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

Intraperitoneal injection of prostaglandin E1 (PGE) produces a transient hypothermia in rats that lasts 1-2 h. Rats exposed to an ambient temperature (Ta) of 26 degrees C displayed a decrease in rectal temperature (Tre) of 0.95 +/- 0.12 degrees C (SE) after injection with PGE (100 micrograms/kg ip). Hypothermia was produced mainly by heat losses, as indicated by increases in tail blood flow. At Ta of 4 degrees C, PGE produced a comparable fall in Tre of 1.00 +/- 0.14 degrees C. However, in the cold the hypothermia was caused solely by decreases in heat production. These results indicate that the PGE-induced hypothermia is not the result of a peripheral vasodilation induced by the direct action of PGE on the tail vascular smooth muscle but is a central nervous system-mediated response of the thermoregulatory system induced by PGE within the peritoneal cavity. Capsaicin injected subcutaneously induces a transient hypothermia in rats because of stimulation of the warm receptors. If administered peripherally in sufficient amounts, it is reputed to impair peripheral warm receptors so that they become desensitized to the hypothermic effects of capsaicin. We measured PGE-induced hypothermias in rats both before and after capsaicin desensitization at Ta of 26 degrees C. Before desensitization the hypothermia was -1.14 +/- 0.12 degrees C, whereas after capsaicin treatment the PGE-induced hypothermia was -0.34 +/- 0.17 degrees C. The biological effects of capsaicin are diverse; however, based on current thinking about the thermoregulatory effects of capsaicin desensitization, our results indicate that peripheral warm receptor pathways are in some manner implicated in the hypothermia induced by intraperitoneal PGE.
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PMID:Effects of cold and capsaicin desensitization on prostaglandin E hypothermia in rats. 238 39

In 7 frogs (Rana esculenta) weighing 70 to 180 g, thermopreferendum (Thp), measured by recording cutaneous temperature (Ts) in the animal placed in the warm end of an aqueous temperature gradient (0 degree C-40 degrees C), equalled 25 +/- 2 degrees C. After an intraperitoneal (IP) injection of 20 mg/kg of capsaicin, Thp was significantly decreased and equalled 3 +/- 1 degree C. The frogs then remained in the cold end of the gradient for 60 minutes. When the time of observation was extended to 3 hours, one frog died from hypothermia. Seven to 24 days after the capsaicin injection, Thp was still decreased in 4 surviving frogs (Thp = 15 +/- 2 degrees C). Capsaicin or isotonic saline solution injected in frogs maintained at 25 degrees C ambient temperature had no effect on Ts or on cloacal temperature. According to results previously obtained in homeothermic species, small doses of capsaicin activated heat-loss responses in the frog.
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PMID:The effect of an intraperitoneal injection of capsaicin on the thermopreferendum in the frog (Rana esculenta). 348 98

Capsaicin was intravenously administered to adult domestic ducks of 1.8-2.6 kg body weight, with a cumulative dose of 1.0 g/kg body weight given in 4-6 single infusions at intervals of 2-3 days. There were no acute, nociceptive or hypothermic effects, as typically seen in mammals. Before and after capsaicin treatment respiratory evaporative heat loss (REHL, w X kg-1), breathing frequency (BF, min-1) and metabolic heat production (M, w X kg-1) were determined in a warm environment (35-38 degrees C) as a function of core temperature, measured in the esophagus (Tes), which was altered by graded heat extraction with a colonic thermode. Capsaicin treatment reduced the rate at which REHL increased with increasing BF, however, this was compensated by a steeper increase of BF with rising Tes so that the relationship between Tes and REHL remained unchanged. The Tes threshold for activation of M was increased by 0.3 degrees C and the slope reduced by 27% after capsaicin, but identical maximum M values were attained before and after capsaicin at identical degrees of hypothermia. Skin temperature measurements revealed no influence of capsaicin on the threshold Tes values for skin vasoconstriction. It is concluded that capsaicin fails to exert effects in birds on those afferents and central neurons which are involved in thermo- and nociception, in contrast to mammals in which these perceptive functions become severely impaired.
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PMID:Capsaicin fails to produce disturbances of autonomic heat and cold defence in an avian species (Anas platyrhynchos). 371 39

