Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cough reflex originates from stimulation of sensory nerve endings located in the upper and lower respiratory tract. Opiates are among the most potent and widely used drugs which inhibit the cough reflex, and it has been generally assumed that they act generally. However, opioid receptors have been identified on the sensory arm of the vagus nerve. Although the functional significance of these receptors is not clear, recent evidence suggests that their activation may be involved in the modulation of airway reflexes. This review briefly examines the evidence to support the hypothesis that opioid receptors on vagal sensory nerves may mediate peripheral opioid-induced antitussive activity.
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PMID:Peripheral opioid receptors and the cough reflex. 185 31

Opiates are known for their stereospecificity. The following studies show that l-codeine was active in the mouse tail-flick test as well as in the hot plate test whether given p.o. or s.c. The ED50 in the first test was 4.09 mg/kg s.c. (2.01-8.34 mg/ kg) and 13.41 mg/kg p.o. (6.91-26.0 mg/kg). In the second antinociceptive test, the ED50 was 20.66 mg/kg s.c. (11.52-37.08 mg/kg) and 20.47 mg/kg p.o. (14.63-28.57 mg/kg). The d-isomer of codeine was inactive ina both tests up to 100 mg/kg but caused hyperexcitability, convulsions and ultimately death. Although l-codeine was more potent than d-codeine inhibiting the cough reflex in the anesthetized cat, the d-compound did have good activity. The ED50 of the l-isomer was 0.27 mg/kgi.v. (0.14-0.47 mg/kg) and that of the d-isomer was 1.61 mg/kg i.v. (0.98-2.65 mg/kg). In these animals, l-codeine did not significantly affect the cardiovascular parameters at the doses tested, whereas d-codeine caused a significant but transient decrease in the blood pressure and heart rate. The specific and nonspecific properties of d- and l-codeine were further delineated in the opiate receptor binding assay. l-Codeine inhibited the stereospecific binding of 2.2 x 10(-9) M [3H]dihydromorphine in mouse brain homogenate with the IC50 being 1.6 x 10(-5) M (1.2 x 10(-5)--2.0 x 10(-5) M). d-Codeine had no effect up to 10(-4) M.
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PMID:Comparative studies of the pharmacological effects of the d- and l-isomers of codeine. 625 35

Opiates, such as morphine, are typically employed to alleviate acute or chronic pain states. However, there are a myriad of side effects including constipation, nausea, respiratory depression, cough suppression, vomiting, sedation, addiction and tolerance. It has also been reported experimentally and clinically that exposure to opiate can elicit paradoxical pain (opiate-induced tactile hyperalgesia; OIH) in regions of the body unrelated to the initial pain complaint. Several mechanisms have been suggested to be responsible for OIH such as sensitization of peripheral nociceptors, enhanced production/release of glutamate and neuropeptides in the spinal cord, protein kinase C gamma-induced signaling, and/or enhanced descending facilitation of nociceptive pathways from the rostral ventromedial medulla; however signaling pathways known to lead to directly to OIH remain undiscovered. Recent publications from our laboratory and others have discovered a potentially important link to OIH that involves the chemokine (chemotactic cytokine), stromal-derived factor 1 (SDF1 also known as CXCL12) and its cognate receptor CXCR4.
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PMID:Opiate-induced hypernociception and chemokine receptors. 1960 47

Asthma is a common chronic inflammatory disorder of the airways associated with hyperresponsiveness, reversible airflow limitation and respiratory symptoms.1 All patients with asthma are at risk for exacerbations that may range from mild to life threatening. Different triggers cause asthma exacerbation by inducing airway inflammation and/or provoking bronchospasm. Allergen-induced bronchospasm results from IgE-dependent release of mediators including histamine, prostaglandins and leukotrienes.2 Opiates are commonly used to treat chronic pain.3 Although hypersensitivity to opiates or accumulation of opiates can cause respiratory depression, opiates are also used in the management of cough and dyspnoea associated with advanced COPD and heart failure.4(,)5 Here, a report is presented on a patient who developed persistent exacerbation of underlying stable asthma after initiating fentanyl transdermal therapy for chronic low back pain. He underwent extensive investigations and a detailed reassessment of history, especially medication history, led to the possible causative factor; once recognised, removal of the offending agent (fenatnyl) resulted in complete improvement in his symptoms within 72 h.
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PMID:Exacerbation of asthma secondary to fentanyl transdermal patch. 2168 75