| Abstract: |
SUMMARY AND CONCLUSIONNitric oxide has been shown to be a mediator of non adrenergic non cholinergic nerve induced smooth muscle relaxation. Some said that NO is the primary peripheral neurotransmitter involved in causing relaxation of the trigonal and urethral smooth muscle. Others, found that normal micturition reflex is relatively insensitive to endogenous NO.Outlet obstruction of the urinary bladder is a symptomatic condition that occurs as a result of either neurogenic or idiopathic factors, including benign prostate hyperplasia, urethral stricture, spina bifida or carcinoma, sclerosis, or fibrosis of the bladder neck.The exact role of L-arg/NO pathway in normal UB contractility and in cases of BOO remains unclear. The aim of the present study is to assess the effect of L-arg/NO pathway in normal UB contractility and in cases of BOO and to determine if L-arg has a protective function on UB in these cases or not.In the present study, 90 adult healthy white albino non pregnant non lactating female rats weighing (180-250gm) and isolated from male contact were used. The used animals were divided into three major groups: the first one is the control group (n=30) which is subdivided into three subgroups: one subgroup (n=10) for DRC estimation. Another subgroup (n=10) rats were given L-arg (150mg/kg b w/day IP for four weeks), then were studied for the probability of the presence of endogenous NO. The third subgroup (n=10) rats were examined to determine the effect of exogenous NO on normal UB contractility.The second group (n=30) which is the sham operated group. It was subdivided into three subgroups: the first one (n=10), were examined after four weeks using CCh (10-5M/ml) only. The second subgroup (n=10) were given (L-arg 150mg/kg b w/day IP for four weeks) after sham operation then were studied for the effect of endogenous NO. The third subgroup (n=10), examined for the effect of exogenous NO on sham operated UB contractility.The third group (n=30) underwent BOO, then, subdivided into three subgroups: the first subgroup (n=10), were examined after four weeks of BOO using CCh (10-5M/ml) only. The second subgroup (n=10) were given (L-arg 150mg/kg b w/day IP for four weeks) after BOO and were studied for the effect of endogenous NO. The third subgroup (n=10), were examined to determine the effect of exogenous NO on BOO UB contractility.From the data showed in the present study, it is clearly apparent that in the female rats, L-arg/NO pathway produced insignificant decrease in the amplitudes of the UB strip contractions in response to CCh in cases of normal UB.On the other hand, L-arg/NO pathway has a significant role in cases of BOO as it showed a significant decrease in UB strips weight in those rats taken L-arg in comparison with those not taken L-arg. Also, there was a significant increase in the amplitudes of the UB strip contractions in response to CCh in those rats taken L-arg in comparison with those not taken L-arg. This means that L-arg administration early in cases of BOO diminishes changes that occur in response to partial obstruction and improves bladder contractility.In conclusion, it is apparent that L-arg/NO pathway has no significant role in cases of normal UB function but, it is able to modulate the bladder response to BOO by keeping UB not markedly hypertrophied and preserving the contractile response of detrusor muscle strips to CCh.This modulative effect could explain the association of voiding dysfunction with cases of BOO such as urethral stricture, fibrosis of the bladder neck and benign enlargement of the prostate (in males).Moreover, this modulative effect of L-arg/NO pathway may be considered a physiological base for a recent trend in treatment of BOO.On the other hand, further work should be done to determine the effect of L-arg supplementation after a long period of BOO. Also, to determine, the effect of relief of chronic obstruction on retaining normal bladder function. Furthermore, to determine effect of other diseases like diabetes on BOO.
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