Body temperature, increase

It is suggested that one reason why the body temperature increases during an infection is to restrict the iron available to the pathogens. The increase in temperature favours uptake by the immune cells and by the liver (Chapter 18). 

Thermoregulation. PG raise the set point of hypothalamic (preoptic) thermoregulatory neurons body temperature increases (fever). 

Schizonepeta multifida (L.) Briquet S. tenuifolia (Benth.) Briquet Jing Jie (aerial part, spikes) Essential oils, d-menthone, d-limonene, campesterol, stigmasterol, beta-sitosterol, hesperidin.33-214 Diaphoresis, antiinflammatory, analgesic, antipyretic, antispasmodic, antidiabetic, lower body temperature, increase blood coagulation, anticonvulsive. 

Colchicine also exhibits a variety of other pharmacological effects. It lowers body temperature, increases the sensitivity to central depressants, depresses the respiratory center, enhances the response to sympathomimetic agents, constricts blood vessels, and induces hypertension by central vasomotor stimulation. It enhances gastrointestinal activity by neurogenic stimulation but depresses it by a direct effect, and alters neuromuscular function. 

Symptoms begin about 72 hours after the last dose and include anxiety, weakness, increased irritability, muscle twitching, kicking movements, significant backache, hot and cold flashes, anorexia, insomnia, muscle spasm, and intestinal spasm. Additional symptoms can include repetitive sneezing, increased body temperature, increased blood pressure, diarrhea, vomiting, increased respiratory rate, and increased heart rate. 

Increased body temperature, increased basal metabolic rate, and/or profuse perspiration may be regarded as cardinal signs of DNOC toxicosis in humans because they are directly related to the mechanism of action of DNOC and occur irrespective of the route of exposure. Based on results from human studies, case reports, and limited animal studies, weight loss and changes in the endocrine system also may be also expected to occur in humans exposed to DNOC. 

SAFETY PROFILE A deadly human poison by ingestion. An experimental poison by ingestion, inhalation, intravenous, intraperitoneal, subcutaneous, and intramuscular routes. Moderately toxic by skin contact. Experimental teratogenic and reproductive effects. Human systemic effects body temperature increase, change in heart rate, coma. A skin irritant. Mutation data reported. Phytotoxic. A pesticide. An explosive. Forms explosive salts with alkalies and ammonia. When heated to decomposition it emits toxic fumes of NOx. See also NITRO COMPOUNDS of AROMATIC HYDROCARBONS. 

Increased body temperature Increased blood pressure Pupil dilation Tearing, runny nose Diarrhea... 

Ethynyl estradiol can cause nausea or vomiting, body temperature increase and other menopausal symptoms, and blood clotting. The lowest published toxic dose is 21 mg kg (21 day) intermittent. 

Intermediate-Duration Exposure. Occupational exposure to 2,4-DNP resulted in death from pyrexia in some cases, and fatigue, elevation of body temperature, increased respiratory rate, profuse perspiration, and weight loss in some of the workers (Gisclard and Woodward 1946 Perkins 1919). Exposure occurred by the inhalation and also probably by the dermal route. Gastrointestinal symptoms (nausea, vomiting) were also noted (Perkins 1919). Autopsy of the fatal cases did not reveal any characteristic lesions, other than pulmonary edema, which was thought to be secondary to vasomotor effects. Hence many of the effects of 2,4-DNP in humans do not appear to be route-specific. No exposure levels were reported in these studies. 

The effects of LSD are unpredictable. They depend on the amount taken the user s personality, mood, and expectations and the surroundings in which the drug is used. Usually the user feels the first effects of the drug 30 to 90 minutes after taking it. The physical effects include dilated pupils, higher body temperature, increased heart rate and blood pressure, sweating, loss of appetite, sleeplessness, dry mouth, and tremors. 

Body Temperature, Blood Flow, and Laminitis. In cattle and sheep, blood flow to the peripheral tissues decreased and body temperature increased when tall fescue seed was included in the diet (Rhodes et al., 1991). The reduction in blood flow to the peripheral tissues is likely related to increased body temperature, because the animal is less efficient in cooling itself. Unlike cattle and sheep, pregnant mares exhibit no increase in body temperature when exposed to the endophytic toxins (Monroe et al., 1988 Putnam et al., 1991). However, horses sweat more freely than cattle and are more capable of cooling themselves. Putnam et al. (1991) observed increased sweating in gravid mares grazing E+ tall fescue. 

Frequent Drowsiness anticholinergic effects postural hypotension increase in body temperature increased salivation ECG changes... 

The word "pyrogen" means "fever-producing" and has been used to cover any substance which causes a body temperature increase on injection. In fact, the first compendial pyrogen test was published in the 1942 edition of the United States Pharmacopeia. It involved the measurement of the rise of body temperature in rabbits upon intravenous injection of a test product. More recently (1977), the FDA approved the Limulus amebocyte lysate (LAL) test which can be run for less than 10% of the cost of a rabbit test. 

Body temperature (increased with fever) Environmental temperature (increased in cold) Thyroid status (increased in hyperthyroidism) Pregnancy and lactation (increased)... 

Immune system activity contributes to body temperature increase. 

Body metabolism tends to increase as body temperature increases. 

One important neuronal TRH control center appears to be the paraventricular nucleus, but TRH Is widely distributed in the hypothalamus and highly concentrated in the median eminence (4). One important ipactor regulating TRH production is environmental temperature. Both peripheral thermal receptors and preoptic neuronal thermal receptors monitor environmental and central body temperature these receptors modulate preoptic neuronal outflow to the paraventricular nucleus and other TRH synthesizing neurons in the hypothalamus and median eminence which. In turn, modulate TRH secretion (4). Decreasing environmental and/or core body temperature Increase TRH output and increase the tonic level of TSH release. Somatostatin (SRIF) and dopamine can inhibit TSH release by actions at the pituitary level, and these inhibitory transmitters contribute to central nervous system modulation of TSH release (4). There is evidence that serotonin may be inhibitory in the adult rat, but this does not seem to be so in other species. Norepinephrine also may be inhibitory. Glucocorticoid can inhibit TSH release at the hypothalamic level, but the mechanism is not known. The exact roles of TRH and non-TRH regulatory factors in TSH control are not clear. Administration of somatostatin antiserum to adult rats increases basal TSH levels and potentiates the TSH response to cold (19). Inhibitory factors probably also play a role in the diurnal variation in TSH secretion, in the inhibitory reactions to stress, in the variation in thyroidal activity in psychosis, etc. 

A 21-year-old woman, who used cocaine regularly and occasionally other drugs of abuse, took moclobemide 1800 mg at 15.00 h and venlafaxine 1800 mg at 18.00 h. At 20.14 h she was conscious but restless and agitated. She had excessively clammy skin with a normal body temperature, increased symmetrical reflexes, ataxia, increased muscle tone, and dilated pupils her blood pressure was 180/120 mmHg, pulse rate 105/minute, and respiratory rate 16/minute. She deteriorated at around 23.30 h, with loss of verbal contact, severe agitation, hallucinations, periodic coma, continuously dilated pupils, a tachycardia of 124/minute and a blood pressure of 105/90 mmHg. Two hours later, her respiratory rate was 34/minute, and her temperature 41-42 °C. She had bloody respiratory secretions and loose bloody stools. Her heart rate increased to 170/minute and she developed ventricular fibrillation. Deflbrillation was unsuccessful and she died. 

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