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Biomedical subjects

I Reimann

Publications and source records attributed to I Reimann.

At least 55 records · Page 3Linked to original sources
PubMed1983

Serum concentrations of tobramycin after intraarticular administration. An experimental study in the rabbit.

Serum concentration of the aminoglycoside tobramycin was followed for 120 min after intraarticular injection of 20 mg tobramycin in six rabbit knee joints. Highest concentration was observed after 15-30 min, and compared with the values after intramuscular injection the serum half life was equal. No pathological changes were observed by histological examination of the synovial membrane and articular cartilage. It was concluded that no damage of the joint has been demonstrated after intraarticular injection of tobramycin, but the serum concentration must be monitored due to the rapid transport from the joint cavity.

Animals↗
PubMed1982

Experimental osteoarthritis in the rabbit. A study of 133xenon washout rates from the synovial cavity.

Synovial perfusion in 6 rabbit knees, with experimentally induced osteoarthritis (joint instability), was studied by recording the initial 133Xe washout rates from the joint space. The unstable osteoarthritic knee was compared with the contralateral sham operated control knee at intervals of 6 to 96 weeks postoperatively. Within the first half year the ratio between the 133Xe washout rates in the osteoarthritic and control joints was significantly increased. These findings were supported by the increased blood flow to the joint region, visualized by scintigraphy of osteoarthritic rabbits given 99mTc-microspheres intracardially. However, methodological sources of error do not allow any conclusions regarding the much less increased 133Xe washout rates found in advanced osteoarthritis. The initially increased synovial blood flow coincided with the existence of joint effusion and the early development of osteophytes, all conditions supposed to be a consequence of posttraumatic synovitis. Attention is drawn to these pathogenic phenomena in studies dealing with the initial changes in experimental models of osteoarthritis and to a possible etiological significance.

Animals↗
PubMed1982

Influence of diphenylhydantoin on isotope release and bone enzymes in vitro.

The acute effect of diphenylhydantoin isotope release in an in vitro system using mouse calvaries was studied. A depressive effect on bone resorption was found involving radioactive calcium as well as tritiated proline. Bone resorption and formation were further investigated by semiquantitative histochemistry. Depressed activity of both alkaline and acid phosphatase was found, indicating a direct inhibitory effect of diphenylhydantoin on bone turnover.

Acid Phosphatase↗
PubMed1982

Observations of reversibility of glycosaminoglycan depletion in articular cartilage.

Observations of reversibility in the surface depletion of glycosaminoglycans in articular cartilage after experimental surgical operations focussed attention on whether the depletion always leads to osteoarthritis or may be an early nonspecific response of articular cartilage to differing injuries. Histologic sections obtained from the patellae of 42 rabbits were investigated at different postoperative intervals. On sections stained metachromatically with Toluidine blue at pH 3, visual measurement by light microscopic examination as well as measurement of optical density, were performed to estimate the degree of surface depletion of glycosaminoglycans. In addition, the glycosaminoglycan level in the areas below the depleted zones was measured by optical densitometry. The results obtained by both methods demonstrated a marked depletion of glycosaminoglycans one week after surgery, reaching a maximum after four weeks. Subsequently, significant decreased depletion continued until 26 weeks. The mean level of glycosaminoglycans was always lower than normal. Concurrent with the surface depletion of glycosaminoglycans were histologic signs of synovitis. Reversible surface depletion of glycosaminoglycans may occur in articular cartilage with normal morphology. It presumably represents a nonspecific reaction of cartilage as well as an early sign of osteoarthritis before "the state of no return."

Animals↗
PubMed1981

Clearance of diazepam can be impaired by its major metabolite desmethyldiazepam.

