The thermoregulatory mechanism of melatonin-induced hypothermia in chicken

1998 ◽  
Vol 274 (1) ◽  
pp. R232-R236 ◽  
Author(s):  
I. Rozenboim ◽  
L. Miara ◽  
D. Wolfenson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Body Temperature ◽  
Heat Losses ◽  
Induced Hypothermia ◽  
White Leghorn ◽  
Evaporative Water ◽  
Dose Dependent ◽  
Respiratory Evaporation

The involvement of melatonin (Mel) in body temperature (Tb) regulation was studied in White Leghorn layers. In experiment 1, 35 hens were injected intraperitoneally with seven doses of Mel (0, 5, 10, 20, 40, 80, or 160 mg Mel/kg body wt) dissolved in ethanol. Within 1 h, Mel had caused a dose-dependent reduction in Tb. To eliminate a possible vehicle effect, 0, 80, and 160 mg/kg body wt Mel dissolved in N-methyl-2-pyrrolidone (NMP) was injected. NMP had no effect on Tb, with Mel again causing a dose-dependent hypothermia. In experiment 2 ( n= 30), Mel injected before exposure of layers to heat reduced Tb and prevented heat-induced hyperthermia. Injection after heat stress had begun did not prevent hyperthermia. Under cold stress, Mel induced hypothermia, which was not observed in controls. In experiment 3 ( n= 12), Mel injection reduced Tband increased metatarsal and comb temperatures (but not feathered-skin temperature), respiratory rate, and evaporative water loss. Heart rate rose and then declined, and blood pressure increased 1 h after Mel injection. Heat production rose slightly during the first hour, then decreased in parallel to the Tbdecline. We conclude that pharmacological doses of Mel induce hypothermia in hens by increasing nonevaporative skin heat losses and slightly increasing respiratory evaporation.

scholarly journals Heat Stress and Cardiovascular, Hormonal, and Heat Shock Proteins in Humans

2012 ◽  
Vol 47 (2) ◽  
pp. 184-190 ◽  
Author(s):  
Masaki Iguchi ◽  
Andrew E. Littmann ◽  
Shuo-Hsiu Chang ◽  
Lydia A. Wester ◽  
Jane S. Knipper ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Heat Shock ◽  
Body Temperature ◽  
Controlled Trial ◽  
Whole Body ◽  
Cord Injury ◽  
Whole Body Heat Stress ◽  
Body Heat

Context: Conditions such as osteoarthritis, obesity, and spinal cord injury limit the ability of patients to exercise, preventing them from experiencing many well-documented physiologic stressors. Recent evidence indicates that some of these stressors might derive from exercise-induced body temperature increases. Objective: To determine whether whole-body heat stress without exercise triggers cardiovascular, hormonal, and extra-cellular protein responses of exercise. Design: Randomized controlled trial. Setting: University research laboratory. Patients or Other Participants: Twenty-five young, healthy adults (13 men, 12 women; age = 22.1 ± 2.4 years, height = 175.2 ± 11.6 cm, mass = 69.4 ± 14.8 kg, body mass index = 22.6 ± 4.0) volunteered. Intervention(s): Participants sat in a heat stress chamber with heat (73°C) and without heat (26°C) stress for 30 minutes on separate days. We obtained blood samples from a subset of 13 participants (7 men, 6 women) before and after exposure to heat stress. Main Outcome Measure(s): Extracellular heat shock protein (HSP72) and catecholamine plasma concentration, heart rate, blood pressure, and heat perception. Results: After 30 minutes of heat stress, body temperature measured via rectal sensor increased by 0.8°C. Heart rate increased linearly to 131.4 ± 22.4 beats per minute (F6,24 = 186, P < .001) and systolic and diastolic blood pressure decreased by 16 mm Hg (F6,24 = 10.1, P < .001) and 5 mm Hg (F6,24 = 5.4, P < .001), respectively. Norepinephrine (F1,12 = 12.1, P = .004) and prolactin (F1,12 = 30.2, P < .001) increased in the plasma (58% and 285%, respectively) (P < .05). The HSP72 (F1,12 = 44.7, P < .001) level increased with heat stress by 48.7% ± 53.9%. No cardiovascular or blood variables showed changes during the control trials (quiet sitting in the heat chamber with no heat stress), resulting in differences between heat and control trials. Conclusions: We found that whole-body heat stress triggers some of the physiologic responses observed with exercise. Future studies are necessary to investigate whether carefully prescribed heat stress constitutes a method to augment or supplement exercise.

