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PubMed1987

Drug interactions with the calcium-entry blockers.

The increasing use of the calcium-entry blockers has led to an enhanced potential for drug interactions with a variety of different drugs. Interactions with cardiovascular agents are of great concern because of the consequences of synergistic negative dromotropism or inotropism. We therefore assessed the concomitant use of calcium-entry blockers and cardiac glycosides, beta-blockers, antiarrhythmic agents, and other chemical types of calcium-entry blockers from a standpoint of clinical relevance. We also evaluated reported drug interactions with H2-receptor antagonists, anticonvulsants, lithium carbonate, general anesthetics, cytostatic drugs, rifampin, and sulfinpyrazone with regard to clinical implications, along with the modification of calcium-entry blocker dose for concurrent social drug use, such as cigarette smoking and ethanol intake. Although a myriad of potential drug interactions exists for these agents, combination therapy is still a reasonable alternative if doses are adjusted appropriately.

Adrenergic alpha-Antagonists↗

PubMed1985

Studies of suloctidil in experimental thrombosis in baboons.

Suloctidil has been evaluated in the baboon for its antithrombotic efficacy using models of both acute and chronic arterial thrombogenesis. Acute thrombus formation was initiated by Dacron vascular grafts inserted as extension segments into chronic arteriovenous shunts. 111In-platelet deposition was measured by scintillation camera imaging for one hour. The results after oral administration of suloctidil (100 mg/kg/d in two divided doses) were not different from control studies. Moreover, concurrent heparin anticoagulation did not affect 111In-platelet deposition compared with control data. In contrast, ticlopidine (20 mg/kg/d) significantly decreased platelet deposition that was reduced further by the addition of heparin. Chronic arterial-thromboembolism was initiated by segments of polyurethane (Biomer) cannula introduced into chronic arteriovenous shunts. Thrombus formation by the polyurethane cannula was measured as 111In-platelet turnover (corrected for removal of senescent platelets). Cannula platelet consumption was unaffected by suloctidil (20 mg/kg/d given in two divided doses for two days preceding and throughout the period of platelet survival measurement). In contrast, dipyridamole (10 mg/kg/d) and sulfinpyrazone (100 mg/kg/d) completely interrupted cannula platelet consumption. We conclude that suloctidil probably has little or no effect on platelet-dependent thrombus formation.

Acute Disease↗

PubMed1986

Anterior ischemic optic neuropathy in type I diabetes.

Anterior ischemic optic neuropathy (A.I.O.N.) may cause optic disc edema in type-I diabetes. A.I.O.N. affects diabetic patients of all ages. Such optic neuropathy is more likely to become bilateral in diabetics than in the non-diabetic subjects. A 41-year-old diabetic insulin-dependent woman presented A.I.O.N. in RE; 5 years later, the same affection occurred in LE. The clinical course was relatively benign in both eyes, with good functional restitution. The patient was treated by high doses of Sodium Salicylate and Sulfinpyrazone. The pathogenesis of optic disc edema in type-I diabetes is, according to Hayreh (1981), ischemia of different grade in the district of the posterior ciliary arteries: microangiopathy, rheological anomalies and atherosclerotic added lesions produce a variability of clinical pictures of increasing seriousness. Our case has an intermediate position in such a continuous spectrum. The VEP supported the diagnosia of A.I.O.N.

Adult↗

PubMed1987

Drug inhibition of penicillin tubular secretion: concordance between in vitro and clinical findings.

Using the rabbit kidney slice model of active tubular secretion, I studied the active accumulation of penicillin (PEN) in the absence and presence of competing drugs to evaluate the feasibility of using in vitro uptake to predict in vivo secretion. Active accumulation of PEN by these slices was saturable at high PEN concentrations and was inhibited by incubation conditions which decreased ATP production. PEN uptake in the presence of 1 mM concentrations of mannitol, tolazoline and tetraethylammonium was unchanged. However, PEN uptake in the presence of eight weak organic acid drugs (probenecid, phenylbutazone, sulfinpyrazone, salicylate, sulfamethizole, chlorothiazide, sulfamethoxypyridazine and indomethacin) was inhibited significantly. This inhibition appeared to be competitive in nature and the inhibitor-transport carrier protein dissociation constant (Ki) for each inhibitory drug was calculated (range, 0.38-74.8 X 10(-5) M). When these values for Ki obtained with PEN were compared to values obtained with methotrexate and p- aminohippurate, the values of Ki were similar, implying the presence of a similar transport carrier protein for PEN, methotrexate and p-aminohippurate. The effects of these eight drugs upon PEN clearance in vivo were extrapolated from the medical literature. The relative inhibitory strengths of these drugs based upon in vitro findings (drug plasma concentration/Ki ratios) and clinical findings (inhibition of PEN clearance) were concordant. This in vitro model for assessing inhibition of renal tubular secretion may be of general utility in predicting clinically important drug interactions between weak organic acid drugs.(ABSTRACT TRUNCATED AT 250 WORDS)