The pharmacokinetics of a single intravenous dose of diazepam 0.1 mg/kg was studied in 6 healthy volunteers, in random order under controlled conditions and following pretreatment with its major metabolite, desmethyldiazepam (20 mg/kg/day) for one week. In the two subjects with the highest plasma concentration of desmethyldiazepam (990 and 1100 ng/ml, respectively), total plasma clearance (Cl) of diazepam was reduced after desmethyldiazepam, by 31% and 54%, respectively. In three individuals there was a moderate decrease of 14% to 21%, and no effect was seen in one volunteer. Cl was significantly reduced (11.5 +/- 1.8 vs. 9.1 +/- 3.3 ml/min; p = 0.015) and elimination half-life tended to be prolonged (38.5 +/- 10.4 vs. 65.8 +/- 67.1 h; p = 0.15). It is concluded that high concentrations of desmethyldiazepam can influence the elimination of its parent drug diazepam by product inhibition.

Adult↗
PubMed1981

Elevation of steady-state diazepam levels by cimetidine.

The effect of cimetidine (1000 mg/day) on steady-state diazepam (5 mg/day) kinetics was investigated in six healthy subjects. During placebo-controlled treatment for 11 days, trough steady-state plasma levels were 130 +/- 33 ng/ml and steady-state concentration averaged 185 +/- 57 ng/ml (mean +/- SD). During concomitant treatment with diazepam and cimetidine these concentrations rose to 194 +/- 52 ng/ml and 255 +/- 46 ng/ml (P less than 0.002). The 40% to 50% increase was due to reduction (P = 0.026) of total body clearance from 20.9 +/- 9.5 ml/min (control) to 14.0 +/- 3.0 ml/min (with cimetidine). Diazepam elimination half-life was also prolonged (P = 0.02, from 39.5 +/- 16.6 hr to 101 +/- 58.1 hr) by cimetidine.

Adult↗
PubMed1980

Identification of the major metabolite of prostacyclin and 6-ketoprostaglandin F1 alpha in man.

Human volunteers were infused with 3H- and 2H-labeled prostacyclin or 3H-labeled 6-ketoprostaglandin F1 alpha and, in separate experiments, with the unlabeled prostanoids. The urine was purified by different chromatographic steps and finally separated into several fractions by high-performance liquid chromatography. The major fractions contained 20.5 and 23.0% of the eluted readioactivity for the metabolites of prostacyclin and 6-ketoprostaglandin F1 alpha, respectively. The structure of both metabolites was identified by gas-liquid chromatography-mass spectrometry as dinor-6-ketoprostaglandin F1 alpha. It is concluded that the major metabolite of prostacyclin and 6-ketoprostaglandin F1 alpha in man is dinor-6-ketoprostaglandin F1 alpha.

6-Ketoprostaglandin F1 alpha↗
PubMed1980

Influence of cimetidine on the pharmacokinetics of desmethyldiazepam and oxazepam.

The pharmacokinetics of single oral doses of desmethyldiazepam 20 mg or oxazepam 50 mg were studied in 5 healthy volunteers under controlled conditions, before and following a 24 h pretreatment with cimetidine 200 mg x 5. Cimetidine significantly impaired (p = 0.03) the elimination of desmethyldiazepam, as shown prolongation of its elimination half-life from 51.7 +/- 21.9 h to 72.6 +/- 39.4 h (mean +/- SD), and a decrease in total plasma clearance from 12.0 +/- 2.7 ml/min to 8.6 +/- 3.3 ml/min. The disposition of oxazepam was not affected. From these results, and recently published data on diazepam and chlordiazepoxide, it is concluded that cimetidine impairs the hepatic elimination of those benzodiazepines which are metabolized by phase I reactions.

Adult↗
PubMed1980

The effect of joint position on juxta-articular bone marrow pressure. Relation to intra-articular pressure and joint effusion--an experimental study on horses.