scholarly journals Heat Stress, Physiological Response, and Heat-Related Symptoms among Thai Sugarcane Workers

2020 ◽  
Vol 17 (17) ◽  
pp. 6363
Author(s):  
Pongsit Boonruksa ◽  
Thatkhwan Maturachon ◽  
Pornpimol Kongtip ◽  
Susan Woskie
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Body Temperature ◽  
Health Effects ◽  
Heat Strain ◽  
Control Measures ◽  
Muscle Cramp ◽  
Factory Workers ◽  
Limit Values

Prolonged or intense exposure to heat can lead to a range of health effects. This study investigated heat exposure and heat-related symptoms which sugarcane workers (90 sugarcane cutters and 93 factory workers) experienced during a harvesting season in Thailand. During the hottest month of harvesting season, wet bulb globe temperature was collected in the work environment, and workloads observed, to assess heat stress. Urine samples for dehydration test, blood pressure, heart rate, and body temperature were measured pre- and post-shift to measure heat strain. Fluid intake and heat-related symptoms which subjects had experienced during the harvesting season were gathered via interviews at the end of the season. From the results, sugarcane cutters showed high risk for heat stress and strain, unlike factory workers who had low risk based on the American Conference of Governmental Industrial Hygiene (ACGIH) threshold limit values (TLVs) for heat stress. Dehydration was observed among sugarcane cutters and significant physiological changes including heart rate, body temperature, and systolic blood pressure occurred across the work shift. Significantly more sugarcane cutters reported experiencing heat-related symptoms including weakness/fatigue, heavy sweating, headache, rash, muscle cramp, dry mouth, dizziness, fever, dry/cracking skin, and swelling, compared to sugarcane factory workers. We conclude that the heat stress experienced by sugarcane cutters working in extremely hot environments, with high workloads, is associated with acute health effects. Preventive and control measures for heat stress are needed to reduce the risk of heat strain.

Effects of Reserpine on the Fowl

1958 ◽  
Vol 194 (1) ◽  
pp. 184-186 ◽  
Author(s):  
Paul D. Sturkie ◽  
Wayne K. Durfee ◽  
Mary Sheahan
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Body Temperature ◽  
Heart Rate Response ◽  
Assay Method ◽  
White Leghorn ◽  
Body Temperatures ◽  
Significant Drop ◽  
General Behavior ◽  
Intramuscular Injections

The effects of intramuscular injections of reserpine (Serpasil) on blood pressure, heart rate, body temperature and general behavior were determined on adult white leghorn capons 4 hours, and up to 24 hours after injection. The dosages used ranged from 0.006 to 0.75 mg/kg. Dosages from 0.006 upwards caused a significant drop in blood pressure, but the extent of drop was not appreciable at the lower doses. Doses from 0.01 to 0.75 significantly depressed heart rate, and the effects were greater and more consistent than for blood pressure. The changes in blood pressure and heart rate with log-dose were linear, but the heart rate response exhibited a closer fit to linearity. Moreover, the results suggest that heart rate response is an efficient assay method for reserpine-containing compounds. Dosages up to 0.10 mg/kg had no effect on body temperature but above this level body temperatures were depressed significantly. The tranquilizing dose for capons is between 0.10 and 0.2 mg/kg.

“On-” and “off-” cells in the rostral ventromedial medulla of rats held in thermoneutral conditions: are they involved in thermoregulation?

