Carbon monoxide (CO) is known as a gaseous toxin, which is produced in tissues during the degradation of haemoblobin. Recently it has been shown that CO is a physiological vasodilator in blood circulation. As enteric neurons, the key players in the regulation of intestinal transport, express the enzymes for CO production, the aim of the present study was to investigate whether CO induces changes in ion transport and to study the mechanisms involved.

Mucosa-submucosa-preparations of the rat colon were voltage-clamped in an Ussing-chamber. In these preparations, tricarbonyldichloro-ruthenium(II) dimer (RuCO), a CO-donor, evoked a concentration-dependent increase in short-circuit current (ISC). The effect showed a strong segment-dependency, i.e. it was more pronounced in the distal compared to the proximal colon. Repeated application of RuCO resulted in a desensitivation of the tissue. Anion substitution experiments suggests that a secretion of chloride and bicarbonate underlye the RuCO-induced current. This is supported by transport inhibitor experiments, where glibenclamide, a blocker of the apical CFTR-channel, and bumetanide, a blocker of basolateral Na⁺-K⁺-2Cl^--transporter, inhibited the ISC after addition of the CO donor. A partial inhibition by the neurotoxin, tetrodotoxin, suggests the involvement of secretomotor neurons in this response.

In ongoing experiments, the stimulation of apical and basolateral ion conductances by CO shall be measured at epithelia, in which one membrane is permeabilized.