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

The alpha 1-adrenergic receptor blocking effect of ketanserin, the blocking properties of this compound for nonspecific stimulation with angiotensin II, and the alpha-adrenergic receptor blocking properties and the blood pressure lowering effect of phentolamine, ritanserin, and the combination of both compounds were studied in patients on cardiopulmonary bypass (constant flow rate, mild hypothermia) undergoing coronary artery bypass grafting. Phenylephrine was used as alpha 1-adrenergic agonist. Ketanserin reduces the alpha 1-agonistic effect of phenylephrine on blood pressure in a dose-dependent manner up to a dose of 10 mg. Ketanserin did not block the nonspecific vasoconstriction, as induced by angiotensin II. The moderate blood pressure lowering effect of phentolamine was substantially potentiated by ritanserin, which in itself did not affect blood pressure. The findings in this study indicate that the blood pressure lowering activity of ketanserin results from a combined blockade of alpha 1-adrenergic and S2-serotonergic receptors.
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PMID:The alpha-adrenergic receptor blocking effect of ketanserin and the interaction between alpha-adrenergic and S2-serotonergic receptor blockade. 245 16

The mechanisms of the hypothermic effect of angiotensin II (AII) injected into the lateral ventricle were investigated in unanesthetized rats at an ambient temperature of 18 degrees C. Mean blood pressure (BP), heart rate (HR), metabolic rate (M), colonic temperature (Tcol), and temperatures of the interscapular brown adipose tissue (TBAT), and the tail skin (Tsk) were continuously monitored. AII at a dose of 5 micrograms produced a sharp and marked elevation in BP accompanied by bradycardia, and a decrease of M and Tco1 in the sinoaortic baroreceptor intact rats. The difference between TBAT and Tcol decreased significantly, which suggests a suppression of nonshivering thermogenesis of the BAT. Tsk was not changed by the AII injection. After sinoaortic denervation, however, the decrease in Tcol and M with AII injection was significantly reduced despite a marked elevation in BP. In addition, intravenous arginine-vasopressin antagonist pretreatment suppressed the elevation in BP and the decrease in HR, Tcol, and M after AII injection. From these results, it is concluded that the hypothermia which occurred after AII injection into the lateral ventricle can be largely attributed to the baroreflexive suppression of M, and to some extent to the direct effect on the thermoregulatory center in rats.
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PMID:Contributions of baroreceptor reflex to the hypothermic effect of intraventricular angiotensin II in rats. 404 35

Systemic administration of angiotensin II (AII) to the rat has previously been shown to induce a dose-dependent, hypothermic response manifested by a fall in colonic temperature (CT), a decrease in heat production and an increase in tail skin temperature (TST). The factors mediating AII-induced hypothermia and their site of action were the subjects of the present investigation. To this end, intracerebroventricular administration of 1 microgram of AII induced a 0.4 degrees C reduction in CT and a 2.4 degrees C increase in TST. In contrast, SC administration of 200 micrograms angiotensin III/kg induced a slight increase in CT but had no affect on TST. Pretreatment with the AII-receptor antagonist, saralasin, at either 1 or 10 micrograms/kg, SC did not affect either the fall in CT or the increase in TST induced by administration of 200 micrograms AII/kg, SC. However, the administration of 100 micrograms saralasin/kg, SC attenuated both the fall in CT and the increase in TST induced by either 100 or 200 micrograms AII/kg. Since both the presynaptic alpha adrenoceptor agonist, clonidine, and the opioid antagonist, naloxone, modulate the pressor and dipsogenic responses to AII, their effects on AII-induced hypothermia were tested. Both clonidine (25 micrograms/kg, SC) and naloxone (1 mg/kg, IP) enhanced the fall in CT. Clonidine lengthened the duration of the increase in TST while naloxone had no effect. Pretreatment with the presynaptic adrenoceptor antagonist, yohimbine (300 micrograms/kg, SC), did not alter the hypothermic response to administration of AII. To determine whether vasodilation of the tail of the rat was mediated by AII-induced prostaglandin release, indomethacin (4 and 6 mg/kg) was administered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Factors affecting angiotensin II-induced hypothermia in rats. 407 24

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

Profound hypothermia below 20 degrees C achieved by surface cooling using simple ice water bath equipment and deep ether anaesthesia is used with the aid of autonomic nerve blocking agents to obtain cardiac arrest for periods of over one hour for open-heart surgery. Blood levels of ether were between 40.6 mg/dl and 285.7 mg/dl during anaesthesia. No arrhythmia occurred and vital signs were quite stable. Hypocarbia throughout the procedure, severe base deficit after circulatory arrest, spontaneous recovery of metabolic acidosis, and a nearly normal cH+ (pH) were observed. Catecholamine increased moderately after circulatory arrest, but was far below shock levels. Plasma renin activity was markedly elevated but angiotensin II stayed at non-significant levels throughout the procedure. Excess lactate showed no significant change. Hyperglycaemia was noted. The mortality rate was 7.7 per cent and neurological disorders occurred in less than 5.8 per cent of the recent 52 cases.
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PMID:A study of profound hypothermia by surface cooling. 677 40

The effects of intracerebroventricular injections of angiotensin II on thermoregulatory responses of conscious rats to ambient temperatures (Ta) of 8, 22, and 30 degrees C were assessed. Administration of angiotensin II produced dose-dependent hypothermia in rats at both Ta 8 and 22 degrees C. The hypothermia in response to angiotensin II was due to decreased metabolic heat production. In addition, angiotensin II produced cutaneous vasoconstriction at Ta 8-22 degrees C. However, at Ta 30 degrees C angiotensin II produced no change in rectal temperature or other thermoregulatory responses. Furthermore, the hypothermia induced by angiotension II was antagonized by pretreatment with 6-hydroxytryptamine (a selective catecholamine neurotoxin) and propranolol (a selective beta-adrenergic antagonist) but not either 5,6-dihydroxytryptamine (a selective serotonin neurotoxin), atropine (a cholinergic antagonist), or phentolamine (a selective alpha-adrenergic antagonist). The data indicate that angiotension II inhibits both heat production and heat loss mechanisms which lead to an alteration in body temperature, probably via the activation of central adrenergic receptors.
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PMID:Angiotensin II inhibits both heat production and heat loss mechanisms in the rat. 722 29

Intraventricular administration of either norepinephrine, tyramine or angiotensin II produced dose-dependent hypothermia, decreased metabolism and lowered cutaneous temperatures in Taiwan monkeys at ambient temperatures of 4 and 22 degrees C. The hypothermia reflected the heat storage consequent to the net effects of decreased heat production and decreased heat loss. In heat (35 degrees C), these agents produced dose-dependent hyperthermia in monkeys. The hyperthermia was brought about mainly by a decrease in dry heat loss.
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PMID:Effects of intraventricular administration of sympathomimetic agents on metabolic, vasomotor and temperature responses in Taiwan monkeys. 732 10

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

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


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