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PubMed1995

Sulphoxide reduction by rat intestinal flora and by Escherichia coli in vitro.

The caecal microflora from female rats show a greater ability to reduce the sulphoxide group of sulindac than either the liver or kidneys. Studies on sulphoxide reduction by Escherichia coli showed that NADH, NADPH and dithiothreitol (DTT), but not acetaldehyde could act as cofactors. The cytosolic fraction was responsible for about 90%, 80% and 60% of the total reducing activity with sulindac, diphenyl sulphoxide and sulphinpyrazone, respectively. The main NADPH linked activity in the E. coli cytosol was dependent on thioredoxin, since the activity was essentially abolished by passing through a G50 column or by the addition of anti-thioredoxin anti-serum. Partial purification and separation of sulphoxide reducing activity by DEAE-cellulose chromatography separated two main protein bands, each of which possessed sulindac reducing activity. The importance of thioredoxin for much of the NADPH dependent activity was confirmed but the eluate fractions also showed the presence of other activities with NADH, NADPH and DTT that were independent of thioredoxin. Incubation of the DEAE-cellulose eluate fractions with flosequinan and sulphinpyrazone showed that the reducing activity in the two main protein peaks showed different substrate specificities and that there were multiple sulphoxide reductase systems present in E. coli cytosol.

Animals↗
PubMed1982

Inhibition by sulphinpyrazone of the platelet-dependent bronchoconstriction due to platelet-activating factor (PAF-acether) in the guinea pig.

Platelet-activating factor (PAF-acether) injected into guinea-pigs induced platelet-dependent bronchoconstriction and thrombocytopenia. Treatment of the animals with sulphinpyrazone suppressed bronchoconstriction without affecting thrombocytopenia. When tested ex vivo and in vitro, sulphinpyrazone suppressed the PAF-acether-induced platelet release reaction, as measured by the release of ATP, more efficiently than platelet aggregation. In contrast, bronchoconstriction and thrombocytopenia in vivo, as well as platelet aggregation and the release reaction ex vivo and in vitro, induced by arachidonic acid (AA), were suppressed by sulphinpyrazone. This effect is accounted for by the known anti-arachidonate cyclooxygenase activity of sulphinpyrazone. Finally, aggregation by ADP was only marginally inhibited by sulphinpyrazone, and the inhibition was easily surmounted when the amounts of ADP added were increased. Sulphinpyrazone exerts a specific and cyclooxygenase-independent protective effect towards platelet activation by PAF-acether, which results in inhibition of platelet-dependent bronchoconstriction even though aggregation, and consequently in vivo thrombocytopenia, may persist.

Adenosine Diphosphate↗
PubMed1996

Transport of the glutathione conjugate of ethacrynic acid by the human multidrug resistance protein MRP.

The multidrug resistance protein MRP has been shown to mediate the transport of glutathione S-conjugates across membranes. In this study we demonstrate that the glutathione S-conjugate of the diuretic drug ethacrynic acid, which is an efficient inhibitor of glutathione S-transferases, is a high-affinity substrate and inhibitor of the glutathione S-conjugate pump associated with MRP. This implies that ethacrynic acid may modulate drug resistance of tumor cells not only by inhibiting glutathione S-transferase activity, but also by inhibiting the export of drug conjugates from the cell by MRP.

ATP-Binding Cassette Transporters↗
PubMed1977

Inhibition of platelet adhesion to rabbit aorta by sulphinpyrazone and acetylsalicylic acid.

A technique for the isolation of rabbit thoracic aorta in a form in which it can withstand normal pressure and a new in vitro system in which it was tested is described. Segments of aorta were selectively damaged with a balloon catheter by the Baumgartneer technique and supensions of washed platelets, labelled with 51Cr, were perfused through them. More platelets adhered to the damaged surface than to the undamaged surface. Suophinpyrazone was more effective than aspirin in inhibiting platelet adherence to both the damaged and undamaged surface.

Animals↗
PubMed1992

Flow cytometric analysis of transport activity in lymphocytes electroporated with a fluorescent organic anion dye.

Organic anion transport in polarized epithelia and macrophages has previously been studied by monitoring the efflux of fluorescent organic anion dyes from cells. We adapted this strategy to the study organic anion transport in lymphocytes. Cloned lymphoma cells and normal and activated human T cells were loaded with a membrane-impermeant, organic anion dye (Lucifer Yellow) by electroporation. Dye efflux in lymphocytes was rapid, energy-dependent, and inhibitable by organic anion transporter inhibitors. Dye efflux could not be attributed to the effects of electroporation. In addition, electroporated, dye-loaded T helper cells retained the ability to properly respond to specific antigen. Thus, dye loss occurred in viable, functionally competent cells. These experiments demonstrate that electroporation is an effective means of loading cells with Lucifer Yellow, and that lymphocytes possess organic anion transporters that are functionally similar to those previously described for secretory epithelia and macrophages.

