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

A short review of the role of cyclic nucleotides and prostaglandins (PGs) in normal and pathological functions of the heart is given. Possible interrelationships of these two regulatory systems have been studied by using spontaneously beating rat atria preparations. Addition of noradrenaline (NA) to the incubate (1 . 10(-6) M) caused an increase in amplitude and frequency which was preceded and parallelled by an elevation of the tissue cAMP level. A transient increase in cGMP and PGE values was also seen. Propranolol (5 . 10(-6) M) abolished the increase in amplitude and frequency as well as in cAMP and PGE concentrations. Indomethacin (1 . 10(-5) M) inhibited the formation of PGE. The increase in cGMP was blocked by phenoxybenzamine. Interchange between beta- and alpha-receptors according as the temperature is lowered has been described earlier. Hypothermia (20 degrees C) had a positive inotropic effect on the atria and increased the tissue cAMP concentration. Loading of the atria caused an increase in cAMP without any effects on cGMP or PGs. Slight hypoxia did not change the cAMP or PG levels, but elevated the cGMP values. Arrhythmias induced by hypo- or hyperpotassemia did not modify the biochemical parameters measured. PGF2alpha (1. 10(-5) M) normalized the atrial rhythm and increased the amplitude without changing cyclic nucleotide or PG levels. PGE1 (1 . 10(-4) M) increased the amplitude of normorhythmic atria and the tissue concentration of cAMP. PGE2 was the only PG tested which stimulated the heart adenylate cyclase in vitro. There seems to be close but complicated relationships between cyclic nucleotides and PGs in the heart.
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PMID:The role of cyclic nucleotides and prostaglandins in heart function. 21 11

While some salicylates (salicyclic acid and salicylaldehyde, especially) are as potent as aspirin as acute, orally-active anti-flammatory drugs in the rat, they are either inactive or far less potent as PG synthesis inhibitors when added directly to isolated platelets or when given orally. Although PGE1 and PGE2 produce anti-ulcerogenic effects when given to rats in the presence of selected non-steroidal anti-flammatory drugs, they fail to inhibit the acute anti-flammatory and anti-nociceptive effects of these drugs. They are anti-flammatory and anti-nociceptive under certain experimental conditions. PGE1 and PGE2 can also behave as hypothermic agents when given subcutaneously. Related studies, using PG synthesis stimulators in vivo and in vitro (substituted phenylureas), also cause anti-nociception and hypothermia. All of these indirect studies, when taken together, infer that PG synthesis inhibition per se fails to explain, entirely, the pharmacologic effects of non-steroidal anti-inflammatory drugs. They also suggest that the precise role of certain PGs in toxicopharmacology is far from simple and straightforward.
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PMID:Anomalous biological effects of salicylates and prostaglandins. 49 43

It is known that central administration of prostaglandins of the E series has marked effects on body temperature. The purpose in the present experiments was to learn whether stable analogs of the cyclic endoperoxide precursors of PGE2, PGF2alpha and PGD2, injected into the primary temperature control in the preoptic/anterior (PO/AH) hypothalamic region and into a presumed secondary control in the medulla oblongata, can produce rises in body temperature similar to those caused by PGE2. Injection of the analogs U-44069 and U-46619 (1.0 and 2.0 microng) into the PO/AH region of the rat, where both PGE2 and PGE1 caused hyperthermia, had no effect on Tre. Likewise, injections into the medulla oblongata, in the region where PGE2 and PGE1 caused hypothermia, were ineffective in altering body temperature. That neurons important to the control of body temperature are selectively sensitive to PGE2 and not to analogs of prostaglandin precursors suggests that local cyclic endoperoxides can influence body temperature only through bioconversion to prostaglandin.
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PMID:Analogs of endoperoxide precursors of prostaglandins: failure to affect body temperature when injected into primary and secondary central temperature controls. 84 28

