An opioid receptor-independent mechanism underlies motility dysfunction and visceral hyperalgesia in opioid-induced bowel dysfunction

Keyphrases

• Motility Disorders 100%
• Opioid Receptors 100%
• Visceral Hyperalgesia 100%
• Receptor-independent 100%
• Opioid-induced Bowel Dysfunction 100%
• Fecal Retention 85%
• Cyclooxygenase-2 57%
• Visceral Hypersensitivity 57%
• Nerve Growth Factor 42%
• Muscle Contractility 42%
• Colon 28%
• Constipation 28%
• Abdominal Pain 28%
• Morphine Treatment 28%
• Fecal Output 28%
• Clear Liquid Diet 28%
• Therapeutic Potential 14%
• Morphine 14%
• Rodent Models 14%
• Pathogenic Role 14%
• Dorsal Root Ganglion Neurons 14%
• Pathogenic Factors 14%
• Mechanotranscription 14%
• Smooth muscle 14%
• Smooth muscle Function 14%
• Colorectal Distension 14%
• Neuronal Excitability 14%
• Anti-nerve Growth Factor 14%
• Nerve Growth Factor Inhibitors 14%
• Visceromotor Response 14%
• Bowel Movement 14%
• Liquid Diet 14%
• Cellular Excitability 14%
• Colorectal Cells 14%

Medicine and Dentistry

• Hypersensitivity 100%
• Cyclooxygenase 2 100%
• Hyperpathia 100%
• Opioid Receptor 100%
• Muscle Contractility 75%
• Nerve Growth Factor 75%
• Morphine 75%
• Colon 50%
• Constipation 50%
• Smooth Muscle 50%
• Abdominal Pain 50%
• Excitability 50%
• Clear Liquid Diet 50%
• Upregulation 25%
• Muscle Function 25%
• Nerve Growth Factor Antibody 25%
• Dorsal Root Ganglion 25%
• Liquid Diet 25%
• Colonic Muscle 25%

Pharmacology, Toxicology and Pharmaceutical Science

• Opiate Receptor 100%
• Cyclooxygenase 2 100%
• Hyperalgesia 100%
• Erethism 100%
• Nerve Growth Factor 75%
• Morphine 75%
• Constipation 50%
• Abdominal Pain 50%
• Nerve Growth Factor Antibody 25%