Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increased sensitivity to certain drugs is believed to contribute to dysthermia in the elderly. To learn whether the temperature-altering effects of an opiate are increased in aged primates, injections of morphine sulfate (0.5-4 mg/kg) were given SC in randomly assigned order to squirrel monkeys ranging in age from 3.5 to over 17 years. Hyperthermia was the predominant response with no clear relationship to age, although hypothermic and biphasic responses also occurred, most commonly after the highest dose. Lateral cerebral ventricular injections of 0.625 and 1.25 micrograms morphine sulfate evoked hyperthermia in monkeys over 8 years of age but did not affect the temperature of animals less than 5 years old. Doses of 2.5 and 5 micrograms usually elicited hyperthermia regardless of age, but 10 micrograms induced hypothermia in a majority of monkeys. Naloxone was given intraventricularly to several monkeys to limit the degree of hypothermia after high doses of morphine given peripherally or centrally. Thus in these primates, as in other species such as the rat, lower doses of morphine usually evoked hyperthermia, but sufficiently high doses caused body temperature to fall. Unlike the case in the squirrel monkey with diazepam and with endogenous substances such as leukocytic pyrogen and taurine, there was not a strong or consistent relationship between age and morphine-induced temperature changes.
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PMID:Effects of morphine on body temperature of squirrel monkeys of various ages. 685 Mar 59

We have previously shown in mice that opiate agonists produce either hypothermia or hyperthermia or both, depending on the dose used and the ambient temperature. We have also shown that both temperature effects are blocked by the antagonists, naloxone and naltrexone. In order to confirm that these are specific opiate effects, the present studies to explore the development of tolerance to both temperature effects were undertaken. Mice were treated chronically with twice-daily injections of 2.5, 10, 40 or 160 mg/kg of morphine sulfate. Rectal temperature changes were monitored at 20 degrees, 25 degrees or 30 degrees C ambient temperature after the initial injection and at weekly intervals thereafter. At 20 degrees and 25 degrees C, the initial hypothermic response was replaced by hyperthermia after 7 weeks of twice-daily injections. At 30 degrees C, the initial hyperthermia became more pronounced and no evidence of tolerance was seen at any dose. A challenge dose of 160 mg/kg was given to all animals at 20 degrees C ambient temperature after 9 weeks of injections. There was a diminution of the hypothermic response inversely related to the chronically administered dose. At 30 degrees C, the 160 mg/kg challenge dose at 9 weeks showed little evidence of tolerance to the hyperthermia. Morphine-base pellet implantation, however, resulted in profound tolerance to both the hypo- and hyperthermic response within 1 day after implantation, peaking at 4 days and somewhat reduced by 1 week. Tolerance to the hypothermic effects induced by chronic administration of levorphanol and morphine-levorphanol cross-tolerance was also observed. It appears that both the hypo- and hyperthermia induced by the opiate and opioid agonists are opiate receptor effects because both effects can be blocked by the opiate antagonists and tolerance and cross-tolerance can be developed to both effects as well.
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PMID:Opiates and thermoregulation in mice. IV. Tolerance and cross-tolerance. 714 33