1. In unanaesthetized restrained rats kept at an ambient temperature of 21-23degrees C, rectal temperature was continuously monitored and the temperature effects of injections of prostaglandins, endotoxin from Salmonella abortus equi, lipid A, and antipyretics were examined. 2. Fever occurred when prostaglandin E1, E2, F1alpha or F2alpha (PGE1, PGE2, PGF1alpha, PGF2alpha) was injected into the cerebral ventricles in doses of 200 ng and 2 mug. PGE2 was the most potent prostaglandin followed in descending order by PGE1, PGF2alpha, and PGF1alpha. The fever produced by 2 mug of PGE1 and PGE2 was short and followed by a fall in temperature to below the pre-injection level. 3. I.V. injections of endotoxin and lipid A in doses of 3 or 10 mug usually caused a long lasting fall in temperature, but when injected into the cerebral ventricles in doses of 400 ng or 1 mug, they produced long lasting fevers. 4. Injected I.V. or I.P., indomethacin and paracetamol had a hypothermic action of their own. Indomethacin was more potent than paracetamol and both were more potent than injected I.P. 5. I.V. and I.P. injections of indomethacin and paracetamol did not reverse the hypothermia in response to I.V. endotoxin or lipid A, but the fever responses to their injection into the cerebral ventricles were prevented and abolished by the antipyretics. 6. It is concluded that in rats endotoxin and lipid A, or the endogenous pyrogens produced by them, do not readily pass through the blood-brain barrier into the brain tissue. If they do reach brain tissue, as when injected into the cerebral ventricles, they stimulate synthesis and release of prostaglandin in rats as they do in other species, and thereby produce fever. The hypothermia in response to I.V. endotoxin or lipid A, on the other hand, is thought to be independent of prostaglandin synthesis and to result from a direct toxic action on the skin vessels.
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PMID:Prostaglandins, endotoxin and lipid A on body temperature in rats. 117 7

The effect of 48 hours of hypothermic renal ischemia utilizing Euro-Collins flush and short term reperfusion on renal prostaglandin synthesis was studied in dogs. Hypothermic ischemia followed by 60 minutes of reperfusion in-vivo resulted in significant elevations in renal Thromboxane B2 (TXB2) production in the outer cortex, inner cortex, and medulla, relative to non-ischemic kidneys. Prostaglandin E2 (PGE2) and 6-keto Prostaglandin F1 alpha (6-K PGF1 alpha) production were not significantly affected by ischemia and reperfusion. Enhanced TXB2 production was not seen with ischemia alone (without reperfusion) or with reperfusion with O2 saturated buffer, indicating a blood born source or stimuli. Early postreperfusion renal blood flow after hypothermic ischemia followed a biphasic pattern; blood flow increased for the first 10 minutes of reperfusion to achieve normal values, and then steadily declined over the next 20 minutes. This pattern was not altered by the cyclooxygenase inhibitors Idomethacin (5 mg/kg, P.O.) or Mefenamic acid (10 mg/kg, I.V.). Administration of the TXA2 synthesis inhibitor CGS-12970 (3 mg/kg, I.V.) or the TXA2/endoperoxide receptor antagonist SQ-29548 (80 micrograms/min, I.A.) significantly increased renal blood flow during reperfusion but neither agent altered the basic time dependent pattern observed in the control group. These data indicate that 48 hours of hypothermic renal ischemia results in dramatic changes in intrarenal TXA2 synthesis at the time of reperfusion. Enhanced TXA2 production is not dependent on reoxygenation per se, but rather requires reperfusion with blood suggesting a circulatory source.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prostanoids and hypothermic renal preservation injury. 228 Nov 20

Exposure of rats to 1-15 Gy of gamma radiation induced hyperthermia, whereas exposure to 20-150 Gy produced hypothermia. Since radiation exposure induced the release of prostaglandins (PGs) and histamine, the role of PGs and histamine in radiation-induced temperature changes was examined. Radiation-induced hyper- and hypothermia were antagonized by pretreatment with indomethacin, a cyclooxygenase inhibitor. Intracerebroventricular administration of PGE2 and PGD2 induced hyper- and hypothermia, respectively. Administration of SC-19220, a specific PGE2 antagonist, attenuated PGE2- and radiation-induced hyperthermia, but it did not antagonize PGD2- or radiation-induced hypothermia. Consistent with an apparent role of histamine in hypothermia, administration of disodium cromoglycate (a mast cell stabilizer), mepyramine (H1-receptor antagonist), or cimetidine (H2-receptor antagonist) attenuated PGD2- and radiation-induced hypothermia. These results suggest that radiation-induced hyperthermia is mediated via PGE2 and that radiation-induced hypothermia is mediated by another PG, possibly PGD2, via histamine.
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PMID:Involvement of prostaglandins and histamine in radiation-induced temperature responses in rats. 230 Jun 72

