Abstract

Immediately after spinal cord transection, normal bladder reflex activity is lost and voiding contractions in response to cholinergic drugs can no longer be elicited. Intravesical pressure responses to s.c. and i.a. bethanechol were studied in male cats before and after spinal cord transection at T6 to T7. Bethanechol s.c. enhanced spontaneous bladder activity and produced a sustained bladder contraction. The sustained response was abolished by spinal transection. The response of the bladder to i.a. bethanechol consisted of two phases. The first, dose-related phase, which resembled the response to i.a. acetylcholine, was unchanged by spinal cord transection, rhizotomy (L7-S3) or by ganglion blockade with hexamethonium. The second sustained phase, like the s.c. response, was markedly reduced by all three treatments. Because the response to bethanechol in vitro did not differ in control and transected preparations, it is unlikely that the depressant effects are due to a persistent change in bladder muscle responsiveness. No contractions were observed regardless of s.c. injection site; hence, altered drug absorption and distribution are not sufficient to explain the diminished responses observed. Because interruption of pelvic parasympathetic reflex pathways by rhizotomy and ganglion blockade interfered with the responses to s.c. and i.a. bethanechol, we conclude that bethanechol requires intact pelvic reflex pathways in order to produce sustained contractions. The prolonged action of bethanechol is an important feature contributing to its effectiveness. Removal of reflex functions by spinal cord transection might explain the ineffectiveness of cholinergic drugs in both patients and experimental animals in the acute, areflexic stage after spinal cord transection.