4-Amino-6-methoxy-1-phenyl-pyridazinium methyl sulfate (ameziniummetilsulfate, LU 1631, Regulton), in this study briefly called amezinium, was tested for possible central effects taking particular account of the mechanisms of action found for this substance in other studies. 1. The most conspicuous action of amezinium was in modifying reserpine-induced ptosis and reserpine-induced hypothermia. When amezinium is given before reserpine, the ED50 values are 0.15 and 3.9 mg/kg p.o. for both mouse and rat. These effects can be explained by a peripheral site of action since peripheral sympathomimetic effects can also be demonstrated in this dose range. Higher doses (10 mg/kg and upwards p.o.) were required to abolish reserpine-induced hypothermia 17 h after reserpine administration, an effect which probably requires a central site of action. But for imipramine, desipramine and pargyline the effective doses are the same in both experimental models (administration before and after reserpine, respectively). 2. Amezinium potentiated the effect of a threshold dose of L-dopa. Based on the central symptoms, higher doses (10 mg/kg p.o.) were also required for this effect. 3. With blood pressure increasing doses, the sleeping-waking pattern was modified in that duration and number of REM-episodes were reduced; in cats there was no parallel increase of wakefulness whilst in rats there was a slight relative increase of wakefulness. 4. Amezinium, particularly at high doses (46.4 mg/kg and upwards), exhibited a central depressant effect on the spontaneous behaviour of mice and rats and on orientational hyperactivity of mice. Based on the modification of aggregation toxicity, the effect of methamphetamine was reduced. In no dose range was there any evidence of methamphetamine-like effects (increase of motor activity, inhibition of food intake and increase of aggregation toxicity). 5. Amezinium did not affect the duration of hexobarbital anaesthesia or the coordination of mice on a rotating rod. 6. The acute toxicity of amezinium in mice and rats was low. The oral LD50 for mice was 1630 mg/kg and for rats 1410 mg/kg.
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PMID:Pharmacology of amezinium, a novel antihypotensive drug. VI. Effect on central nervous functions. 719 73

The effects of the Chinese herb Chou-Mou-Li, clerodenron fragrans (Ventenaceae) on metabolic, respiratory and vasomotor activities as well as body temperature were assessed in conscious rats at three different ambient temperatures (Ta) of 8, 22 and 30 degrees C. Intraperitoneal administration of Chou-Mou-li produced dose-dependent hypothermia in rats at both 8 and 22 degrees C Ta- At 8 degrees C Ta the hypothermia in response to Chou-Mou-Li was due to decreased metabolism, while at 22 degrees C Ta the hypothermia was due to both decreased metabolism and cutaneous vasodilatation. There was no change in respiratory evaporative heat loss. Furthermore, the hypothermia induced by Chou-Mou-Li was greatly antagonized by pretreatment of animals with p-chlorophenylalanine (a selective depletor of brain serotonin), but not by either atropine sulfate (a selective blocker of cholinergic receptors), regitine (a selective blocker of alpha-adrenergic receptors) or DL-propranolol (a selective blocker of beta-adrenergic receptors). However, at 30 degrees C Ta, systemic administration of Chou-Mou-Li produced no change in rectal temperature or other thermoregulatory responses. On the other hand, direct administration of serotonin into the lateral cerebral ventricle of conscious rats also produced dose-dependent hypothermia at 8 and 22 degrees C Ta. Again, the hypothermia in response to serotonin was due to decreased metabolism at 8 degrees C Ta and was due to both decreased metabolism and cutaneous vasodilatation at 22 degrees C Ta. At 30 degrees C Ta administration of serotonin also produced no change in thermoregulatory functions. The data indicate that Chou-Mou-Li produces hypothermia by increasing sensible heat loss and decreasing metabolic heat production, probably via the release of endogenous serotonin within brain.
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PMID:Serotoninergic mechanisms of the hypothermia induced by clerodenron fragrans (Ventenaceae) in the rat. 734 19

A new myocardial support system has been developed and a study of this system is reported. Cardioplegia was induced by continuous infusion of potent "cardioplegic" agents (potassium chloride and potassium chloride with propranolol) at the aortic root in 12 dogs subjected to cardiopulmonary bypass with total body hypothermia (20 degrees C). A low-flow normal-pressure perfusion was maintained with the aid of a norepinephrine drip. During the period of hypothermia the blood pH was maintained at 7.6 and serum magnesium concentration was increased to an average of 2.1 mmol/l by parenteral infusion of magnesium sulfate. At no time was ischemia induced and the aorta was not cross-clamped. The functional recovery to normal and preservation of the ultrastructure of the subendocardium after 4 hours of perfusion in cardioplegia were remarkable. The control hearts from hypothermic dogs that were allowed to fibrillate spontaneously showed severe damage.
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PMID:Perfusion in cardioplegia: an experimental study. 736 75