2,4-Dinitrophenol↗

PubMed1978

Antiplatelet drugs in arterial thrombosis: a review.

The thrombotic process, basic mechanisms of action of antiplatelet drugs, and clinical trials with platelet inhibitors are reviewed. The role of prostaglandins in platelet reactions and the mechanisms of aspirin's, dipyridamole's and sulfinpyrazone's inhibition of platelet function are discussed. Clinical studies of the use of these three drugs, alone or in combination with each other or with anticoagulants, for the treatment of thrombotic disorders associated with valvular heart disease, prosthetic heart valves, cerebral vascular disease (e.g., transient ischemic attacks), coronary artery diseases (including myocardial infarction), peripheral vascular disease, renal disease and renal allograft rejection are reviewed and evaluated. Clinical evidence suggests that antiplatelet drugs are useful in preventing thromboembolism associated with coronary and cerebral vascular disorders. In peripheral vascular and renal diseases and in renal allografts, their benefits have not been proved. Further controlled clinical studies of the preventive use of these drugs for arterial thrombosis are needed.

Arterial Occlusive Diseases↗

PubMed1985

Indications and contraindications for the use of nonsteroidal antiinflammatory drugs in urology.

Prostaglandins are ubiquitous biologically active compounds that are involved in inflammatory reactions, hemostasis, and, under certain circumstances, the maintenance of renal function. NSAIDs, which inhibit PG synthesis, are used therapeutically most often as antiinflammatory agents in conditions of inflammation and pain, mostly of a nonurologic nature. However, since NSAIDs inhibit systemic PG synthesis, administration of NSAIDs can lead to adverse side effects. For example, the gastrointestinal irritation caused by NSAIDs probably reflects removal of a cytoprotective effect of gastrointestinal PGs. Similarly, the kidney may be especially susceptible to adverse effects of NSAIDs. In diseases such as peptic ulcers, diabetes, hypertension, congestive heart failure, liver disease with ascites, and renal insufficiency, PGs seem to play a protective role in the kidney. This protective role, which results from increased synthesis of vasodilator PGs in the face of elevated vasoconstrictors, is diminished in the presence of NSAIDs. Other side effects include the antagonism by NSAIDs of the action of diuretics, such that the dose of the diuretic must be adjusted accordingly. The diuretic triamterene should not be used in conjunction with indomethacin due to several reported cases of toxicity. Another drug interaction involves the salicylates, which have been shown to diminish the uricosuric effects of probenecid and sulfinpyrazone. Likewise, since corticosteroids increase the renal clearance of salicylates, it is important to monitor the patient carefully following termination of steroid treatment in patients receiving large doses of salicylates, since this change in elimination can precipitate toxicity. In addition, the NSAIDs bind to plasma proteins and, as such, can displace or be displaced by other drugs that bind in the same manner and can result in either decreased efficacy or toxicity. Despite the fact that the kidney may not be the target of NSAID therapy, renal function may be adversely affected by NSAID treatment. It has therefore been proposed that a renal-sparing NSAID would be a very useful therapeutic agent. Sulindac (Clinoril) has been suggested to be such an agent, eg, able to inhibit systemic PG synthesis (usually monitored by measuring serum thromboxane synthesis) without an apparent effect on renal PG synthesis (monitored by measurement of urinary PGs). However, recent data have suggested that Sulindac does inhibit renal PG synthesis and does not exhibit selectivity. The reasons for the discrepancy are not clear, but may relate to the doses or time intervals examined.(ABSTRACT TRUNCATED AT 400 WORDS)

Acute Kidney Injury↗

PubMed1979

Platelet survival in patients previously resuscitated from out-of-hospital ventricular fibrillation.