Animals↗
PubMed1983

Veno-venous allografts: patency, subendothelial proliferation, and the role of platelet-active agents.

Patency and histology of 81 vein allografts and 10 autografts in the canine femoral venous system were compared and the effect of platelet active agents in altering patency rates and subendothelial proliferation in allografts was examined. It was found that allografts thrombose at a predictable interval after operation (18 +/- 7 days) and have significantly worse survival than autografts (P less than 0.001). Platelet-active agents did not alter allograft patency rate of the incidence of subendothelial proliferation in this model.

Animals↗
PubMed1985

Sulphinpyrazone dose schedule in hyperuricemic patients with cardiovascular diseases: tolerability assessment.

Renal tolerability of four different dose schedule of sulphinpyrazone (S) was evaluated in a bi-centre, 2-week long open study performed in fifty-six cardiovascular patients of both sexes (47 males, 9 females; mean age 64 yrs) at different risk as regards serum uric acid levels. Each patient was allocated, according to his/her baseline values of serum uric acid or serum creatinine to four different sulphinpyrazone incremental dosage schedules. Renal function and other biochemical assessments (liver function; blood lipids; blood glucose) were assessed at the entry, after the 1st and the 2nd week. Reported signs and symptoms were collected at the 1st and the 2nd week, too. Renal function did not show any statistically and clinically significant impairment during the whole trial. General tolerability, both objective and subjective was particularly good. Only one patient was withdrawn because of reasons unrelated to the ongoing treatment. Sulphinpyrazone can be safely administered also in patients at risk as regards uric acid levels if the proposed therapeutic program is adopted.

Allopurinol↗
PubMedDate not supplied

Myocardial infarct expansion, infarct extension, and reinfarction: pathophysiologic concepts.

Infarct expansion and infarct extension are events early in the course of myocardial infarction with serious short- and long-term consequences. Infarct expansion, disproportionate thinning, and dilatation of the infarct segment probably begin within hours of acute infarction and usually reach peak extent within seven to 14 days. Clinical data suggest that infarct expansion occurs in approximately 35% to 45% of anterior transmural myocardial infarctions and to a lesser extent in infarctions at other sites. Although expansion usually develops in large infarcts, the extent of transmural necrosis rather than absolute infarct size predicts its occurrence. Expansion has an adverse effect on infarct structure and function for several reasons. Functional infarct size is increased because of infarct segment lengthening, and expansion results in over-all ventricular dilatation. Thus, patients with expansion of an infarct have poorer exercise tolerance, more congestive heart failure symptoms, and greater early and late mortality than those without expansion. Infarct rupture and late aneurysm formation are two additional structural consequences of infarct expansion. Experimental and clinical data suggest that the incidence and severity of expansion can be modified by interventions. Increased ventricular loading conditions and steroidal and nonsteroidal antiinflammatory agents make expansion more severe. Reperfusion of the infarct segment and pharmacologic interventions that decrease ventricular afterload lessen the severity of expansion. Previous myocardial infarction and preexisting ventricular hypertrophy may also limit the development of infarct expansion. Infarct extension is defined clinically as early in-hospital reinfarction after a myocardial infarction. The pathologic finding of infarct extension is necrotic and healing myocardium of several different recent ages within the same vascular territory. Although this pathologic criterion usually cannot be verified, studies employing invasive and noninvasive assessment of patients with early reinfarction provide evidence that the new myocardial injury is usually in the same vascular risk region as the original infarction. A variety of different criteria have been applied in the clinical diagnosis of infarct extension, and this has resulted in a large range of estimated frequencies from under 10% to as high as 86%. High estimates are found in studies using one or two nonspecific criteria such as ST segment shift or reelevation of total CK. The lowest rates have been found when combinations of criteria are used.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic beta-Antagonists↗
PubMed1980

Changing trends of mortality in gout.

Patients with primary gout live as long as the nongouty male in the general population. Coronary heart disease is the leading cause of death in the gouty and nongouty population. There is a parallel decline in mortality particularly from coronary heart disease as that in the general population. This phenomenon is related to a number of specific and nonspecific factors. The changes in life styles and major risk factors may be counted as important influences. It is also clear that the impact of the disturbance of uric acid metabolism has not placed a particular individual in a category with any significantly inherent greater risk from intimately or remotely related causes of morbidity or mortality.

Aged↗