2014 ◽  
Vol 112 (9) ◽  
pp. 2199-2217 ◽  
Author(s):  
Nabil El Bitar ◽  
Bernard Pollin ◽  
Daniel Le Bars
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Body Temperature ◽  
Core Body Temperature ◽  
Rostral Ventromedial Medulla ◽  
Sequence Of Events ◽  
Ventromedial Medulla ◽  
Cyclic Variations ◽  
On And Off Cells ◽  
Core Body

In thermal neutral condition, rats display cyclic variations of the vasomotion of the tail and paws, synchronized with fluctuations of blood pressure, heart rate, and core body temperature. “On-” and “off-” cells located in the rostral ventromedial medulla, a cerebral structure implicated in somatic sympathetic drive, 1) exhibit similar spontaneous cyclic activities in antiphase and 2) are activated and inhibited by thermal nociceptive stimuli, respectively. We aimed at evaluating the implication of such neurons in autonomic regulation by establishing correlations between their firing and blood pressure, heart rate, and skin and core body temperature variations. When, during a cycle, a relative high core body temperature was reached, the on-cells were activated and within half a minute, the off-cells and blood pressure were depressed, followed by heart rate depression within a further minute; vasodilatation of the tail followed invariably within ∼3 min, often completed with vasodilatation of hind paws. The outcome was an increased heat loss that lessened the core body temperature. When the decrease of core body temperature achieved a few tenths of degrees, sympathetic activation switches off and converse variations occurred, providing cycles of three to seven periods/h. On- and off-cell activities were correlated with inhibition and activation of the sympathetic system, respectively. The temporal sequence of events was as follows: core body temperature → on-cell → off-cell ∼ blood pressure → heart rate → skin temperature → core body temperature. The function of on- and off-cells in nociception should be reexamined, taking into account their correlation with autonomic regulations.

SKULL METASTASES OF FOLLICULAR CARCINOMA THYROID: A RARE CASE REPORT

2021 ◽  
pp. 24-25
Author(s):  
Smriti Kumari ◽  
Manoj Kumar Paswan ◽  
Nishat Ahamad
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Case Report ◽  
Body Temperature ◽  
Thyroid Gland ◽  
Basal Metabolic Rate ◽  
Rare Case ◽  
Follicular Carcinoma ◽  
Rare Case Report ◽  
Follicular Carcinoma Thyroid

The thyroid gland, usually located below and anterior to the larynx, consists of two bulky lateral lobes connected by a relatively thin isthmus. The thyroid is divided by thin brous septae into lobules composed of about 20 to 40 evenly dispersed follicles, lined by a cuboidal to low columnar [1] epithelium, and lled with PAS-positive thyroglobulin. The thyroid secretes hormones that control the heart rate, blood pressure, body temperature and basal metabolic rate

scholarly journals Heat stress alters hemodynamic responses during the Valsalva maneuver

2010 ◽  
Vol 108 (6) ◽  
pp. 1591-1594 ◽  
Author(s):  
Scott L. Davis ◽  
Craig G. Crandall
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heat Stress ◽  
Phase Ii ◽  
Valsalva Maneuver ◽  
Late Phase ◽  
Thermal Conditions ◽  
Whole Body ◽  
Hemodynamic Responses ◽  
Arterial Blood

The Valsalva maneuver can be used as a noninvasive index of autonomic control of blood pressure and heart rate. The purpose of this investigation was to test the hypothesis that sympathetic mediated vasoconstriction, as referenced by hemodynamic responses during late phase II (phase IIb) of the Valsalva maneuver, is inhibited during whole body heating. Seven individuals (5 men, 2 women) performed three Valsalva maneuvers (each at a 30-mmHg expiratory pressure for 15 s) during normothermia and again during whole body heating (increase sublingual temperature ∼0.8°C via water-perfused suit). Each Valsalva maneuver was separated by a minimum of 5 min. Beat-to-beat mean arterial blood pressure (MAP) and heart rate were measured during each Valsalva maneuver, and responses for each phase were averaged across the three Valsalva maneuvers for both thermal conditions. Baseline MAP was not significantly different between normothermic (88 ± 11 mmHg) and heat stress (84 ± 9 mmHg) conditions. The change in MAP (ΔMAP) relative to pre-Valsalva MAP during phases IIa and IIb was significantly lower during heat stress (IIa = −20 ± 8 mmHg; IIb = −13 ± 7 mmHg) compared with normothermia (IIa = −1 ± 15 mmHg; IIb = 3 ± 13 mmHg). ΔMAP from pre-Valsalva baseline during phase IV was significantly higher during heat stress (25 ± 10 mmHg) compared with normothermia (8 ± 9 mmHg). Counter to the proposed hypothesis, the increase in MAP from the end of phase IIa to the end of phase IIb during heat stress was not attenuated. Conversely, this increase in MAP tended to be greater during heat stress relative to normothermia ( P = 0.06), suggesting that sympathetic activation may be elevated during this phase of the Valsalva while heat stressed. These data show that heat stress does not attenuate this index of vasoconstrictor responsiveness during the Valsalva maneuver.