Platelet survival times were measured in 11 ambulatory patients within 5 to 21 months of out-of-hospital ventricular fibrillation unassociated with acute myocardial infarction. The mean platelet survival time of 7.7 +/- 2.1 days was shortened when compared with 28 normal controls of similar age (9.0 +/- 1.0 days, p less than 0.03) but not different from 56 other patients with stable angina pectoris (6.85 +/- 1.81 days, p less than 0.2). One patient with a near normal survival time of 7.5 days experienced recurrent ventricular fibrillation without associated acute myocardial infarction 1 month following the platelet survival study. Although one platelet inhibitory agent, sulfinpyrazone, may lower the incidence of sudden cardiac death following acute myocardial infarction, the shortened platelet survival time in the group of patients experiencing out-of-hospital ventricular fibrillation did not distinguish them from others with coronary artery disease.

Aged↗

PubMed1979

Antiplatelet drugs and the generalized Shwartzman reaction in the pregnant rat.

Several antiplatelet drugs (aspirin, sulfinpyrazone, hydroxychloroquine, dipyridamole, BL-3459, pyridinolcarbamate) were assayed for their ability to prevent the generalized Shwartzman reaction initiated by endotoxin in the pregnant rat, and compared to glucocorticoids (dexamethasone, hydrocortisone). The drugs were administered in a single large dose a few hours before provocation of the reaction. In opposition to glucocorticoids and beside BL-3459 which interfere with other mechanisms involved in the phenomenon, the tested inhibitors of platelet aggregation were found incapable of preventing or reducing the severity of the Shwartzman reaction.

Animals↗

PubMed1979

The effect of certain antiplatelet drugs on in vitro malonylaldehyde (MDA) production.

Several antiaggregating agents were tested with regard to their effect on platelet malonylaldehyde (MDA) production which seems to be a good marker of prostaglandin metabolism. Non-steroidal antiinflammatory compounds, namely acetylsalicylic acid (ASA), ditazole and sulfinpyrazone, showed a sure, statistically significant, inhibitory effect on MDA production while theophylline, adenosine and alpha-blocking agent nycergoline did not. Dipyridamole on the contrary, was demonstrated to have a mild but still statistically significant effect on the inhibition of platelet MDA production.

Blood Platelets↗

PubMed1984

Platelet accumulation on collagen: drugs which inhibit arachidonic acid metabolism and affect intracellular cyclic AMP levels.

We have studied the accumulation of washed platelets on collagen-coated glass from flowing platelet-red blood cell suspensions in the presence and absence of drugs. Glass tubes were 10 cm long and the flow rate was 1 ml/min, 80 s-1. For all experiments, platelet accumulation was greatest near the tube's inlet with a continuous decrease to the exit. A common feature, of those drug treatments which lead to reduced accumulation at the inlet, was an increase in outlet accumulation when compared with outlet control values. Platelet-collagen adhesion resulted in maximal release of 3H-serotonin in the presence of agents that prevent platelet aggregation on collagen. Only drug treatment known to raise cAMP levels (PGE1 and dipyridamole) or prevent the formation of prostaglandins and thromboxanes (sulfinpyrazone, indomethacin and ASA) were found to inhibit aggregate growth. Platelet aggregation on collagen in the absence of thrombin likely proceeds through the liberation of prostaglandins and thromboxanes from surface-bound platelets into the flow where they may stimulate flow-born cells. An alternate hypothesis is that such treatments affect the release of alpha-granule components necessary for aggregation.

Alprostadil↗

PubMed1983

Secondary prevention of myocardial infarction with drugs.