1. In rats and guinea-pigs a subcutaneous or intraperitoneal injection of capsaicin, the substance responsible for the pungency of red pepper, produces profound hypothermia associated with skin vasodilatation.2. After large doses of capsaicin rats and guinea-pigs become insensitive to the hypothermic action of capsaicin. This densensitization is apparently irreversible since it is present months after the capsaicin treatment.3. Capsaicin-desensitized animals are no longer able to protect themselves against overheating but respond with pronounced hyperthermia to high ambient temperatures (32-40 degrees C). Temperature regulation against cold exposure, however, is not impaired.4. They also respond with an enhanced hyperthermia to painful stimuli such as repeated pinching of the tail or repeated introduction of the thermometer probe into the rectum.5. The enhanced hyperthermias are not due to increased heat production but to impairment of the heat dissipating mechanisms, which in rats and guinea-pigs acts mainly through evaporation of saliva, and skin vasodilatation.6. Acylamides with pungent action related to capsaicin such as piperine, caprinoyl-p-aminophenol and propionyl vanillylamide also cause hypothermia followed by desensitization and their efficacy is dependent on their pungency. The non-pungent nonenoyl benzylamide produces neither hypothermia nor desensitization.7. Capsaicin and its related pungent acylamides appear first to stimulate and then to desensitize the hypothalamic warmth detectors. By stimulating them the acylamides evoke reflexly the hypothermic response, whereas after desensitization the protective thermoregulatory reflexes for heat dissipation are no longer activated in response to high ambient temperature and to painful stimuli.
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PMID:Irreversible impairment of thermoregulation induced by capsaicin and similar pungent substances in rats and guinea-pigs. 549 2

Capsaicin modulates animal pain perception, increasing chemosensitive and pressure thresholds following systemic administration, increasing thermal thresholds following intrathecal administration, and decreasing electric shock thresholds following intracerebroventicular (ICV) administration. Since morphine analgesia is decreased in a dose-dependent manner following ICV capsaicin, the present study examined whether ICV injections of capsaicin (0, 25, 50, 100 micrograms) would alter other analgesic responses as well. Experiment 1 demonstrated that the analgesic response to a 450 mg/kg dose of 2-deoxy-D-glucose was significantly reduced by the 25 and 50, but not the 100 micrograms capsaicin dose. Further, while analgesia induced by cold-water swims (CWS) in a 2 degrees C bath was significantly attenuated by the 25 micrograms capsaicin dose, the entire dose range eliminated analgesia induced by CWS in a 15 degrees C bath. Experiment 2 indicated that the capsaicin-induced alterations in CWS analgesia were not attributable to parallel changes in CWS hypothermia. Experiment 3 demonstrated that capsaicin failed to alter both the non-opioid analgesic response induced by 20 inescapable foot shocks (FS) and the opioid analgesic response induced by 80 FS. These data are discussed in terms of the similarities to and/or dissimilarities from capsaicin-induced effects upon morphine analgesia.
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PMID:Capsaicin treatment and stress-induced analgesia. 668 8

Naturally occurring pungent agents (zingerone, capsaicin), beside their hypothermic action, produced an anaesthesia-like state and/or potentiated hexobarbital sleeping time in rats. This effect was correlated to the sensory stimulating potency of these substances; actually non-pungent capsaicin congeners induced neither hypothermia nor anaesthesia. Capsaicin desensitization known to impair the function of the hypothalamic warmth detectors, greatly inhibited or completely abolished these responses. The anaesthetic action of some synthetic ketones possessing sensory stimulating effect was also greatly inhibited or abolished by capsaicin.
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PMID:Anaesthesia-like condition and/or potentiation of hexobarbital sleep produced by pungent agents in normal and capsaicin-desensitized rats. 739 32

