Objective—To determine effects of short-chain fatty
acids (SCFA) on canine colonic smooth muscle.
Sample Population—Colonic tissue obtained from
14 healthy dogs.
Procedure—Short-chain fatty acid (SCFA; acetate,
propionate, and butyrate; 1 to 100 mmol/L)-induced
contractions were compared with responses
obtained with acetylmethylcholine (AMCh; 10-4 mol/L).
Roles of enteric neurons, cholinergic receptors, calcium
stores in the sarcoplasmic reticulum, and extracellular
calcium in the SCFA-induced responses were
investigated by incubating muscle strips with
tetrodotoxin (1 µmol/L), atropine (1 µmol/L), ryanodine
(10 µmol/L), nifedipine (1 µmol/L), ethylene glycol-bis (β-aminoethylether)-N,N,N',N'-tetra-acetate
(EGTA; 0.1 mmol/L), or an extracellular calciumdepleted
(zero extracellular calcium) solution prior to
the addition of propionate or butyrate.
Results—Incubation with SCFA elicited isometric
stress responses (0.25 to 2.15 × 104 N/m2) in colonic
longitudinal smooth muscle. Maximal responses to
butyrate and propionate (50 mmol/L) were 37 and
23%, respectively, of the maximal AMCh response.
Acetate was least effective in stimulating contractile
responses. Tetrodotoxin and atropine did not affect
SCFA-induced contractions. Nifedipine and zero extracellular
calcium solution abolished responses to
butyrate and propionate, whereas EGTA attenuated (>
60%) but did not abolish those responses. Ryanodine
did not affect SCFA-induced contractile responses.
The SCFA did not affect colonic circular smooth muscle.
Conclusions and Clinical Relevance—The SCFA
stimulate longitudinal but not circular colonic smooth
muscle contractions via a direct effect on smooth
muscle. The mechanism of the SCFA effect appears
to involve the influx of extracellular calcium. These
findings may account for some of the effects of
canine colonisc motility. (Am J Vet Res 2002;63:295–300 )