Hidehisa Soejima

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.

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)

Pheochromocytoma of the Spermatic Cord: A Case Report

A case of pheochromocytoma arising from the left spermatic cord in a 52-year-old man is presented. The tumor had been present for about 10 years without hormonal symptoms. A diagnosis of pheochromocytoma was presumed because of a marked elevation of blood pressure at operation.

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).

Intrarenal Prostaglandins: Effect of Sodium and Indomethacin on PGE2 and PGF2α in Rabbits

The levels of prostaglandins (PGS) E2 and F2α in different parts of the rabbit kidney were determined to observe the effect of sodium and indomethacin. After the pretreatment with injections of saline or with indomethacin, tissues from inner and outer medulla and cortex were separated, extracted, analyzed for PGE2 and PGF2α by radioimmunoassay. In the normal rabbit kidney, the greatest amount of PG was found in the inner medulla. Saline injections appeared to increase PGE2 (but not PGF2α), especially in the inner medulla. Repeated injections of saline, on the other hand, markedly reduced PGE2 in the inner medulla but increased outer medullary PGE2. Indomethacin reduced the production of PGS in all kidney segments. These results suggest the bidirectional effect of sodium on PG concentration in the rabbit kidney. Acute administration of sodium may directly stimulate the synthesis of PGE2 in the inner medulla but chronic stimulation with sodium may alter the pattern of PGE2 synthesis.

Studies on Intrarenal Prostaglandins

The unilateral renal artery in rabbits was constricted, and lipid droplet count in the medullary interstitial cells of the ‘opposite’ kidney was performed 1 week after surgery. Lipid droplet count in

Interrelationships between the Renal Kallikrein-Kinin and Prostaglandin Systems in Furosemide-Induced Diuresis

The relationships between the renal kallikrein-kinin (K-K) and prostaglandin (PG) systems under conditions of furosemide-induced diuresis were studied in normal rats. Urinary PGE and PGF2 alpha were measured by radioimmunoassay, and urinary kallikrein by enzymatic activity. The diuretic and natriuretic effects of furosemide were accompanied by a concomitant increase in the urinary excretion of kallikrein and PGE. The urinary excretion of kallikrein and PGE was closely related to the urinary excretion of sodium, potassium and chloride. The urinary excretion of kallikrein also showed a highly significant correlation with the urinary excretion of PGE. Pretreatment of the animal with indomethacin or aprotinin inhibited furosemide-induced diuresis and natriuresis. Aprotinin inhibited the urinary excretion of PGE, while indomethacin did not exert any inhibitory action on the urinary excretion of kallikrein. Although the urinary excretion of kallikrein was closely related to the urinary excretion of potassium, both indomethacin and aprotinin had no effect on the urinary excretion of potassium. The results indicate that the potassium-sodium exchange caused by furosemide in the distal nephron might stimulate the renal K-K system to result in increasing synthesis of PGE, which would, at least in part, participate in the diuretic and natriuretic effects of furosemide.

Intrarenal Prostaglandins E2 and F2α in Experimental Renovascular Hypertension

To study the role of renal prostaglandins (PGs) in renovascular hypertension, PGE2 and PGF2α concentrations in both inner and outer medullae of the kidney were measure

[Questionnaire survey of peri-operative management of transurethral prostate resection in Japan].

OBJECTIVESnWe investigated perioperative management for transurethral resection of the prostate (TURP) in Japan.nnnMETHODSnThe questionnaire survey was conducted in 1,213 educational institutions for urology.nnnRESULTSnThe questionnaires were returned from 722 (60%) institutions. Admission to hospital was most frequently scheduled on preoperative day 1; termination of continuous drip infusion, starting meal intake and walking on postoperative day 1; intravenous antibiotics for three days; removal of Foley catheter on postoperative day 4; oral antibiotics for 7 days; and discharge from hospital on postoperative day 7.nnnCONCLUSIONnAlthough hospitalization was 14 days or less at most institutions, several procedures, especially the administration of prophylactic antibiotics, were fairly varied. Discussions from various perspectives might be needed to standardize the perioperative management of TURP in Japan.