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At least 127 records · Page 7Linked to original sources
PubMed1975

[In vitro investigations on the influence of various antirheumatic drugs on the enzymes of the purine salvage pathway (author's transl)].

On testing the effect of 5 drugs (azapropazone, flufenamic acid, indomethacin, oxyphenbutazone and prednisolone) commonly used in the therapy of rheumatic diseases on 3 enzymes of the purine salvage pathway (adenine-phosphoribosyltransferase, guanine-phosphoribosyltransferase and hypoxanthine-phosphoribosyltransferase) a distinct inhibitory effect of oxyphenbutazone and flufenamic acid was noted. A particularly marked effect was observed on adenine-phosphoribosyltransferase at the applied concentration (50 mug%) by both drugs but also guanine-phosphoribosyltransferase and hypoxanthine-phosphoribosyltransferase indicated reduced activities.

Adenine Phosphoribosyltransferase↗
PubMed1975

[The effect of so-called basic therapeutics and symptomatically effective antirheumatic drugs on the enzymes of DNA synthesis and DNA repair].

Investigation of DNA-synthesis and DNA-repair are important for evaluating mutagenic effects of drugs. Among the tested non steroidal antirheumatic drugs metiacinic acid, ketoprofene, and azapropazone do not show any effect on these mechanisms. Tolmetin and indometacine, however, inhibit DNA-synthesis only, whereas naproxene, oxyphenylbutazone, and flufenamic acid inhibit both DNA synthesis and repair. Gold does not influence DNA synthesis or repair, D-penicillamine inhibits DNA-synthesis only. However, Chloroquine and metabolised cyclophosphamide respecitvely impair both DNA-synthesis and repair. This effect may be also caused by azathioprine in high dosage. Application of two repair- inhibitors or of one DNA-repair-inhibitor and one directly mutagenic acting drug, e.g. cyclophosphamide, should therefore be avoided.

Apazone↗
PubMed1992

Measurement of non-steroid antiinflammatory drugs induced gastric microbleeding.

The damage of the mucous membranes in the gastrointestinal tract caused by non-steroid antiinflammatory drugs are well known. The gastrointestinal microbleeding was measured by the method of Fischer and Hunt before and after the intake of indomethacin (4 x 25 mg), naproxen-sodium (4 x 275 mg), diclofenac (3 x 50 mg) and azapropazone (2 x 600 mg). In the indomethacin group microbleeding increased from 0.91 +/- 0.12 ml/24 h to 7.30 +/- 1.20 ml/h. In the naproxen-sodium group from 1.22 +/- 0.16 ml/24 h to 3.56 +/- 0.40 ml/24 h, in the diclofenac group from 0.86 +/- 0.14 ml/24 h to 3.18 +/- 0.28 ml/24 h, in azapropazone group from 0.92 +/- 0.18 ml/24 h to 2.50 +/- 0.20 ml/24 h, respectively. All non-steroid antiinflammatory drugs increased the gastric microbleeding, however, there were considerable differences in the degree of enhancement. This can be explained by the different inhibitory activities of the drugs on the cyclooxygenase enzyme activity.

Adult↗
PubMed1992

Quantitative contribution of endogenous compounds and hypoalbuminemia in reducing the binding of furosemide in the plasma of newborn infants.

The protein binding of furosemide was studied in the plasma of newborn infants and adult subjects. Plasma consisted of two pools obtained from 25 newborns and adult subjects. The concentrations of albumin were 36.8 (newborn) and 48.3 g/l (adult). The unbound fraction of furosemide was 1.38 +/- 0.15 (adult) and 2.03 +/- 0.13% (newborn; p < 0.001). After extensive dialysis of the plasma, the unbound fraction of furosemide was 1.12 +/- 0.15 (adult) and 1.39 +/- 0.09% (newborn; p < 0.0001), suggesting that dialyzable endogenous compounds interfere with the binding of furosemide. The addition of human albumin to the newborn plasma to give a final albumin concentration of 48.3 g/l yielded an unbound fraction of furosemide of 1.63 +/- 0.08 (nondialyzed plasma) and 1.17 +/- 0.08% (dialyzed plasma; p < 0.0001). The addition of albumin to the dialyzed newborn plasma, to give a final albumin concentration similar to that in adult plasma, decreased the unbound furosemide to the level of the dialyzed adult plasma. The binding defect of furosemide in newborn plasma reflects either the effects of the endogenous inhibitors or of hypoalbuminemia. The intrinsic binding properties for furosemide of newborn dialyzed plasma are similar to those of dialyzed adult plasma. This consideration corroborates our previous results on the binding of furosemide and diazepam, salicylic acid and digitoxin to newborn and adult albumin. The displacement of furosemide by salicylic acid, tolbutamide and azapropazone is 70% greater in newborn than in adult plasma. The greater displacing effect is largely due to hypoalbuminemia.

Aging↗
PubMedDate not supplied

[The potentiating effects of azathioprine and azapropazone on the enzyme activity in experimental inflammation].

The influence of prednisolone, azathioprine, and azapropazone on the activity of collagen peptidase, acid phosphatase (complete), and the lactate dehydrogenase of granulation tissue was studied using a model of proliferative inflammation i.e. the cotton-granuloma in rats. The authors observed significant decreases in the activities of the collagen peptidase and acid phosphatase during treatment with prednisone and under combined treatment with azathioprine and azapropazone. In contrast, administration of either azathioprine or azapropazone by itself caused no changes in these enzyme activities as compared with a control group. These studies suggest that the last mentioned drugs potentiate each other in their inhibiting effect upon these enzyme activities. Whether or not these findings are of importance in the clinical treatment of chronic bacterial inflammations must be studied in further trials.

Acid Phosphatase↗
PubMed1991

Myocardial cytoprotective efficacy of azapropazone in a swine model of regional myocardial ischemia/reperfusion injury.

The purpose of the present study is to determine the myocardial cytoprotective efficacy of azapropazone (AZA) on regional myocardial function in anesthetized swine model of regional myocardial ischemia/reperfusion injury. AZA was administered (100 mg/kg, i.v.) 15 minutes prior to reflow. The left anterior descending (LAD) coronary artery occlusion was maintained for a total of 30 minutes and then reperfused for 120 minutes. The effects of AZA on regional segmental shortening (% SS) as well as on neutrophil migration were examined in the (proximal) central and border (distal) zones within the area at risk (AAR). AZA reduced the incidence of myocardial fibrillation which occurred in some animals during the LAD occlusion/reperfusion periods. AZA produced a significant recovery of left ventricular segmental shortening (% SS) in the border, but not in the central zones within the AAR. No significant differences in the hemodynamic parameters were observed between the AZA (n = 14) and the saline-treated (n = 17) groups. AZA produced a significant inhibition of neutrophil migration (as evident from the decrease in myeloperoxidase activity) into epi- and endocardium central and border zones within the AAR. It is concluded that AZA may elicit its cardioprotection in moderately but not in severely injured myocardium by inhibiting the neutrophil migration.

Animals↗
PubMed1989

[Post-traumatic edema as a limiting factor in early functional treatment measures and its pharmacodynamic modification].

Post-traumatic oedema is a limiting factor of early functional exercise following fractures. A review of drug prophylaxis used in many clinical studies is given. A 30% reduction of oedema development following bimalleolar fractures was achieved with cyclooxigenase inhibitors (azapropazone) and aprotinin. It is pointed out that non-steroidal antiphlogistic drugs inhibit the collagen metabolism during the healing of rat skin-wounds.

Ankle Injuries↗