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Biomedical subjects

H Olsen

Publications and source records attributed to H Olsen.

At least 73 records · Page 4Linked to original sources

Bactericidal capacity against Neisseria meningitidis of normal human serum and sera with functional deficiencies of the third and eight complement factor.

The bactericidal capacity of serum with C3 deficiency secondary to circulating C3 nephritic factor, serum with C8 deficiency and normal human serum were assessed in vitro against Neisseria meningitidis groups A-C. Normal human serum and C8-deficient serum, originating from a 28-year-old male with two episodes of meningococcal meningitis, showed significant bactericidal capacity against meningococci groups A and B. Against group C meningococci the C8-deficient serum revealed significant bactericidal capacity, whereas normal human serum showed no bactericidal effect. Serum with C3 deficiency, obtained from a 16-year-old female with two episodes of meningococaemia, showed no bactericial effect against meningococci groups A-C. Incubation of normal human serum and C8-deficient serum with isolated nephritic factor resulted in C3 depletion and abolished the bactericidal effect.

Adolescent↗

Effects of ethanol on human blood fibrinolysis and coagulation.

The effect of ethanol (serum concentrations 10 and 22 mM) on whole blood clotting time, thromboplastin activity and whole blood clot lysis time were studied in eight healthy humans. Each subject serving as its own control. Ethanol (22 mM) increased the whole blood clotting time by 26 +/- 29% (p less than 0.05), whereas the thromboplastin activity (in both unstimulated and endotoxin stimulated monocytes) was significantly decreased in presence of ethanol (both 10 and 22 mM). The whole blood clot lysis time was increased by 83 +/- 9 and 260 +/- 178 percent in presence of 10 and 22 mM ethanol respectively. After the high ethanol doses, ten hours after the end of the voluntary ethanol intake, the whole blood clot lysis time was increased with 133 +/- 105 percent. According to the present findings, acute ethanol intake affect blood fibrinolysis activity, as measured by whole blood clot lysis time, in a way which might precipitate a state of increased risk of thrombotic diseases.

Adult↗

The effect of ethanol intake on propoxyphene absorption and biotransformation in dogs.

The effect of ethanol (0.5 and 1.0 g/kg) on gastrointestinal absorption and presystemic biotransformation of propoxyphene (4 mg/kg) was studied in dogs in a crossover design. Low ethanol doses (0.5 g/kg) had no effect on the bioavailability of propoxyphene. High ethanol doses (1.0 g/kg) enhanced the bioavailability of orally administered propoxyphene significantly (p less than 0.05). With this dose of ethanol, the area under the blood concentration versus time curve (AUC)0-5 h of propoxyphene was approximately 200% of the control value. The level of norpropoxyphene, a major metabolite of propoxyphene, was significantly decreased (p less than 0.05) after administration of high ethanol doses. In all blood samples, after propoxyphene administration, an unidentified metabolite of propoxyphene was found, which formation was dose dependently inhibited by ethanol.

Administration, Oral↗

Ethanol inhibition of codeine and morphine metabolism in isolated rat hepatocytes.

Suspensions of isolated hepatocytes from male Wistar rats were prepared according to a two step Ca++-free collagenase perfusion method. Codeine, morphine or norcodeine were incubated with hepatocytes at 37 degrees C for up to 90 min in the absence and presence of ethanol. The elimination rate constant (Kel) of codeine and morphine was reduced with approximately one-third and one-fourth, respectively, in the presence of 60 mM ethanol, whereas the presence of ethanol did not alter the Kel of norcodeine significantly. The inhibition of codeine metabolism was dose-dependent, extending from approximately 15% at 10 mM ethanol to 40 to 50% at 100 mM. A 3-fold increase in the ratio of morphine concentration (formed from codeine) to the amount of codeine metabolized was observed in the presence of ethanol as compared to control cells. The mean morphine concentration was 170% higher in the ethanol-treated suspensions than in the controls. The ratio of norcodeine concentration to codeine metabolized was unchanged. The inhibition of morphine metabolism was accompanied by a similar reduction of morphine-3-glucuronide formation. The accumulation of morphine observed in the cell medium in the presence of ethanol might be due to inhibition of other metabolic pathways from codeine, thus shunting to morphine formation, combined with the inhibitory effect of ethanol on morphine metabolism per se.

Animals↗

Lack of evidence of increased lethality due to propoxyphene overdose in the presence of ethanol in male Wistar rats.

The primary purpose of the present investigation was to evaluate if the presence of ethanol increased lethality induced by propoxyphene. A secondary aim was to study the effect of naloxone on propoxyphene lethality alone, and on the concomitant administration of propoxyphene and ethanol. Male Wistar rats (210-330 g) were used as test animals. Propoxyphene (175 mg/kg) and ethanol (2 g/kg) were administered by gastric intubation, naloxone (2 mg/kg) by subcutaneous injection. Four groups, each consisting of 19 rats, received either of the following drug treatments: Propoxyphene, ethanol + propoxyphene, naloxone + propoxyphene, and naloxone + ethanol + propoxyphene respectively. The drugs were given in the sequence mentioned at the beginning of the experiment. Naloxone was also given 45 and 90 min later. Mortality was reduced to 42% in the group that received ethanol and propoxyphene compared to 73% in the group that received propoxyphene only. Naloxone protected against lethality in both groups. Some animals died despite naloxone administration, possibly due to a nonopioid cardiotoxic effect of propoxyphene or its metabolite. An increase in the propoxyphene/norpropoxyphene (P/N) ratio due to an increase in the absolute concentrations of propoxyphene and a decrease in the absolute levels of norpropoxyphene in blood, brain, and heart tissues was observed in the ethanol + propoxyphene group, compared to the propoxyphene group. In the animals which died, the highest P/N ratio was observed in brain tissue and the lowest in heart muscle. Despite the pharmacokinetic data obtained in this investigation indicating impaired propoxyphene metabolism in the presence of ethanol, ethanol did not enhance propoxyphene-induced lethality.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Enterocutaneous fistulization due to Actinomyces odontolyticus. Report of a case.

