ABSTRACT
PURPOSE: In order to compare stone metabolic risk factors in recurrent stone formers, we researched lithogenic factors according to sex and age. MATERIALS AND METHODS: We performed stone metabolic studies on recurrent stone formers (77 men, 33 women) and grouped them according to age; under 40 (n=38), from 40 to 59 (n=56) and over 60 (n=16). We evaluated excretion rate differences of lithogenic and inhibitory constituents such as volume, sodium, uric acid, calcium, oxalate, and citrate from 24-hour urine samples, and calcium, sodium, uric acid, phosphate, potassium, and chloride from serum samples. We analyzed the incidence of stone metabolic risk factors between the age groups and the sexes. RESULTS: The most common detectable risk factor in all groups of recurrent stone formers was hypocitraturia. This finding was more remarkable in males aged under 60. The incidence of hypocitraturia was higher in males and in the younger group, whereas hypercalciuria was more frequent in the elder group. CONCLUSIONS: The most important cause of urolithiasis was hypocitraturia in recurrent stone formers, and this was apparent in males aged under 60.
Subject(s)
Humans , Male , Calcium , Citric Acid , Hypercalciuria , Incidence , Potassium , Risk Factors , Sodium , Uric Acid , UrolithiasisABSTRACT
PURPOSE: There is little data on the effects of botulinum toxin A (BoTx A) on detrusor muscle published in the literature. An experimental study was conducted to investigate the effect of BoTx A on the detrusor muscle in rats. MATERIALS AND MTHODS: Sprague-Dawley rats were used to make the detrusor muscle strip (length: 8mm, width: 2mm). An isometric force transducer in the physiologic salt solution was used to measure the contraction and relaxation of this muscle strip. A contraction was induced by acetylcholine (ACh) and electrical field stimulation (40V, 20Hz, 3sec), and relaxation was induced by verapamil and sodium nitroprusside. The BoTx A concentration was 0.1U/ml. The relaxation and contraction of the detrusor muscle in the BoTx A-treated group were analyzed and compared with those in the control group. RESULTS: The time to the maximum contraction induced by electrical field stimulation was lengthened and the time of recovery to the basal state after terminating electrical field stimulation was also increased by BoTx A (p<0.05). However, the contractile reaction induced by ACh and the relaxing reaction induced by verapamil and sodium nitroprusside after maintaining the maximum contraction induced by ACh 10 4M was not influenced by BoTx A. CONCLUSIONS: The results of this experimental study suggest that the time delay of the maximum contraction induced by electrical field stimulation occurred by blocking ACh release at the neuronal endings and the time delay of the recovery to the basal state after terminating electrical field stimulation occurred by reducing cholinesterase activity.
Subject(s)
Animals , Rats , Acetylcholine , Botulinum Toxins , Cholinesterases , Neurons , Nitroprusside , Rats, Sprague-Dawley , Relaxation , Transducers , Urinary Bladder , VerapamilABSTRACT
PURPOSE: There is little data on the effects of botulinum toxin A (BoTx A) on detrusor muscle published in the literature. An experimental study was conducted to investigate the effect of BoTx A on the detrusor muscle in rats. MATERIALS AND MTHODS: Sprague-Dawley rats were used to make the detrusor muscle strip (length: 8mm, width: 2mm). An isometric force transducer in the physiologic salt solution was used to measure the contraction and relaxation of this muscle strip. A contraction was induced by acetylcholine (ACh) and electrical field stimulation (40V, 20Hz, 3sec), and relaxation was induced by verapamil and sodium nitroprusside. The BoTx A concentration was 0.1U/ml. The relaxation and contraction of the detrusor muscle in the BoTx A-treated group were analyzed and compared with those in the control group. RESULTS: The time to the maximum contraction induced by electrical field stimulation was lengthened and the time of recovery to the basal state after terminating electrical field stimulation was also increased by BoTx A (p<0.05). However, the contractile reaction induced by ACh and the relaxing reaction induced by verapamil and sodium nitroprusside after maintaining the maximum contraction induced by ACh 10 4M was not influenced by BoTx A. CONCLUSIONS: The results of this experimental study suggest that the time delay of the maximum contraction induced by electrical field stimulation occurred by blocking ACh release at the neuronal endings and the time delay of the recovery to the basal state after terminating electrical field stimulation occurred by reducing cholinesterase activity.
Subject(s)
Animals , Rats , Acetylcholine , Botulinum Toxins , Cholinesterases , Neurons , Nitroprusside , Rats, Sprague-Dawley , Relaxation , Transducers , Urinary Bladder , VerapamilABSTRACT
Female sexual dysfunction is now of great concern and have a relatively high prevalence. It is related with psychosocial disorder, organic disease and iatrogenic cause. But until recently, basic science and clinical study on it is limited and medical therapy stays in early experimental steps except conventional hormone replacement therapy. Hormonal based female sexual dysfunction can be caused by dysfunction of the hypothalamic-pituitary axis, surgical or medical castration, menopause and premature ovarian failure. We report two cases of female sexual dysfunction derived from hormonal deficiency. One case is about premature menopause induced and the other is about rare form of adult onset idiopathic hypogonadotropic hypogonadism.