Keiichi Ikegami

Carcinosarcoma of the ureter.

A rare case of carcinosarcoma of the ureter is reported. Histologically, this neoplasia was an unusual heterologous carcinosarcoma of the ureter. 2 years after the initial total nephroureterectomy, the patient died from recurrence.

Fungus ball formation of aspergillus in the bladder. an unusual case report.

An unusual case of fungus ball formation of Aspergillus in the bladder without any evidence of disseminated and renal aspergillosis is presented. A 49-year-old man whose chief complaint was progressively worsening dysuria after a stomach operation was admitted. Cystoscopy revealed many ball-like masses on the retrotrigone and left wall. Histological studies showed that these masses were composed of many Aspergilli. The uniqueness of the case and the route of infection are discussed.

Effects of Some Prostaglandins on Urinary Bladder and Urethra Isolated from the Dog

Effects of prostaglandins (PGs) E1, E2, E2 and F2 alpha on the vesical and urethral smooth muscles of dogs were isometrically investigated in vitro. In vesical smooth muscles, 10(-8)-10(-6) PGE1/ml produced biphasic responses in the dome preparations; relaxation at 10(-8) g/ml and contractions at 10(-7)-10(-6) g/ml. In the trigone preparations, 10(-8)-10(-6) g PGE1/ml caused dose-dependent contractions. 10(-8)-10(-6)M g PGE2/ml and 10(-7)-10(-6) g PGF2 alpha /ml induced dose-dependent contractions of the dome and the trigone preparations. In urethral smooth muscles, 10(-8)-10(-6) g PGE1/ml and 10(-8)-10(-6) g PGE2/ml produced dose-dependent relaxations, while 10(-8)-10(-6) g PGF2 alpha /ml caused dose-dependent contractions. Results indicate that PGE, particularly PGE2, is able to stimulate micturition through vesical contraction and urethral relaxation.

Effect of Adrenergic and Cholinergic Drugs on the Noradrenergic Transmission in Bladder Neck Smooth Muscle

Strips of bladder neck smooth muscle were isolated from the dog and noradrenaline stores in the peripheral sympathetic nerve terminals were labelled with (-)3H-noradrenaline. Transmural electrical stimulation was applied and the released radiolabeled noradrenaline in the superfusate was measured with a liquid scintillation counter. Autonomic drugs were administered in the superfusate to examine their effect on noradrenaline release evoked by electrical stimulation. The general conclusions drawn from the data are that: there are two autonomic receptor systems on sympathetic nerve terminals of bladder neck--alpha-adrenergic receptors and muscarinic receptors, the activation of alpha-adrenergic receptors or muscarinic receptors depresses noradrenaline release and parasympathetic nerve excitement inhibits noradrenaline release in bladder neck.

Chemotherapy for bladder cancer with neocarzinostatin: Evaluation of systemic administration☆

Abstract Thirty patients with newly diagnosed bladder cancer were treated with i.v. neocarzinostatin. In 2 patients (6.7%) , the tumors disappeared completely. In 16 patients (53.3%) , a reduction to less than half of the initial size of the tumor was observed. In another 5 patients (16.7%) , the tumor was moderately reduced in size. In 6 patients (20%) , no effect was observed cystoscopically. Tumor growth was seen in 1 patient (3.3%) . Anorexia, general fatigue, slight weight loss and leukopenia appeared in most patients. Slight increase of S-GOT level was detected in 3 patients. However, these side effects were reversible and disappeared with the interruption of chemotherapy. All patients underwent transurethral resection after chemotherapy. Up to this date, although the periods of observation after treatment were 12–46 months, 5 recurrences (16.7%) have occurred. The recurrence rate was 3.3% (130) within 6 months , 6.7% (230) within 1 yr and 26.3% (519) within 2 yr . These results suggest that neocarzinostatin may be of value in treatment of bladder cancer.

The Possible Role of Prostaglandin E2 in Urinary Stone Formation

To investigate the role of prostaglandin E2 in urinary stone formation, urinary prostaglandin E2 was measured by radioimmunoassay in 28 men with recurrent idiopathic urolithiasis (14 normocalciuric and 14 hypercalciuric patients) and 6 healthy male volunteers. Urinary prostaglandin E2 levels were significantly higher (p less than 0.01) in the hypercalciuric group than in the normocalciuric and healthy control groups, and they showed a positive correlation with urinary calcium excretion. Urinary prostaglandin E2 and calcium excretions in the hypercalciuric and normocalciuric groups were suppressed significantly by indomethacin. Creatinine clearance was not reduced by indomethacin. The results suggest that renal prostaglandin E2 may participate in calcium stone formation by regulating the renal tubular handling of calcium.

Role of sodium and renal prostaglandin E2 in the maintenance of hypertension in the chronic phase of two-kidney one-clip renovascular hypertension in rabbits.