Six metacarpo-phalangeal joints of adult horses were studied. Pressure measurements were made in the joint and the metacarpal bone with simultaneous measurement of the systemic arterial blood pressure. Investigations performed to study the effect of joint position on juxta-articular bone marrow pressure showed that an increase in joint flexion was always followed by a rise in intraosseous pressure with a significant increase at flexion above 60 degrees. Increase in intra-articular pressure which was achieved by injection of saline was always followed by a slower rise in intraosseous pressure. Furthermore, it was shown that even a few millilitres of saline in the joint caused a rise in intra-articular pressure. The findings indicate that changes in joint position as well as effusion may block the drainage vessels from the bone marrow as they pass through the joint.

Animals↗
PubMed1980

Metabolism of prostacyclin and 6-keto-prostaglandin F1 alpha in man.

The major metabolites of prostacyclin and 6-keto-prostaglandin F1 alpha in man were investigated. Healthy male volunteers were infused with the labeled and unlabeled prostanoids. The urine was chromatographed on different systems including high-pressure liquid chromatography (HPLC). The material under the major peak was derivatized to the methyl ester methoxime trimethyl silyl ether and analyzed by gas chromatography-mass spectrometry (GC-MS). Open bed reversed-phase chromatography of the urine obtained from PGI2 infusion resulted in two peaks. On further separation by two different HPLC systems one major peak containing 20.5 % of the radioactivity was obtained and was shown by GC-MS to be identical with dinor-6-keto-prostaglandin F1 alpha. Urine obtained from 6-keto-prostaglandin F1 alpha infusion was chromatographed similarly. Its major peak on HPLC appeared with a retention volume and mass spectrum identical with the major metabolite of PGI2. It is concluded that the major metabolite of PGI2 and 6-keto-prostaglandin F1 alpha in human urine is dinor-6-keto-prostaglandin F1 alpha.

6-Ketoprostaglandin F1 alpha↗
PubMed1980

The synovial membrane in human coxathrosis: light and electron microscopic studies.

Changes of the synovium are in integral part of osteoarthritis. Most authors regard these changes as secondary to cartilage degeneration. However, synovitis is a very early feature in osteoarthritis, and increased knowledge of changes in the chemical composition of the synovia focused our attention on the histologic characteristics of osteoarthritic synovium. Light and electron microscopic studies of the synovial membrane from patients with osteoarthritis and rheumatoid arthritis of the hip joints were performed. Two distinct types of osteoarthritic synovitis were observed: an early proliferative from characterized by venous stasis with edema, free erythrocytes and hemosiderine deposits in the interstitial tissue, that suggested increased capillary permeability. In the late form, fibrous synovitis, the microscopic picture was dominated by dense fibrous tissue. Synovium from rheumatoid arthritis showed the same vascular changes as in osteoarthritis. In addition, the histologic picture was characterized by severe inflammatory changes. In osteoarthritis the signs of inflammation were moderate or absent. The development from proliferative into fibrous synovitis is probably the result of long-standing chronic venous insufficiency. The essential feature of osteoarthritic proliferative synovitis--venous stasis with increased capillary permeability--correlates well with most of the known changes in the composition of the synovial fluid.

Arthritis, Rheumatoid↗
PubMed1979

Indomethacin increases plasma lithium.

The effects of indomethacin on plasma lithium concentrations and renal lithium clearance were investigated in three psychiatric patients and four normal volunteers. After steady-state plasma lithium concentrations had been reached, the subjects received indomethacin placebo for three to seven days, indomethacin (50 mg thrice daily) for seven days, and placebo again for three to seven days. Indomethacin increased plasma lithium concentrations by 59% in the psychiatric patients and 30% in the volunteers. Renal lithium clearance was reduced by indomethacin by 31% in the group as a whole, and prostaglandin synthesis, determined by measuring the major metabolite of PGE2 with mass spectrometry, was reduced by 55%. These results show that indomethacin reduces renal lithium clearance to an extent which may be clinically important. They also suggest that the renal clearance may be affected by a prostaglandin-dependent mechanism, possibly located in the distal tubule.

Drug Interactions↗