The antipyretic, analgesic, antinflammatory and antiulcerogenic properties of a new compound 1,4 dihydro-1-ethyl-7-phenylpyrrol (1,2-a)-pyrimidine-4-one (V33) are described. V33 on a mg/kg basis possesses antipyretic and analgesic properties at doses lower than paracetamol and which do not produce hypothermia or motor impairment. V33 possesses antiinflammatory activity and decreases the production of LTB4 from inflammatory exudates without affecting PGE2 content. V33 is not only devoid of gastric ulcerogenic properties but exerts antiulcer activity toward various ulcerogenic stimuli. Lethal dose 50% (LD50) of V33 is higher that of paracetamol.
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PMID:The pharmacological properties of 1,4-dihydro-1-ethyl-7-phenylpyrrol (1,2-a)-pyrimidine-4-one, a new antipyretic and analgesic drug. 282 81

We have investigated the ability of three hyperthermic stimuli (PGE2, 5-HT and ACh) to elicit hyperthermia in the Helium-Cold (He-Cold) hypothermic hamster. Hamsters in these conditions are poikilothermic and will passively follow room temperature in a regulated cold room. Animals were injected centrally at AH/POA sites via an indwelling guide tube at body temperatures maintained between 9-12 degrees C. Active sites in the AH/POA were determined prior to the experiment by PGE2 injection. PGE2 injection at an effective AH/POA site immediately reversed the anesthetic induced hypothermia in warm air. Hamsters were induced into hypothermia by the He-Cold induction method and body temperatures were maintained in a 9 degrees C cold room. Colonic temperatures were monitored at 5 minute intervals by a YSI thermistor probe and telethermometer. Central injections of 5-HT (2 micrograms/microliter) and ACh (50 micrograms/microliter) at effective AH/POA sites evoked significant increases in colonic temperature in He-Cold hamsters. PGE2 injections were not different from saline control injections and did not elicit pronounced temperature changes in these animals. Specific blockade of the 5-HT and ACh temperature increases was demonstrated with specific antagonist injections. The results suggest that the central organization of heat-gain mechanisms in the AH/POA is the same as normothermic animals even at temperatures well below those previously investigated.
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PMID:Organization of central hyperthermic mechanisms in helium-cold hypothermic hamsters. 346 74

In this study we have examined the interactions of bombesin (1 microgram ICV), neurotensin (1 microgram ICV), TRH (10 micrograms ICV), somatostatin (10 micrograms ICV), PGE2 (10 micrograms ICV) and naloxone (10 mg/kg SC) on thermoregulation in the rat at room temperature (20 +/- 1 degree C). Given alone, bombesin, neurotensin, somatostatin and naloxone all produced hypothermia (bombesin greater than neurotensin greater than somatostatin congruent to naloxone). PGE2 was hyperthermic, and TRH had no effect. Bombesin and PGE2 neutralized one another's effects. Neurotensin had no effect on PGE2-induced hyperthermia. Naloxone enhanced the hypothermic effect of bombesin and somatostatin enhanced the rate of onset of hypothermia after bombesin. TRH had no effect on bombesin-induced hypothermia. TRH, somatostatin and naloxone had no effect on neurotensin-induced hypothermia. TRH antagonized the hypothermia due to naloxone and somatostatin.
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PMID:Neuropeptides and thermoregulation: the interactions of bombesin, neurotensin, TRH, somatostatin, naloxone and prostaglandins. 612 11

In previous research, intracerebroventricular (ICV) injection of serine (1-4 mg) caused dose-related hypothermia in rabbits and reduced rises in body temperature caused by leukocytic pyrogen (LP) and prostaglandin E2 (PGEs). Since serine is the major precursor of the putative neurotransmitter glycine, these effects of serine may be due to its conversion to glycine. To assess this possibility, glycine was administered centrally to see if its effects on body temperature are similar to those of serine. ICV injections of glycine (0.25-1.0 mg) caused dose-related decreased in body temperature in a 10 degrees C environment but had no significant effect at 23 degrees C. Glycine (1 mg) delayed the normal rise in temperature in 30 degrees C environment and reduced LP fever and PGE2 hyperthermia. ICV glycine and serine in combination were, however, subadditive in producing hypothermia, which suggests that these amino acids act at different central sites. A difference in the interaction of serine and glycine with strychnine in producing hypothermia also suggests that the action of serine is not entirely mediated by glycine. Since serine and glycine have similar effects on normal body temperature and fever some portion of the effects of serine may be caused by its conversion to glycine. The subadditivity data and the difference in temperature effects when the amino acids are given with strychnine suggest that serine and glycine probably have separate central sites of action.
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PMID:Comparison of the effects of central administration of serine and glycine on body temperature of the rabbit. 678 12


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