The effects of cholinomimetic drugs such as mecholyl (methacholine) and pilocarpine on autonomic functions (including sudomotor, metabolic, respiratory, vasomotor, and temperature responses) were assessed at room temperature (24 degrees C) in three groups of individuals, including normal, hyperhidrotic, and denervated subjects. The normal group had no palmar hyperhidrosis, with intact T2-3 ganglia, the hyperhidrotic group had palmar hyperhidrosis with intact T2-3 ganglia, and the denervated group had palmar hyperhidrosis treated with T2-3 ganglionectomy. Subcutaneous administration of mecholyl and pilocarpine each produced a fall in oral temperature in the normal group. The hypothermia was brought about by a decrease in metabolic rate, an increase in local sweating rate (mainly of the upper limb and trunk), and an increase in cutaneous circulation (estimated by an increase in the upper limb and trunk skin temperatures). The autonomic functions induced by these cholinomimetic drugs were antagonized by pretreatment with atropine sulfate (an antagonist of cholinergic receptors). Moreover, the hypothermia induced by mecholyl or pilocarpine was greatly reduced in the hyperhidrotic group. The reduction in the cholinomimetic-induced hypothermia in the hyperhidrotic group was due to the reduced sudomotor and metabolic responses after the injections of these cholinomimetic drugs, as compared to those of the normal group. However, neither the excessive sweating of the palms nor the reduced cholinergic responses in the hyperhidrotic group was observed after T2-3 ganglionectomy. The data indicate that the T2-3 ganglia play a role in the elaboration or modulation of the sudomotor and metabolic responses induced by activation of certain cholinergic receptors in humans.
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PMID:Effects of cholinomimetic drugs on sudomotor, metabolic, respiratory, vasomotor, and temperature response in palmar hyperhidrosis. 743 Oct 77

Current hematologic approaches to minimize postoperative bleeding have focused principally on antifibrinolytic agents. To explore whether a need might exist to promote clot stabilization independent of steps that might be taken to prevent lysis, we followed levels of the functional A-chain of factor XIII (fibrin stabilizing factor) immunologically in 19 patients undergoing coronary artery bypass grafting. The levels of factor XIIIA together with alterations in fibrinogen were followed at five stages of operation: (1) initial catheter placement (control), (2) heparinization, (3) initiation of cardiopulmonary bypass, (4) discontinuation of cardiopulmonary bypass, and (5) heparin neutralization with protamine sulfate. Significant (p < 0.05) inverse correlations were observed between postoperative chest-tube drainage volumes and levels of XIIIA at stages 1 through 3, and borderline associations (p < 0.1) were observed for stages 4 and 5. Pronounced losses of factor XIIIA accompanied initiation of cardiopulmonary bypass, when levels fell to 43% +/- 12% (standard deviation) of the control value, significantly below the 59% +/- 9% of the control value expected from hemodilution. By comparison, fibrinogen concentrations fell only to the extent attributable to hemodilution, unaccompanied by substantial degradation as indicated by electrophoretic, functional, and immunologic assays. There was a reversible heparin-induced precipitation of fibrin complexes and fibrinogen dimers from the blood on initiation of hypothermia, but these components returned to the circulation on restoration of normothermia. This precipitation was unrelated to losses of factor XIIIA. The findings warrant inference that XIIIA supplementation in deficient states should be considered as an adjunct to other therapies for postoperative bleeding.
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PMID:Low factor XIIIA levels are associated with increased blood loss after coronary artery bypass grafting. 791 67

