to environmental temperature.

Separation of peripheral and central cardiovascular actions of angiotensin II

1997 ◽  
Vol 273 (6) ◽  
pp. H2620-H2626 ◽  
Author(s):  
Jaspal S. Kooner ◽  
Clive N. May ◽  
Stanley Peart ◽  
Christopher J. Mathias
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Angiotensin Ii ◽  
Sympathetic Nervous System ◽  
Plasma Norepinephrine ◽  
Ang Ii ◽  
Vascular Effects ◽  
Before And After ◽  
Sympathetic Nervous ◽  
Conscious Rabbits

The pressor and vasoconstrictor action of angiotensin II (ANG II) is considered to be caused by a combination of its direct and indirect vascular effects, the latter mediated by the sympathetic nervous system. The purpose of this study was to determine the extent to which the direct and indirect actions of ANG II contribute to its pressor and vascular effects. Blood pressure, cutaneous vascular, and plasma norepinephrine responses to intravenous ANG II were measured in conscious rabbits before and after inhibition of central sympathetic outflow with intravenous and intracisternal clonidine and after ganglionic blockade with intravenous pentolinium. Intravenous ANG II caused a similar dose-related rise in blood pressure before and after sympathetic blockade with intravenous clonidine, intracisternal clonidine, and intravenous pentolinium. In contrast, the dose-related fall in cutaneous ear blood flow and cutaneous ear temperature and rise in cutaneous ear vascular resistance induced by intravenous ANG II were abolished after intravenous clonidine, intracisternal clonidine, and intravenous pentolinium. Heart rate was unchanged after ANG II. There were no changes in back skin or rectal temperature. There was a nonsignificant fall in plasma norepinephrine and no change in epinephrine after ANG II. These results demonstrate that the acute pressor response to intravenous ANG II is mediated by its direct vascular effects and is not dependent on central or ganglionic stimulation of the sympathetic nervous system, in contrast to the effect of ANG II on cutaneous ear vasoconstriction, which is predominantly caused by a centrally mediated increase in sympathetic nervous activity. Our results separate, in conscious rabbits, the direct vascular effects of ANG II from its indirect vascular actions, which are mediated by central sympathetic stimulation in the brain.

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