Moderate hypothermia significantly diminishes consequences of spinal and cerebral anoxia. One component of this neuroprotection has been hypothesized to be suppression of excitotoxic transmitter release. Whether this suppression is attributable to reduced hypoxic injury that induces release or an alteration of the release process itself is unclear. We sought to characterize the temperature sensitivity (Q10) of basal and evoked calcitonin gene-related peptide (CGRP) and amino acid release from dorsal horn slices of rat spinal cord over a range of temperatures from 40 to 8 degrees C. At 40 degrees C, potassium (60 mM) and capsaicin (10 microM) evoked a 21- and 32-fold increase in basal CGRP concentrations, respectively. Capsaicin had no effect on glutamate release, but potassium evoked a 2.7-fold increase. Release evoked by either potassium or capsaicin was reduced in a biphasic fashion with declining temperature. Over the range of 40 to 34 degrees C, the Q10 values for evoked release for CGRP were 11.3 (potassium) and 39.7 (capsaicin) and for glutamate, 5. 5 (potassium). Over the range of 34 to 8 degrees C, Q10 values were near unity for all evoked release (0.8 and 1.3 for CGRP and 1.2 for glutamate). Although serine, glycine, glutamine, taurine, and citrulline showed no evoked release, basal levels were reduced at temperatures below 34 degrees C. The pronounced temperature dependency of evoked transmitter release between 40 and 34 degrees C is consistent with the profound cerebral protection observed with mild hypothermia in which metabolic activity is only slightly depressed.
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PMID:Temperature dependency of basal and evoked release of amino acids and calcitonin gene-related peptide from rat dorsal spinal cord. 915 57

Capsaicin, the vanilloid responsible for the pungent taste of hot peppers, binds to receptors found primarily in polymodal nociceptors. Capsaicin initially stimulates polymodal nociceptors and subsequently inhibits them from responding to a variety of stimuli. This property makes it useful clinically as an analgesic and anti-inflammatory compound. There is mounting, albeit indirect, evidence for the existence of several subtypes of vanilloid receptors. One such piece of evidence comes from studying analogues of capsaicin, such as phorbol 12-phenylacetate 13 acetate 20-homovanillate. This compound binds to (capsaicin) vanilloid receptors on sensory neurons, but unlike capsaicin it is non-pungent and does not produce hypothermia. To determine how sensory neurons respond to phorbol 12-phenylacetate 13 acetate 20-homovanillate, and to compare these responses with those evoked by capsaicin, whole-cell patch-clamp measurements were performed on cultured rat trigeminal ganglion neurons. It was found that 63% of the neurons held at -60 mV were activated by 3 microM, phorbol 12-phenylacetate 13 acetate 20-homovanillate, and 87% of these were also activated by 1 microM capsaicin. In a given neuron, phorbol 12-phenylacetate 13 acetate 20-homovanillate, like capsaicin, could activate kinetically distinct inward currents. The current-voltage curves characterizing phorbol 12-phenylacetate 13 acetate 20-homovanillate responses were asymmetric and had reversal potentials at -5.8 +/- 6.0 mV and 10.4 +/- 4 mV. The averaged dose-response curves for phorbol 12-phenylacetate 13 acetate 20-homovanillate were fit to the Hill equation and had binding constants (K(1/2)s) of 2.73 microM and 0.96 microM and Hill coefficients (ns) of approximately 1 for a rapidly- and slowly-activating current, respectively. These parameters are consistent with those obtained from binding experiments and calcium-influx experiments on sensory nerves. Repeated applications of phorbol 12-phenylacetate 13 acetate 20-homovanillate every 3 min caused a complete reduction in the rapidly-activating currents leaving only a reduced slowly-activating current. This provides strong evidence for the independence of these currents and the existence of subtypes of vanilloid receptors. Additional evidence for the existence of receptor subtypes is that 10 microM capsazepine, a specific and competitive inhibitor of capsaicin-evoked responses, did not inhibit the phorbol 12-phenylacetate 13 acetate 20-homovanillate-induced currents in some neurons and partially inhibited them in other neurons. Thus, there are capsazepine-sensitive and capsazepine-insensitive subtypes of vanilloid receptors. In summary, we have obtained electrophysiological and pharmacological evidence for distinct subtypes of vanilloid receptors.
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PMID:A non-pungent resiniferatoxin analogue, phorbol 12-phenylacetate 13 acetate 20-homovanillate, reveals vanilloid receptor subtypes on rat trigeminal ganglion neurons. 953 27