Patients undergoing abdominal aortic aneurysm repair routinely have a depressed core body temperature during surgery, and hypothermia is known to cause abnormalities in coagulation. This study was designed to determine whether platelet function is altered as a result of hypothermia or heparin during abdominal aortic aneurysm repair. Ten patients scheduled for abdominal aortic aneurysm surgery were prospectively studied. Bleeding times and temperature were measured every hour beginning preoperatively. Each patient was heparinized intraoperatively, and the effects reversed with protamine sulfate prior to closure. Despite efforts to keep the patients warm, all of them developed hypothermia (mean lowest core temperature 34.8 +/- 0.7 degrees C). A significant linear relationship between the change in core temperature and the change in bleeding time was demonstrated. In 7 of 10 cases the greatest change in bleeding time occurred when patients experienced the lowest mean core temperature and not when they were heparinized. These data suggest that hypothermia has a marked effect on platelet function during abdominal aortic aneurysm repair. Although heparin can cause abnormalities in platelet function, hypothermia may be a more important role in inhibiting normal platelet function. By preventing severe hypothermia (< 35 degree C), excessive bleeding associated with abdominal aortic aneurysm repair may be minimized without the concomitant risk of blood product transfusion.
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PMID:Hypothermia and bleeding during abdominal aortic aneurysm repair. 819 2

Cyclophosphamide-induced neutropenia exacerbates septic shock and multiple organ injury in conscious rats during Escherichia coli (EC) bacteremia despite antibiotics and fluid administration. We hypothesized that such shock and inflammatory organ injury would be mitigated by rBPI23's microbicidal activity and/or binding of EC endotoxins. Four days after 100 mg cyclophosphamide/kg, catheterized rats with < 300 PMNs/microL were pretreated with rBPI23 or the irrelevant 22 kDa protein thaumatin [3.3-6.6 mg/kg, i.v. in 0.9% NaCl (NS)] 5 min before graded i.v. infection with 5 x 10(9) or 1 x 10(10) cfu of EC serotype 055:B5 ending at t = 0. Posttreatment with each protein continued (3.3-6.6 mg/kg in 1 mL NS/h) through 8 h, in addition to penicillin plus amikacin sulfate at t = 1.5 and 8 h. Arterial samples were obtained before pretreatment and at t = 1.5, 4.5, 8, and 24 h when animals were necropsied. One of eight thaumatin + 5 x 10(9) EC rats and none of six thaumatin + 10(10) EC rats survived 24 h. In contrast, rBPI23 significantly reduced mortality after either inoculum, improved bacterial clearance, and led to renormalization of early EC-induced hypotension, hypothermia, tachypnea, hyperoxemia, and hypocarbia. Compared with thaumatin, however, rBPI23 did not reduce circulating endotoxin or bioactive and antigenic tumor necrosis factor-alpha. Sepsis-induced severe neutropenia (< 50 PMNs/microL) evident in all EC rats by t = 1.5 h was reversed with rBPI23 by t = 8 h, but thrombocytopenia (< 5 x 10(4) platelets/microL) evident in all groups by t = 4.5 h was not altered.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The recombinant 23-kDa N-terminal fragment of bactericidal/permeability-increasing protein (rBPI23) decreases Escherichia coli-induced mortality and organ injury during immunosuppression-related neutropenia. 856 60

Repin is a sesquiterpene lactone found in Centaurea solstitialis, a plant responsible for Parkinson-like disease in horses. Repin, on intraperitoneal (i.p.) injection, produces a dose-dependent and highly significant hypothermia in naive rats. The hypothermia is long-lasting with a peak 3 h after the injection and a return to normal temperature after more than 8 h. The effects of atropine sulfate, atropine methylbromide, propranolol, metergoline, ketanserin, diphenhydramine and apomorphine pretreatment on repin-induced hypothermia were investigated. None of the pretreatments directly antagonized repin's hypothermic effect. However, partial but significant reversals of hypothermia by atropine sulfate, metergoline, ketanserin, diphenhydramine and apomorphine were observed 2-4 h after the repin injection. These late-onset effects are probably due to secondary physiological mechanisms. On the other hand, propranolol, at 20 mg/kg i.p., clearly accentuated both the early-onset (30-90 min) and late-onset (2-4 h) hypothermic effects of repin.
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PMID:Effect of various pretreatments on the hypothermic activity of repin in naive rats. 884 89


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