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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiotensin II (AII, 5 micrograms) injected into the cerebral ventricles produced hypothermia in conscious rats at ambient temperatures (Ta) of 18, 23, and 28 degrees C. At Ta of 18 and 23 degrees C, AII-induced hypothermia was attributed to both enhancement of heat loss and suppression of metabolic rate. At Ta of 28 degrees C, AII-induced hypothermia seemed to be mainly attributed to increased heat loss.
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PMID:Effects of intraventricular angiotensin II on heat balance at various ambient temperatures in rats. 402 Dec 20

Polypeptides are endogenous agents, involved in the regulation of many physiologic functions and the pathogenesis of several diseases. Polypeptide antagonists form a group of new chemical entities which may provide valid therapeutic agents. Some polypeptides (angiotensin, kinins) are released through the action of proteolytic enzymes (renin, kallikreins) and act as hormones or autacoids; others (substance P, neurotensin) are synthetized by nervous cells to serve as neurotransmitters or neuromodulators. The main homeostatic role of the renin-angiotensin system is to uphold high systemic arterial blood pressure. Overproduction of renin and insufficient checking of renin secretion are among the most common causes of arterial hypertension. Several forms of arterial hypertension (neurovascular, idiopathic) benefit from a reduction in renin-angiotensin system activity. This is achieved either through decreasing renin secretion, by inhibiting conversion of angiotensin I into angiotensin II, or through blocking the peripheral actions (at the receptor sites) of angiotensin II. Renin secretion is very significantly reduced by beta-blocking agents (propranolol); conversion of angiotensin I into angiotensin II is inhibited by teprotide, captopril and their derivatives; peripheral actions of angiotensin II are blocked by saralasin. Bradykinin and related agents produce vasodilation, increase vascular permeability and stimulate pain fibers. Kinins thus reproduce the cardinal features of inflammation and are held to be mediators of the inflammatory reaction. The substance P neuropeptide is found in the brain and bowel; it may act as a transmitter of the sensation of pain at the spinal cord and central nervous system sites. Among other effects outside of the brain, substance P is a potent vasodilator and inhibits renin secretion. Neurotensin is a neuropeptide which produces hypothermia, muscular relaxation and analgesia. Outside of the brain, this peptide is involved in the regulation of gastric secretion, intestinal motility and insulin and glucagon secretion. The vasoactive intestinal peptide, found in certain cholinergic nerve endings, is a large peptide which inhibits gastric secretion, intestinal motility and vascular tone.
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PMID:[Polypeptides and antagonists]. 620 6

The present studies were performed to investigate the metabolic role of the lungs in the renin-angiotensin system under hypothermia by measuring plasma renin activity, plasma angiotensin I (A I), plasma angiotensin II (A II), plasma aldosterone and plasma angiotensin converting enzyme activity on 14 patients who underwent open-heart surgery with surface-induced simple hypothermia. In addition, dog experiments were performed, in which changes of renal blood flow and angiotensin metabolism in lungs and kidneys under hypothermia were studied in vivo. The following results were obtained: 1) During and after open-heart surgery with surface-induced simple hypothermia, the homeostasis in the renin-angiotensin system is still maintained. 2) An increase of A II may play an important role in maintaining blood pressure under hypothermia. 3) Under hypothermia, the conversion of A I to A II in the kidneys may contribute to an increase of plasma A II.
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PMID:Significance of renin-angiotensin system during and after surface-induced simple hypothermia in open-heart surgery. 630 Apr 82

The effects of intraventricular administration of angiotensin II (10 to 50 micrograms, third cerebral ventricle) on thermoregulatory responses of conscious rabbits to different ambient temperatures (Ta) of 2, 22 and 32 degrees C were assessed. Angiotensin II administration produced dose-dependent hypothermia in rabbits at both 2 and 22 degrees C Ta. The hypothermia in response to angiotensin II was due to decreased metabolic heat production and increased heat losses. The increase in heat loss was shown by an increase in both skin blood flow and respiratory evaporative heat loss. However, at 32 degrees C Ta, angiotensin II produced no change in rectal temperature or other thermoregulatory responses. The data indicate that angiotensin II decreases heat production and increases heat loss mechanisms in the rabbit brain which leads to hypothermia.
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PMID:Effects of angiotensin II on metabolic, respiratory and vasomotor activities as well as body temperatures in the rabbit. 745 27