Clinical trials in the field of secondary prevention of myocardial infarctions are reviewed, with emphasis on those studies that were randomized and included at least 100 patients. Standardized total mortality data, when available, are provided. Five groups of drugs are reviewed: 1) antiarrhythmic drugs, including studies of phenytoin, tocainide, mexiletine and aprindine. Important, commonly used drugs in this group, which apparently have not been submitted to clinical trials, include procainamide and lidocaine; 2) lipid-lowering drugs, including estradiol, conjugated equine estrogen, dextrothyroxine, clofibrate and nicotinic acid; 3) anticoagulant drugs, the oldest and most controversial preventive drug measure. In this group, only the oral drug derivatives of indandione or coumarin have been tested, and no appropriate studies of parenteral heparin were found; 4) platelet-active drugs--six studies dealing with aspirin alone, one combining aspirin and dipyridamole, and one study of sulfinpyrazone are reviewed; and 5) beta-adrenergic blocking drugs, including practolol and timolol.

Adrenergic beta-Antagonists↗

PubMed1980

Experimental prevention of venous thrombosis.

Modern antithrombotics are no more represented merely by anticoagulants. The experiments with a series of thrombosis models enabled us to redefine several new groups appearing as yet under the name "antiplatelet agents" or "antiaggregants". The group comprises particularly acetylsalicylic acid, dipyridamole, hydroxychloroquine, sulfinpyrazone, clofibrate and suloctidyl. It was demonstrated experimentally that these drugs act predominantly by increasing endothelial stability against various noxious agents. This stabilizing effect, independent on the anticoagulant activity, is present also after the administration of oral anticoagulants in doses by one order lower in comparison with the anticoagulant dosage. In fact, the latter dosage has an opposite effect on endothelium and increases the number of circulating endothelial cells. Nevertheless, this unfavourable effect may be inhibited by suitable endotheloprotective drugs (e. g. prenylamine) and in this way an important portion of bleeding complications after oral anticoagulants may be abolished.

Animals↗

PubMed1981

Effects of platelet inhibitors on the platelet aggregation induced by plasma from patients with thrombotic thrombocytopenic purpura.

Antiplatelet drugs have been used in the treatment of thrombotic thrombocytopenic purpura (TTP) but there in vivo efficacy remains controversial. It has been shown that, in vitro, the plasmas obtained from patients with TTP induced the aggregation of washed platelets from normal donors as well as patients in remission. The effects of platelet inhibitors on the TTP plasma-induced platelet aggregation were examined. It was found that aspirin, indomethacin, ibuprofen, sulfinpyrazone, 5, 8, 11, 14-eisacotetraynoic acid, prostaglandin E1, prostaglandin I2, dBcAMP, apyrase, creatine phosphate/creatine phosphokinase, antimycin, 2-deoxy-D-glucose, dipyridamole, clofibrate, dextran 40, dextran 70, dibucaine, xylocaine, methylmaleimide, and ethylenediamine tetraacetic acid had little or no effect at all. These data lead us to conclude that at least in certain cases, antiplatelet drugs probably play a limited role in the treatment of patients with TTP.

Adenosine Diphosphate↗

PubMed1983

[Long-term antithrombotic treatment in coronary disease].

The respective roles of thrombosis and spasm in the pathogenesis of coronary disease is a subject of current discussion. Critical study of trials of long-term secondary prevention of myocardial infarction carried out between 1967 and 1982 have failed to yield any definitive conclusion as to the value of oral anticoagulants, aspirin, sulfinpyrazone or dipyridamole. However oral anticoagulants should be prescribed in the long-term, in the absence of any contra-indication, in cases of myocardial infarction complicated by ventricular ectasia, arrhythmias or cardiac failure with cardiomegaly. The use of better methods in secondary prevention trials would be desirable. Primary prevention of myocardial infarction using drugs raises difficult problems, in particular economic.

4-Hydroxycoumarins↗

PubMed1983

Measurement of flecainide acetate in human plasma by an extraction spectrophotofluorometric method.

