Effect of atropine and diclofenac on the contractility of dog's vesico-urethral smooth muscls vitro

Smooth muscle preparations from various parts of the vesicourethral system of dogs and cats were used. These were suspended in Tyrode's solution at 37°C, bubbled with carbogen. The contractile response was recorded through an isotonic muscle transducer on a chartmover. It was observed that while the response to the ganglion stimulant Dimethyl phenyl piperazinium [D, M.P.P] is variable i.e. contraction, relaxation or no response acetyl choline induced contraction in all specimens. In addition atropine escape phenomenon was not uniformly distributed.Also alpha and beta adrenergic blockers in combination with prostaglandins synthetase inhibitor can induce complete block in response to acetyl choline in areas where atropine escape phenomenon was observed.These observations, in addition to the constant demonstration of atropine escape phenomenon in our in vivo experiments, suggest that a central mechanism plays an important role in atropine escape phenomenon and this phenomenon is variable in our in vitro experiments. Also, prostaglandins may be partially responsible for atropine resistance of the detrusor

Effect of atropine and diclofenac on the contractility of dog's vesico-urethral smooth muscle in vivo

Female dogs were used, the bladder body was surgically separated from the trigone and urethra. A millar transducer was used to record the intravesical pressure.Another double channel transducer records pressure changes at the level of trigone and proximal urethra These transducers were connected to honeywell amplifier. The signals were recorded on a honeywell multichannel vesicorder. The response of the lower urinary tract of chemical or electrical stimulation was recorded as pressure changes which represent either contraction or relaxation. In vivo studies revealed that atropine can block 40% of detrusor and trigonal contractions and 30% of the proximal urethral contractions induced by both intra-arterial injection of dimethyl phenylpiperazinium [D.M.P.P] and electrical stimulation of pelvic nerves. The addition of adrenergic blockers did not block completely the contractions except in the proximal urethra where 90% of the contractile response was blocked. Thus atropine escape phenomenon was mainly manifested in the fundus and trigonal regions. Prostaglandins may be responsible for atropine escape phenomenon since diclofenac [prostaglandins synthetase inhibitor] and the multiple autonomic blockers can block about 90-95% of fundus and trigonal induced contractions meanwhile complete block in the proximal urethra was observed. Injection of prostaglandins after autonomic blockers and diclofenac led to contraction of the bladder body, trigone and urethra [PG F2alpha] and contraction of the bladder body and relaxation of trigone and urethra [PG E2]