The delayed preconditioning of the heart by monophosphoryl lipid A is mediated by endogenous nitric oxide (NO), and the cardioprotection afforded by nitroglycerin is related to stimulation of calcitonin gene-related peptide (CGRP) release. The objective of this study was to explore whether improvement of preservation with cardioplegia by monophosphoryl lipid A is mediated by CGRP. In addition, we examined the effect of monophosphoryl lipid A on the tumor necrosis factor-alpha (TNF-alpha) content of myocardial tissues. The isolated rat heart was perfused in the Langendorff mode. Heart rate, coronary flow, left-ventricular pressure, and its first derivatives (+/-dp/dt(max)) were recorded, and plasma levels of NO and CGRP, the release of creatine kinase in coronary effluent and the content of TNF-alpha in myocardial tissues were measured. Hypothermic ischemia for 4 h caused a decline in cardiac function, and an increase in the release of creatine kinase and in the content of TNF-alpha. Pretreatment with monophosphoryl lipid A (500 microg/kg, i.p.) for 24 h improved the recovery of cardiac function and reduced the release of creatine kinase concomitantly with a decrease in the content of cardiac TNF-alpha. Monophosphoryl lipid A markedly increased plasma concentrations of CGRP and NO. After pretreatment with L-nitroarginine methyl ester (L-NAME), the cardioprotection and the increased release of NO and CGRP induced by monophosphoryl lipid A were abolished. Capsaicin also abolished the cardioprotection and the increased release of CGRP induced by monophosphoryl lipid A, but did not affect the content of NO. The results suggest that monophosphoryl lipid A-induced preconditioning enhances preservation with cardioplegia and that the protective effects of monophosphoryl lipid A are related to stimulation of CGRP release.
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PMID:Monophosphoryl lipid A-induced delayed preconditioning is mediated by calcitonin gene-related peptide. 1140 36

The medial preoptic nucleus (MPN) is the major nucleus of the preoptic area (POA), a hypothalamic area involved in the regulation of body-temperature. Injection of capsaicin into this area causes hypothermia in vivo. Capsaicin also causes glutamate release from hypothalamic slices. However, no data are available on the effect of capsaicin on synaptic transmission within the MPN. Here, we have studied the effect of exogenously applied capsaicin on spontaneous synaptic activity in hypothalamic slices of the rat. Whole-cell patch-clamp recordings were made from visually identified neurons located in the MPN. In a subset of the studied neurons, capsaicin enhanced the frequency of spontaneous glutamatergic EPSCs. Remarkably, capsaicin also increased the frequency of GABAergic IPSCs, an effect that was sensitive to removal of extracellular calcium, but insensitive to tetrodotoxin. This suggests an action of capsaicin at presynaptic GABAergic terminals. In contrast to capsaicin, the TRPV4 agonist 4alpha-PDD did not affect GABAergic IPSCs. Our results show that capsaicin directly affects synaptic transmission in the MPN, likely through actions at presynaptic terminals as well as on projecting neurons. Our data add to the growing evidence that capsaicin receptors are not only expressed in primary afferent neurons, but also contribute to synaptic processing in some CNS regions.
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PMID:Capsaicin augments synaptic transmission in the rat medial preoptic nucleus. 1586 12


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