A case of abdominal actinomycosis originating from the sigmoid colon is presented. Actinomyces odontolyticus was isolated; it is a rarity, but should be suspected in the case of a palpable mass and several fistulas developing after a latent period of weeks to months following surgical or inflammatory trauma. The diagnosis is made by anaerobic cultivation. Primary treatment with large doses of penicillin for several weeks may be supplemented by surgery. The strain isolated in the present case was only moderately sensitive to penicillin and was successfully treated with erythromycin.

Actinomycosis↗

The antiglucocorticoid RU486 inhibits the ethanol-induced increase of tryptophan oxygenase.

The effect of the glucocorticoid-antagonist RU486 (Roussel-Uclaf, France) on the increased activity of hepatic tryptophan oxygenase (TO) after administration of corticosterone and ethanol in rats was studied. RU486 (40 mg/kg per os) inhibited completely the effect of corticosterone (5-15 mg/kg injected intraperitoneally) on TO. Ethanol (4 g/kg) given intraperitoneally is followed by peak corticosterone concentrations comparable to those seen after the administration of 5-10 mg exogenous corticosterone, and increased the TO activity 3-fold 4 h after the injection. RU486 inhibited completely the ethanol-induced increase of TO, indicating that this increase is mediated by corticosterone.

Animals↗

11-Deoxycortisol induces hepatic tryptophan oxygenase in rats.

11-Deoxycortisol (cortexolone) has previously been used as a glucocorticoid antagonist in vitro and in adrenalectomized rats. Antiglucocorticoid properties of 11-deoxycortisol in intact rats were examined by studying the effect of 11-deoxycortisol on the induction of hepatic tryptophan oxygenase (TO) by corticosterone. No antiglucocorticoid effect was observed. When 11-deoxycortisol was injected into rats, the TO activity increased. This was probably mainly caused by an elevation of the serum corticosterone level. The induction of TO by 11-deoxycortisol was inhibited by metyrapone. However, 11-deoxycortisol (100 mg/kg) was still not a glucocorticoid antagonist even in presence of metyrapone.

17-Hydroxycorticosteroids↗

Acute interaction of halothane and enflurane with the metabolism of ethanol in isolated hepatocytes and liver cytosol preparations from the rat.

The effects of halothane and enflurane on ethanol (40 mM) oxidation were studied in isolated rat hepatocytes. Anaesthetic (halothane, enflurane and diethyl ether) effect on the activity of alcohol dehydrogenase (ADH) was studied in incubations of cytosol preparations from rat liver. Mean rates of ethanol metabolism ranged from 0.44 to 0.49 mumol ethanol metabolized/mg cell protein/hour in control hepatocytes from fasted and fed animals. These rates were enhanced by 2- and 3-fold in hepatocytes from fed and fasted animals, respectively, when pyruvate (5 mM) was added. Halothane and enflurane both caused dose dependent inhibition of ethanol metabolism (15-40%) in all hepatocytes without exogenous addition of pyruvate. The inhibitory effect was present also after pyruvate stimulation in hepatocytes from fasted animals, but disappeared in hepatocytes from fed animals when pyruvate was added. The rate of ethanol oxidation by cells from fed rats was enhanced by approximately 40% when the concentration of ethanol was increased from 20 mM to 80 mM. The anaesthetic inhibition of ethanol metabolism was about 20% more pronounced at the higher ethanol concentration compared to the lower concentration when no pyruvate was added. In the presence of pyruvate the effect of anaesthetics was again reversed regardless of ethanol concentration. Halothane (2 mM) and enflurane (2 mM) both caused about 25% inhibition of the ADH-activity in cytosol preparations while ether (30 mM) caused more than 50% inhibition. No inhibition of hepatocyte uptake of ethanol was caused by any of the three anaesthetics.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Dehydrogenase↗

Incision and drainage v. incision, curettage and suture under antibiotic cover in anorectal abscess. A randomized study with 3-year follow-up.

Conventional incision and drainage was compared with incision plus curettage and primary suture of abscess cavity under antibiotic cover in a prospective, randomized trial of 83 patients with acute anorectal abscess with or without low fistula. All the patients were followed up for three years. The time to healing was on average three weeks less after suture than after incision alone. The difference was statistically significant. Primary healing was obtained in 32 of 42 cases after suture. Recurrence of abscess tended to be more frequent after suture, but the time to healing of initial and recurrent abscesses and fistulas in the three-year observation period continued to be three weeks less after suture than after incision alone, making suture the most attractive treatment.

Abscess↗

Prophylactic metronidazole or suction drainage in abdominal hysterectomy.

The efficacy of a two-dose perioperative course of oral metronidazole or suction drainage of the vaginal vault was evaluated in a randomized study of 150 patients undergoing abdominal hysterectomy. Patients receiving metronidazole demonstrated a significant reduction in febrile morbidity (from 48 to 8%), infectious morbidity (from 46 to 16%), urinary tract infections (from 30 to 10%), and pelvic and/or abdominal wound infections (from 18 to 2%). The patients managed with suction drainage showed a marked reduction in febrile and infectious morbidity; however, this reduction was not significant. Overall, 17% of all specific postoperative infections were first diagnosed after discharge from the hospital. No adverse side effects of metronidazole were encountered.

Adult↗