Vasoconstriction is believed to be a dominant cause of high perfusion resistance during kidney preservation at low temperatures. An experiment was performed to study the effects of hypothermia on vasoactivity. Measurements were made on an apparatus that permitted perfusion resistance to be compared simultaneously in two isolated kidneys at different temperatures. With perfusion temperature serving as the variable, the vascular responses to several vasoactive agents were measured. Hypothermia diminished or altered the vascular responses to the agents. For example, no vasoconstriction was observed with Angiotensin II, dopamine, acetylcholine, or BaCl2 and no vasodilation was observed with papaverine or bradykinin in the hypothermic kidney. A significantly altered response was observed with norepinephrine. The responses were reversible upon return to normothermia. From these data, we conclude that myogenic vasoconstriction plays a questionable role in producing the elevated perfusion resistance observed in some hypothermic kidneys.
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PMID:Renal preservation resistance: evidence against myogenic vasoactive factors. 746 89

The blood flow rates of 14 tissues in the body were determined by microsphere method using normal and tumor-bearing rats kept conscious or under urethane anesthesia. The effects on the blood flow rate in the tissues were assessed for multimodal therapy, systemic hypothermia for ischemic brain injury, and local hyperthermia and angiotensin II-induced hypertensive chemotherapy for cancer. Urethane anesthesia showed no effect on cardiac output, while there was a tendency of decrease of blood flow rate and % of cardiac output in each tissue other than muscle tissue, in which they increased as a counterbalance, in normal and tumor-bearing rats. Systemic hypothermia gave results similar to those of urethane anesthesia in normal rats, but for tumor-bearing rats, it decreased cardiac output, and consequently the blood flow rate in most tissues. Brain blood flow rate was about half of that in the conscious rats. Local hyperthermia also decreased the cardiac output and blood flow rate in each tissue, including the tumor tissue. Angiotensin II-induced hypertension showed no effect on cardiac output, had various effects on blood flow rate in each tissue, and led to no increase in the tumor blood flow rate. Simulations based on the physiological pharmacokinetic modeling suggested that intramuscular injection of a lung-specific derivative of ceftazidime would provide the ideal biodistribution to ensure its optimal therapeutic efficacy during systemic hypothermia. This methodology, namely the pharmacokinetic simulation based on the physiological values of the body, will provide a useful piece of information on drug delivery systems under various conditions.
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PMID:Blood flow rate in normal and tumor-bearing rats in conscious state, under urethane anesthesia, and during systemic hypothermia. 989 94

Angiotensin II (ANG II), a bioactive peptide that plays important roles in blood-pressure and body-fluid regulation, has recently been reported to be involved in normal thermoregulation and fever. In the case of thermoregulation, ANG II lowers body temperature when administered centrally or systemically (i.e. "exogenous" ANG II acts as a hypothermia-inducing agent). In contrast, "endogenous" ANG II is involved both in heat-loss responses in a hot environment and in thermogenesis in the cold. It therefore seems likely that endogenous ANG II is involved in maintaining body temperature at the set-point. In the case of fever, it has been reported that endogenous brain ANG II and its type 1 receptor mediate or modulate the fever induced by "restraint stress". At the final step in "pyrogen-induced" fever, brain ANG II facilitates the fever induced by prostaglandin E2 (PGE2) through its action on the type 2 receptor, whereas at its first step the lipopolysaccharide (LPS, 2 microg/kg, i.v.)-induced production of pyrogenic cytokines [such as interleukin-1 (IL-1)] involves an action of endogenous ANG II through its type 1 receptor. On the other hand, it is well known that a very high dose of LPS (50-5000 microg/kg) injected systemically induces hypothermia in rodents. This hypothermia is presumably initiated by tumor necrosis factor (TNF). Since ANG II contributes to the LPS-induced production of cytokines such as IL-1beta, as described above, it is possible that the generation of TNF by LPS involves an action of ANG II, too, and that this TNF production leads to the LPS-induced hypothermia. Together, these findings suggest that ANG II and its receptors make a number of contributions to normal thermoregulation, to fever, and to the hypothermia in systemic inflammation.
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PMID:Angiotensin II: its effects on fever and hypothermia in systemic inflammation. 1476 80