Life sciences
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The present study analyzed the potential antinociceptive effect of the antimigraine drugs sumatriptan, dihydroergotamine or methysergide in rats submitted to the formalin test. Moreover, by using selective antagonists, the role of 5-HT1B/1D serotonergic receptors was investigated in the antinociception induced by these antimigraine drugs. ⋯ The above findings suggest that: (i) the antimigraine drugs sumatriptan, methysergide and dihydroergotamine reduce the acute and chronic nociception induced by formalin; and (ii) this antinociceptive effect results from activation of peripheral 5-HT1B/1D serotonergic receptors.
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Comparative Study
Desflurane but not sevoflurane augments laryngeal C-fiber inputs to nucleus tractus solitarii neurons by activating transient receptor potential-A1.
Volatile anesthetics have distinct odors and some are irritating to the upper airway and may cause cough and laryngospasm, which may result, in part, from stimulation of C-fiber reflex. Local exposure of such anesthetics increases the sensitivity of capsaicin-sensitive laryngeal C-fiber endings compatible with airway irritability presumably by activation of transient receptor potential (TRP) ion channels, but the physiological relevance of this sensitization transmitted to the higher-order neurons in the central reflex pathway and output is unknown. ⋯ Thus, the sensitization of the laryngeal C-fiber endings by irritant volatile anesthetics is transmitted to the NTS via activation of the TRPA1 and is associated with a prolonged reflexively evoked expiratory apnea. The findings may help to explain local deleterious effects of irritant volatile general anesthetics on the airways during inhaled induction or bronchodilator therapy for status asthmatics.
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Recently, we demonstrated that peripheral antinociception induced by δ opioid receptor is dependent of Ca(2+)-activated Cl(-) channels (CaCCs). Because opioid and cannabinoid receptors share some common mechanisms of action, our objective was to identify a possible relationship between CaCCs and the endocannabinoid system. ⋯ These results provide the first evidence for the involvement of CaCCs in the peripheral antinociception induced by activation of the CB1 cannabinoid receptor.
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Trauma/hemorrhagic shock (T/HS) induced gut injury is known to initiate a systemic inflammatory response which can lead to secondary lung injury. We have shown that vagal nerve stimulation (VNS) protects intestinal epithelial integrity after a severe burn insult. We hypothesize that VNS will protect the lung from injury following T/HS by preventing intestinal barrier failure. ⋯ VNS is effective in protecting against acute lung injury caused by hemorrhagic shock through its ability to prevent gut barrier dysfunction.
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The endogenous cannabinoid anandamide (AEA) exerts the majority of its effects at CB1 and CB2 receptors and is degraded by fatty acid amide hydrolase (FAAH). FAAH KO mice and animals treated with FAAH inhibitors are impaired in their ability to hydrolyze AEA and other non-cannabinoid lipid signaling molecules, such as oleoylethanolamide (OEA) and palmitoylethanolamide (PEA). AEA and these other substrates activate non-cannabinoid receptor systems, including TRPV1 and PPAR-α receptors. ⋯ Indeed, pharmacological and genetic FAAH disruption in mice enhances nicotine reward and withdrawal. However, in rats, pharmacological blockade of FAAH significantly inhibits nicotine reward and has no effect in nicotine withdrawal. Studies suggest that non-cannabinoid mechanisms may play a role in these species differences.