Measurement of sympathetic nerve activity in the unanesthetized rat

1989 ◽  
Vol 67 (1) ◽  
pp. 250-255 ◽  
Author(s):  
J. P. Fluckiger ◽  
G. Gremaud ◽  
B. Waeber ◽  
A. Kulik ◽  
A. Ichino ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Blood Pressure Reduction ◽  
Response Curves ◽  
Nerve Activity ◽  
Dose Dependent

A new system was developed in our laboratory to continuously monitor intra-arterial pressure, heart rate, and sympathetic nerve activity in unanesthetized rats. The animals were prepared 24 h before the start of the experiments. Sympathoneural traffic was measured at the level of splanchnic nerve. The amplitude of the spikes recorded at this level was utilized to express sympathetic nerve activity. The amplitude of the residual electroneurogram signal present 30 min after the rats were killed was 32 +/- 2 mV (mean +/- SE; n = 11). For analysis, these background values were subtracted from values determined in vivo. The nerve we studied contains postganglionic fibers, since electrical activity decreased in response to ganglionic blockade with pentolinium (1.25 mg/min iv for 4 min). The amplitude of spikes fell by 43 +/- 4% (n = 4). Sympathetic nerve activity was highly reproducible at a 24-h interval (104 +/- 26 vs. 111 +/- 27 mV for the amplitude of spikes; n = 11). Dose-response curves to the alpha 1-stimulant methoxamine and to bradykinin were established in four rats. The increase in blood pressure induced by methoxamine caused a dose-dependent fall in sympathetic nerve activity, whereas the blood pressure reduction resulting from bradykinin was associated with a dose-dependent activation of sympathetic drive. These data therefore indicate that it is possible with out system to accurately measure sympathetic nerve activity in the awake rat, together with intra-arterial pressure and heart rate.

Centrally induced cardiovascular and sympathetic responses to hydrocortisone in rats

1983 ◽  
Vol 245 (6) ◽  
pp. H1013-H1018 ◽  
Author(s):  
H. Takahashi ◽  
K. Takeda ◽  
H. Ashizawa ◽  
A. Inoue ◽  
S. Yoneda ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Angiotensin Ii ◽  
Sympathetic Nerve ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Angiotensin I Converting Enzyme ◽  
Angiotensin Ii Antagonist ◽  
Dose Dependent

Central effects of hydrocortisone were investigated by injecting it intracerebroventricularly (icv) while recording blood pressure and heart rate in awake rats. Dose-dependent increases in both blood pressure and heart rate occurred following injections of hydrocortisone. Pretreatment by icv injections of the angiotensin II antagonist, [Sar1-Ile8]angiotensin II, completely abolished vasopressor responses to subsequent injections of hydrocortisone. When rats were later anesthetized with urethan to allow recording of abdominal sympathetic nerve activity, hydrocortisone produced vasopressor responses accompanied by corresponding increases in sympathetic nerve firing, which were also abolished by central pretreatment with either [Sar1-Ile8]angiotensin II or angiotensin I converting-enzyme inhibitor, captopril. These results indicate that centrally administered hydrocortisone stimulates the brain renin-angiotensin system to produce vasopressor responses by increasing sympathetic nerve firing.

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