A fluorometric method for the quantitation of 2,5-bis-(2,2,2-trifluoroethoxy)-N-(2-piperidylmethyl)benzamide acetate (R-818, flecainide acetate) in human plasma has been developed. The minimum quantifiable concentration of flecainide acetate by this method is 25 ng/ml with a 2 ml plasma sample; a slightly modified procedure which also requires the use of a microcell in the spectrophotofluorometer further increases the maximum sensitivity to 12.5 ng/ml. The precision, expressed as relative standard deviation is 2.9, 0.7, 5.6, 3.5, and 4.3% for 75, 150, 250, 500, and 700 ng flecainide acetate/ml, respectively. The accuracy, expressed as relative error, is -6.7, -3.3, -0.4, +4.4, and -0.4%, respectively, for the corresponding concentrations specified above. The relative standard deviations for the inter-day variation are 19, 7, 9, 9, 8, 10, 13, 12, and 9% for the 25, 50, 100, 200, 300, 400, 600, 800, and 1000 ng/ml standards, respectively. Preliminary data indicate that propranolol and quinidine interfere with this method while procainamide, disopyramide, hydralazine, methyldopa, diazepam, hydrochlorothiazide, and sulfinpyrazone exhibit little or no interference. The results of the analyses of clinical samples by the fluorometric method agree well with an established GLC method. Thus, the quality of the fluorometric method is considered adequate for estimating plasma flecainide acetate levels during drug therapy in most non-research settings, if careful consideration is given to possible interference by other drugs.

Chromatography, Gas↗

PubMed1983

[Anticoagulants and thrombocyte aggregation inhibitors in the treatment of heart infarct. A survey].

The treatment of causes and complications of myocardial infarction is complicated by variable response to anticoagulants and inhibitors of platelet aggregation. No generally accepted principle for treatment of myocardial infarction is available at present. Following a literature review and after our own experience we suggest an immediate treatment of acute myocardial infarction with heparin and a switch to oral anticoagulants after heparin treatment of the acute phase. Three to four weeks after the acute myocardial infarction invasive diagnostic procedure should be performed. The result will lead to a decision about possibly extended therapy with oral anticoagulants. Left ventricular aneurysma e.g. would lead to prolonged coumarin-therapy. If no oral anticoagulants are necessary long term treatment with sulfinpyrazone or Aspirin plus dipyridamole should be initiated.

Anti-Inflammatory Agents↗

PubMed1981

Inhibition of 5-methyltetrahydrofolic acid transport by amphipathic drugs.

Numerous chemically unrelated drugs after the membrane transport of folate compounds. To investigate drug structure-activity relationships, we measured the effect of amphipathic drugs (that is, compounds with polar-apolar character) on 5-methyltetrahydrofolic acid permeability of human erythrocytes. All drugs tested were inhibitory, but only compounds that exist at least partially in the anionic form were highly active. Ethacrynic acid, sulfinpyrazone, phenylbutazone, sulfasalazine, and furosemide were effective transport inhibitors in micromolar concentrations. In contrast, compounds that are capable of forming cations at physiologic pH, such as chlorpromazine, procaine, tetracaine, and papaverine, were inhibitory only in millimolar concentrations or caused hemolysis before major inhibition was seen. Inhibitory activity correlated with drug dissociation constant (r = 0.87). A double-reciprocal plot analysis of drug effect on 5-methyltetrahydrofolic acid transport showed changes in both Km and Vmax (indicating a mixture of competitive and noncompetitive inhibition) by ethacrynic acid, sulfasalazine, and phlorizin. Inhibitory activity of a series of eight phenoxyacetic derivatives, including ethacrynic acid, correlated highly with measurements of liposolubility (r = 0.87) but only weakly with the Hammet substituent constant (r = 0.56). These results suggest that the effect of amphipathic drugs on 5-methyltetrahydrofolic acid transport is influenced by drug pKa and by the presence of hydrophobic substituents, but is relatively independent of electron-attracting groups.

Adult↗

PubMed1982

[Anti-platelet aggregation therapy and ischaemic cerebral accidents due to atheroma (author's transl)].

Most controlled studies of the effects of anticoagulants on ischaemic cerebral accidents due to atheroma were carried out in the 60's and failed to show long-term beneficial results. Anti-platelet aggregation agents, such as dipyridamole, clofibrate and sulfinpyrazone, did not prove more effective. A well-conducted co-operative Canadian study has recently shown that aspirin in doses of 1300 mg/day reduced by 19% the risk of ischaemic cerebral accident or death and that this risk is further reduced in the subgroup of non-diabetic male patients without history of infarction. Another American co-operative study suggests that aspirin is more effective in patients who had several transient episodes of cerebral ischaemia and that an atheromatous lesion is present. No combination of anti-platelet aggregation agents is demonstrably superior to aspirin. The present tendency is to administer heparin immediately after ischaemic cerebral accidents.

Anticoagulants↗