Prostaglandins (PGs) are well known as one of the chemical mediators of infl ammation. Nonsteroidal anti-infl ammatory drugs (NSAIDs), PG synthesis inhibitors, are used for anti-nociception and/or anti-infl ammation. We examine the effect of loxoprofen, an NSAID, on micturiton in acetic acid-induced bladder infl ammation of the rats. In cystometrogram study with saline infusion into the urinary bladder, loxoprofen did not alter the interval of bladder contraction (IC, 107% of the control). IC was shortened by acetic acid infusion (65% of the control) and loxoprofen prolonged the IC (162% of acetic acid infused period). This prolonged IC was approximately same as the control. Loxoprofen did not alter the threshold pressure and the maximal voiding pressure. These data suggest that PGE 2 might not play a part of normal micturition and may play a part of the micturition refl ex during acetic acid infusion. That is, loxoprofen might be useful for pathological hyperrefl ex of the micturition.Urinary bladder controls two different physiological stages; storage of urine and micturition refl ex. Previous studies have mainly investigated the reflex pathway of the micturition (5, 25). In contrast, recent studies were interested in the storage mechanisms because over active bladder was commonly seen in elder people (2,8,21). During storage of the urine in the bladder, smooth muscles were stretched and it activated the afferent fi bers in the pelvic nerve (18). The activities were mediated through the sacral spinal cord and it stimulated the potine micturition center (6).When inflammation of the urinary bladder occurred, painful sensation was noticed and frequency of the micturition were increased (14). As indicated in many reports, infl ammation of the urinary bladder could excite the detrusor muscles with chemical mediators (17) and activate the afferent nerve terminals (1, 7).Prostagrandins (PGs) have been investigated for one of the chemical mediators of the infl ammation. In general, cyclooxgenase (COX) isoenzymes synthesize PGs from arachidonic acid at many organs including bladder smooth muscles and urothelium (4, 15). Indeed, PGE 2 in the urine was increased at the interstitial cystitis patients (11). Recent animal studies also demonstrated that COX-2 and PGE 2 were increased in cystitis rats (9, 24). Thus PGE 2 must be important for changing the micturition refl ex of the bladder infl ammation.Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used for treatment of the infl ammation. Under anesthesia, NSAIDs increased the bladder capacity during the infl ammation in rats (23). It has been reported that anesthesia have infl uence to the micturition refl ex (26). So unanesthetized animals experiments must be performed. Hence we used

Sirs: We report a case of fatal sepsis complicating rhabdomyolysis on the extremities. A 67-year-old man was referred to our hospital complaining of upper abdominal pain, vomiting, and diarrhea for 1 week in October 1999. He had also suffered from severe muscle pain bilaterally in the anterior arms and distal legs beginning 1 day previously. He had suffered from chronic alcoholic pancreatitis, diabetes mellitus, and alcoholic liver cirrhosis for 5 years. Physical examination revealed a temperature of 39.3 C, blood pressure 176/ 64 mmHg, heart rate 84/min, and respiratory rate 50/min. Consciousness was clear, and no cyanosis was observed. He had slight tenderness in the upper abdominal lesion, and the extremities were extremely swollen with severe pain. Laboratory examination revealed normal blood cell counts except for a platelet count of 90,000/ mm 3 . Slight icterus and slight renal dysfunction were detected. Although serum creatine-phosphokinase level was high at 12500 IU/l, electrocardiography revealed no significant ST-T wave changes. Arterial blood gas examination suggested metabolic acidosis without hypoxia. Plain chest radiography revealed no abnormal findings, but plain abdominal radiography showed a large amount of gas in the small intestine. Acute exacerbation of chronic pancreatitis was initially suspected, but abdominal computed tomography revealed no findings of pancreatitis. Given the severe muscle pain and elevation in serum creatinephosphokinase level, rhabdomyolysis was suspected. Blood cultures were performed, and cefmetazole sodium was given intravenously. However, shock developed within a few hours. Although cardiopulmonary resuscitation was attempted, he died 5 h after admission. Vibrio vulnificus was detected in blood cultures, and death appeared to be due to V. vulnificus septic shock.Infection with V. vulnificus is one of the most severe of all food-borne infectious diseases and causes severe, fulminant sepsis principally in patients with chronic liver diseases [1]. V. vulnificus sepsis has also been reported in immunocompromised hosts such as hemodialyzed patients [2]. Mortality associated with sepsis from V. vulnificus infection is very high, over 50 % or even 90 % in the cases of patients with hypotension manifested within 12 h of the clinical examination [3]. Among patients with primary septicemia a history of raw oyster ingestion or seawater exposure is the prominent epidemiological feature [3]. In this case the patient often ate sushi, and may thus have eaten contaminated seafood. Up to 75 % of primary V. vulnificus septicemia cases develop secondary skin lesion, often noticed within 36 h of the onset of illness. Usually found on the extremities, these skin lesions are erythematous and tender. They may evolve to bullae formation, necrotic ulceration, or even gangrene with major vessel occlusion. Histopathology may show cellulitis with necrosis of subcutaneous fibroadipose tissue and transmural necrotizing vasculitis [4]. About 7 % of bacterial sepsis patients develop rhabdomyolysis,...

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