Journal of the Oslo city hospitals最新文献

Similar distributions of prostaglandins in urine and renal venous blood both during prostaglandin infusion and stimulated synthesis indicated a vascular origin for both urinary and renal venous PGE2 and PGI2. Various stimulation procedures demonstrated that the renal vasculature releases PGE2 and PGI2 in a fixed proportion. Renal degradation of circulating prostaglandins was not influenced by ureteral occlusion and seems to be mainly confined to the blood vessels. The vascular capacity for both synthesis and degradation was much greater for PGE2 than for PGI2. Urinary PGE2 was shown to be of renal origin, but constituted a small and variable fraction of renally produced PGE2, making it a poor estimate of renal PGE2 synthesis. Urinary 6-keto-PGF1 alpha may originate from renal PGI2 production or from circulating 6-keto-PGF1 alpha which readily appears in the urine. Equimolar infusions of PGE2 and PGI2 demonstrated that PGI2 was a more potent stimulator of renin release than PGE2, but the difference seemed to be mainly due to differences in degradation and not to differences in intrinsic potency. Prostaglandins stimulated renin release only when the intrarenal mechanisms for renin release were activated and not at control blood pressure and free urine flow. beta-adrenoceptor agonists stimulated renin release independently of activation of the macula densa, but required activation of the hemodynamic mechanism. Ethacrynic acid activated both the hemodynamic and the macula densa mechanism, but had no direct stimulatory effect on renin release. PGE2 and PGI2 were released during autoregulatory vasodilation, but neither PGE2 nor PGI2 participated in the autoregulatory mechanism. Autoregulatory and prostaglandin mediated vasodilation seems to be independent. Descending autoregulatory vasodilation was demonstrated during successive reductions in RAP, but a more simultaneous dilation of all preglomerular vessels was indicated during successive elevations of ureteral pressure. This difference may be due to participation of TGF together with the myogenic mechanism in autoregulation of RBF. Participation of TGF may also explain why prostaglandin and renin release dissociate during successive reductions in RAP, but increase in parallel during successive elevations of ureteral pressure. It also explains why maximal renin release induced both by the hemodynamic and the macula densa mechanism coincides with the breaking point of the RBF autoregulatory curve, and why loop diuretics induce complete autoregulatory vasodilation at control blood pressure.

One hundred and thirty-six patients operated on with femoropopliteal bypass for arterial occlusive disease are retrospectively examined. In 58% of the cases the reversed saphenous vein was used, while 42% had a Dardick Biograft (umbilical vein graft). Patency rate for all grafts was 62.2% at four years. The most important factor for long term patency in our material is the type of graft used. In the saphenous vein group the four years patency rate was 74%, while in the Dardick group 45%. There was no significant difference in patency rate for patients operated on for claudication and those for limb salvage. We found a significantly lower patency rate when the distal anastomosis was placed below the knee. Patients with good arteriographic runoff had better long term patency. The difference was, however, not significant for the prosthetic group. The perioperative mortality was 1.4%. Early graft failure was 4.8% in the autologous vein group and 33% in the umbilical vein group. The majority of amputations occurred in patients with early failure of umbilical vein grafts.

Twenty-two patients with stable coronary heart disease were randomly assigned to either of two groups. Group I (n = 11) was given acetylsalicylic acid (ASA) 300 mg daily for 1 week, whereafter a daily supplement of 3,4 g eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) as a highly concentrated ethylester, formulation ("K-85", Norsk Hydro) was added for another 4 weeks. Group II (n = 11) was given 3,4 g daily of EPA and DHA for 4 weeks, after which ASA 300 mg daily was added for another week. Determination of serum fatty acids confirmed satisfying absorption of EPA and DHA. A significant increase of the Ivy bleeding time was registered following administration of both "K-85" (240 to 270 sec, median values) and ASA (270 to 360 sec, median values) alone. A slighter increase was noted by a combination of the two principles. A reduction in serum triglycerides of 17% was noted after "K-85" (median values, both groups). Serum total cholesterol decreased after "K-85" administration in group I, but not so in group II. HDL-cholesterol remained unchanged. Serum lipids remained unaffected by ASA. During administration of "K-85" no adverse effects or bleeding episodes were seen.

Mediastinal fibrosis may be part of a multifocal fibrotic disease, including retroperitoneal fibrosis, lung fibrosis and Riedel's struma. A case of mediastinal fibrosis, with a previous history of retroperitoneal fibrosis and lung fibrosis, is discussed. There are many known causes of retroperitoneal and mediastinal fibrosis, but as in the present case the etiology often remains unknown.

Among a group of 14 painters accorded a disability pension, 11 showed signs and symptoms of slight encephalopathy. Five of these 11 painters previously had been pensioned with a diagnosis of musculoskeletal disease, while the encephalopathy was unrecorded in the disability pension records. The combined effect of the two diseases may have caused the disability. We considered occupational solvent exposure the most probable cause of the encephalopathy in four of these five painters. This study indicates that case-referent studies based on diagnoses from disability pension registers may lead to underestimation of the risk of toxic encephalopathy.

Twenty-six patients with previous heavy exposure to organic solvents were admitted to a neurological department during a 1 1/2 year period. They were studied with a battery of tests, including general medical and neurological examinations, neuropsychological tests, electroencephalography (EEG) and neurography with electromyography (EMG), and cerebral computerized tomography (CT). The presenting complaints were compatible with encephalopathy and/or polyneuropathy. When patients with alternative diagnosis were excluded, 17 patients (65%) of the initial group were diagnosed as belonging to the organic solvent syndrome. These patients had a mean time of solvent exposure of 23.9 years, ranging from one to 45 years. EEG and cerebral CT showed minor deviations only as did the neurological examination. These methods proved nevertheless of importance in excluding alternative etiologies. Neuropsychological test performances were markedly reduced, especially short-term memory. All patients were injured by occupational exposure to organic solvents, most often from painting and lacquering. Encephalopathy was a more frequent finding than polyneuropathy, and most often classified as slight or marked, whereas severe encephalopathy was not found in the present group.

A single-blind placebo controlled study on the efficacy of the anticholinergic and calcium blocking agent terodiline (Mictrol) on detrusor hyperreflexia has been done in 10 patients with multiple sclerosis in a stable state. The patients were evaluated by means of micturition charts, uroflowmetry and cystourethrometry, including electromyography of the periurethral sphincter in females and the bulbocavernosus muscle in males. After 6 weeks on terodiline 25 mg twice a day, the volume per voluntary micturition increased 23 per cent. The number of incontinence episodes decreased. Bladder volume at first urge increased 55 per cent, the maximum cystometric capacity increased 52 per cent, and the detrusor pressure of the first involuntary contraction decreased 27 per cent. The number of voluntary micturitions and voided volume per 24-hour, maximum and average flow, residual urine and urethral pressure at first urge remained unaltered. Terodiline is an alternative drug in the treatment of detrusor hyperreflexia. A follow-up investigation indicates that an increase in terodiline dosage may improve the results.