From:
Sukie Crandall
Date: 2008-10-18 21:04:03 UTC
Subject: [ferrethealth] abstract: gastric reflux
To: fhl <ferrethealth@yahoogroups.com>
Now, anyone who has had ferrets long enough knows they can and do burp
(transient LOS relaxation (TLOSR) normally allowing venting of gas),
but I hadn't thought about gastric reflux among ferrets. I wonder if
-- like in humans -- Helicobacter infection makes reflux less
likely? I know that in a human epidemiological study not only did
reflux increase with strict control of Helicobacter but esophageal
malignancy rates increased. So, for people at least there is no
perfect solution, and I wonder if that also is the case for ferrets.
Begin Quoted abstract.
Eur Rev Med Pharmacol Sci. 2008 Aug;12 Suppl 1:33-9.
New insights in the neural regulation of the lower oesophageal
sphincter.
Blackshaw LA.
Nerve Gut Research Laboratory, Department of Gastroenterology,
Hepatology and General Medicine, Hanson Institute, Royal Adelaide
Hospital, Australia.
Gastro-oesophageal reflux disease (GORD) is caused by disordered
control of the gastro-oesophageal reflux barrier, comprised internally
of the lower oesophageal sphincter (LOS) and externally the crural
diaphragm (CD). Both relax briefly to allow bolus passage during
oesophageal peristalsis. Brief relaxation also occurs prior to gastro-
oesophageal reflux, known as transient LOS relaxation (TLOSR),
normally allowing venting of gas. TLOSRs also account for up to 90% of
acid reflux episodes. The development of GORD therefore depends upon
the rate of TLOSR and the physical and chemical nature of refluxate.
We established an animal model of reflux in ferrets, in which similar
patterns of TLOSR are seen to humans. TLOSRs are mediated via a vago-
vagal pathway initiated by tension receptors in the gastric
musculature. They have central terminals in the brainstem which
provide input to a central program generator. The program has 3
simultaneous outputs: 1. brief activation of vagal motor neurones to
the LOS, which activate inhibitory enteric motorneurones, leading to
smooth muscle relaxation: 2. suppression of oesophageal peristalsis:
3. suppression of motor output to the CD. We have investigated several
aspects of the TLOSR pathway in ferrets, and determined that the
optimal site for therapeutic pharmacological intervention is at
gastric vagal tension receptor endings. Their responses to distension
are potently inhibited by gamma-aminobutyric acid type B (GABAB)
receptor agonists and metabotropic glutamate type 5 receptor (mGluR5)
antagonists. These effects translate to inhibition of TLOSR and reflux
in animal models and humans. Clinical studies indicate both types of
drug may have potential in the treatment of GORD.
PMID: 18924442
End Quoted Abstract
http://www.europeanreview.org/articolo.php?id=514
Sukie (not a vet)
Recommended ferret health links:
http://pets.groups.yahoo.com/group/ferrethealth/
http://ferrethealth.org/archive/
http://www.afip.org/ferrets/index.html
http://www.miamiferret.org/fhc/
http://www.ferretcongress.org/
http://www.trifl.org/index.shtml
http://homepage.mac.com/sukie/sukiesferretlinks.html
[Non-text portions of this message have been removed]
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