To study the role of sodium and renal prostaglandin E2 in the chronic phase of two-kidney one-clip renovascular hypertension, urinary excretion rates of sodium and prostaglandin E2 were measured in rabbits with hypertension induced by left renal artery constriction during alteration in sodium intake. The arterial blood pressure, the increasing rate of body weight and sodium balance during alteration in sodium intake were directly proportional to the amount of sodium intake in the hypertensive rabbits, but not in the control ones. Plasma renin activity and plasma aldosterone concentration, which had no significant difference between hypertensive and control rabbits, were inversely proportional to the amount of sodium intake in both rabbits. Urinary excretion rates of sodium in the clipped kidneys of the hypertensive rabbits were significantly lower than the control values in all dietary regimens (p less than 0.01). Urinary excretion rates of sodium in the nonclipped kidneys were not significantly higher and in the total kidneys were significantly lower than the corresponding control values during sodium load (p less than 0.01). Urinary excretion rates of prostaglandin E2 were inversely proportional to the amount of sodium intake in both groups. Urinary excretion rates of prostaglandin E2 in the clipped kidneys were significantly lower than the control values in all dietary regimens (p less than 0.001). Urinary excretion rates of prostaglandin E2 in the nonclipped kidneys were significantly higher during sodium restriction (p less than 0.01) but not during sodium load than the control values. Furthermore, urinary excretion rates of prostaglandin E2 in the total kidneys were significantly lower than the control values in all dietary regimens (p less than 0.01). These results suggest that two-kidney one-clip renovascular hypertension in rabbits seems to be partly sodium-dependent in the chronic phase because the nonclipped kidney fails to excrete sodium sufficiently. There may also be disorders of renal prostaglandin E2 metabolism influencing these disorders of sodium in the nonclipped kidneys.

Pseudohyperaldosteronism (riddle’s Syndrome): A Case Report

AbstractA 22-year-old man was hospitalized because of hypertension, hypokalemic alkalosis and suppressed plasma renin activity. Although these findings were similar to hyperaldosteronism, plasma aldosterone concentration and urinary aldosterone excretion were lower than the normal range. Adrenocortical function also was normal except for aldosterone. Treatment with spironolactone, salt restriction and potassium supplementation improved the hypokalemia but not the hypertension. Blood pressure decreased markedly after administration of triamterene.

Role of Renal Prostaglandin E2 in Two-Kidney, One-Clip Renovascular Hypertension in Rabbits

To investigate the role of renal prostaglandin E2 (PGE2) in renovascular hypertension, urinary PGE2 was measured in rabbits with hypertension produced by left renal artery constriction. In the acute phase of renovascular hypertension (1 week after the constriction), urinary excretions of PGE2 and sodium were significantly increased without correlations with changes in the systemic blood pressure (delta BP). In this phase, delta BP was directly proportional to plasma renin activity and plasma aldosterone concentration (p less than 0.001). In the intermediate phase (5 weeks), delta BP lost significant correlations with plasma renin activity and plasma aldosterone concentration and had a inverse correlation with urinary sodium excretion (p less than 0.01). In the maintenance phase (10 weeks), delta BP showed inverse correlations (p less than 0.01) with both PGE2 and sodium excretions, although their excretions decreased to normal levels. In the clipped kidney, only urinary PGE2 excretion in the acute phase was significantly elevated (p less than 0.02), and both sodium and PGE2 excretions were significantly decreased (p less than 0.01) in the maintenance phase. In the nonclipped kidney, urinary PGE2 and sodium excretions were elevated in the acute and intermediate phases, but decreased to the control levels in the maintenance phase. In this phase, delta BP showed inverse correlation (p less than 0.01) with both PGE2 and sodium excretions from the nonclipped kidney. The infusion of saralasin, an angiotensin II analogue, dose dependently reduced the blood pressure in the acute phase, but showed no effect in the intermediate and maintenance phases.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of the Renal Prostaglandins in Furosemide-Induced Diuresis

The role of the renal prostaglandin (PG) system in the renal effects of furosemide was assessed by using indomethacin, an inhibitor of PG synthetase, in conscious rats under conditions of vasopressin infusion (or dehydration). Urinary PGE and PGF2 alpha were measured by radioimmunoassay under conditions of furosemide-induced diuresis. The diuretic and natriuretic effects of furosemide were accompanied by a concomitant increase in the urinary excretion of PGE. In normal rats the pretreatment of indomethacin at 10 mg/kg failed to alter the diuretic effect of furosemide (5 mg/kg). In contrast, the diuretic effect of furosemide in vasopressin (2 U/kg)-infused (or dehydrated) rats was greatly inhibited by indomethacin. In regard to the natriuretic effect of furosemide, indomethacin did impair this response to furosemide both in normal and vasopressin-infused (or dehydrated) rats, but inhibited more strongly in the latter than in the former. These results suggest that the renal PGE is necessary for furosemide to produce optimal diuretic and natriuretic effects under conditions of vasopressin infusion (or dehydration).