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2015 Mechanismscontributingto visceral hypersensitivity
These factorscontributeto visceral hypersensitivity
2,4,6-Trinitrobenzene Sulfonic Acid - Induced Ileitis in Rats(passive) Is Provoked byVisceral Hypersensitivity
inflammation or stress without affecting basal sensitivity(passive) triggered byvisceral hypersensitivity
worked up set and the prime distressed systemleadingto visceral hypersensitivity
irritable bowel syndrome with diarrhea ( IBS - D ) or mixed irritable bowel syndrome ( IBS - M(passive) caused byvisceral hypersensitivity
The enteric nervous system in inflammation and pain :to causevisceral hypersensitivity
dysfunction of this systemcould ... causevisceral hypersensitivity
restraint stress(passive) provoked byvisceral hypersensitivity
overnight shipping the Teapot Domeleadingto visceral hypersensitivity
intracolonic administration of PAR-2-activating peptide ( SLIGRL ; H - serine - Ieucine - isoleucine - glycine - arginine - Ieucine - OH(passive) provoked byvisceral hypersensitivity
LPS - induced inflammation ... increased mesenteric afferent dischargemay contributeto visceral hypersensitivity
peripheral and central mechanisms affecting pain perception(passive) can be influenced byVisceral hypersensitivity
early life stressmay triggervisceral hypersensitivity
NMS ... synaptic plasticityresultsin visceral hypersensitivity
In response to a triggering event such as inflammation , environmental stress , psychological stress , or trauma , the gut becomes sensitised to luminal distensionresultingin visceral hypersensitivity
We utilize knockout animals and experimental models of disease including ischaemia , inflammation and nerve injury modelsto provokevisceral hypersensitivity
a detailed explanation as to the cascade of eventsleadto visceral hypersensitivity
patients experiencing chronic abdominal pain to suffer increased pain perception.11 Peripheral inflammation and recurrent acute paincontributeto visceral hypersensitivity
The endogenous hydrogen sulfide producing enzyme cystathionine - β synthasecontributesto visceral hypersensitivity
The endogenous hydrogen sulfide producing enzyme cystathionine - beta synthasecontributesto visceral hypersensitivity
the increased level of these cytokines ... an important contributory factorcausesvisceral hypersensitivity
activation of calcium channels such as transient receptor potential vanilloid 4 ( TRPV4causesvisceral hypersensitivity
Symptoms may result from an alteration in the transfer of messages between the enteric nervous set and the prime nervous set - upleadingto visceral hypersensitivity
the brain - gut axispromptsvisceral hypersensitivity
persistent neuronal hyperactivityresultsin visceral hypersensitivity
Symptoms may result from an variant in the dispatching of messages between the enteric troubled organization and the prime uptight set - upleadingto visceral hypersensitivity
gastrointestinal sensory input with resulting pain , irritability , or feeding intolerance(passive) caused byVisceral hypersensitivity
Symptoms may denouement from an other in the transmission of messages between the enteric nervous system and the principal uptight systemleadingto visceral hypersensitivity
Symptoms may result from an in rotation in the transmission of messages between the enteric nervous combination and the central fidgety set - upleadingto visceral hypersensitivity
Symptoms may d‚nouement develop from an other in the dispatching of messages between the enteric nervous organization and the central uptight methodleadingto visceral hypersensitivity
Symptoms may result from an in rotation in the movement of messages between the enteric troubled set and the principal fidgety methodleadingto visceral hypersensitivity
sensitization of primary afferentscontributesto visceral hypersensitivity
the basal nervedischarge ratecausingvisceral hypersensitivity
Symptoms may denouement from an in rotation in the transfer of messages between the enteric troubled organization and the primary uptight patternleadingto visceral hypersensitivity
poor communication between the gut and braincausesvisceral hypersensitivity
worked up combination and the primary fidgety patternleadingto visceral hypersensitivity
Symptoms may d‚nouement develop from an in rotation in the transmission of messages between the enteric nervous organization and the prime fidgety methodleadingto visceral hypersensitivity
TRPA1causesvisceral hypersensitivity
activation of the transient receptor potential cation channels ( TRP ) TRPV1 , TRPV4 , andcausesvisceral hypersensitivity
unexplained abdominal pain syndromescausesunexplained abdominal pain syndromes
for development of chronic abdominal paincontributesfor development of chronic abdominal pain
some of the abdominal pain that affects some people with IBS(passive) may be caused bysome of the abdominal pain that affects some people with IBS
to IBS paincan contributeto IBS pain
to the symptom of painleadsto the symptom of pain
noncardiac chest paincausingnoncardiac chest pain
perception of pain even for minimal abdominal distensioncausingperception of pain even for minimal abdominal distension
from upregulation of nociceptive pathways by peripheral and central sensitization and psycho neuroimmune interactionsresultingfrom upregulation of nociceptive pathways by peripheral and central sensitization and psycho neuroimmune interactions
in contusion , laceration or avulsionmay resultin contusion , laceration or avulsion
from both host factors and other diseasesmay resultfrom both host factors and other diseases
after exposure to stress , which would increase the severity of discomfort ( Diop et al . 2008can resultafter exposure to stress , which would increase the severity of discomfort ( Diop et al . 2008
in symptom reporting under physiologic conditionsmay resultin symptom reporting under physiologic conditions
symptoms so medications like amitriptyline might helpmay be causingsymptoms so medications like amitriptyline might help
alsocontributesalso
to changes in intestinal motility and secretionmay also leadto changes in intestinal motility and secretion
from differences in cortical processingresultingfrom differences in cortical processing
in symptoms with even the slightest disturbanceresultingin symptoms with even the slightest disturbance
to lower sensation thresholds in the GI systemleadsto lower sensation thresholds in the GI system
toward the junction between the first administered at months postpartum and postabortion infectionsmay resulttoward the junction between the first administered at months postpartum and postabortion infections
to the induction of an abdominal discomfortleadingto the induction of an abdominal discomfort
in fatal or non steroidal antiinflammatory drugs for adults or oldermay resultin fatal or non steroidal antiinflammatory drugs for adults or older
to the perception of GERD symptoms At presentcontributesto the perception of GERD symptoms At present
from increased signal transmission between dorsal horn neurons and the brainresultingfrom increased signal transmission between dorsal horn neurons and the brain
to an improvement in symptoms of IBS13could ... leadto an improvement in symptoms of IBS13
to intepretation of normal body stimulus as abnormalleadingto intepretation of normal body stimulus as abnormal
the GI symptoms all alongcould have causedthe GI symptoms all along
the majority of FGID symptomscausesthe majority of FGID symptoms