Risk of deep venous thrombosis in drain clamping with tranexamic acid and carbazochrome sodium sulfonate hydrate in total knee arthroplasty.

The aim of this randomized prospective study was to clarify risks associated with a drain-clamping method using tranexamic acid and carbazochrome sodium sulfonate hydrate after total knee arthroplasty (TKA). Subjects comprised 100 patients scheduled to undergo TKA, randomized into 2 groups: 50 patients received the drain-clamping method using tranexamic acid and carbazochrome sodium sulfonate hydrate and 50 patients received drain-clamping with saline. Although bleeding volume was significantly lower in the group with tranexamic acid and carbazochrome sodium sulfonate hydrate, risk of asymptomatic deep venous thrombosis as detected by ultrasonography was comparable between groups. Tranexamic acid and carbazochrome sodium sulfonate hydrate in the drain-clamping method help reduce bleeding after TKA without increasing the risk of deep venous thrombosis.

Double-blind, randomized clinical trial of troxerutin-carbazochrome in patients with hemorrhoids.

This multicenter, double-blind, randomised study was undertaken to determine the efficacy and safety of a combination of troxerutin 150 mg and carbazochrome 1.5 mg compared to carbazochrome alone in patients with acute uncomplicated hemorrhoids. Patients were administered by the intramuscular route (one ampoule) twice daily for one week. Both subjective and objective efficacy variables significantly improved in the combination drug group only, thus demonstrating the rationale for a combination therapy. Treatments were safe and well tolerated either at a local or systemic level.

Effect of serotonin antagonists on patients with atypical facial pain.

The effect of the serotonin antagonist iprazochrome was studied in 30 patients with atypical facial pain and 10 control nonpain volunteers. The aim of the study was to investigate the effect of a single dose of iprazochrome and of its short-term administration in patients with chronic pain. Twelve of the 30 patients reported increased pain, 16 reported no effect, and two reported pain relief for some hours after taking iprazochrome. None of the controls reported any effect from iprazochrome. Four of the 12 patients who reported increased pain also reported increased pain in distant organs, especially in the joints. A hypothesis of the mechanism is presented and a possible use of iprazochrome as a diagnostic tool is suggested.

Protective effect of sulfinpyrazone against catecholamine metabolite adrenochrome-induced arrhythmias.

Single intravenous injection of adrenochrome (10 to 50 mg/kg body weight), an oxidation product of catecholamines, has been shown to induce arrhythmias and cause death in anesthetized rats in a dose-dependent manner. Sulfinpyrazone, which is an inhibitor of platelet aggregation, was found to protect animals from these adrenochrome effects. It is suggested that sudden death due to arrhythmias in patients following the first attack of myocardial infarction of during other stressful situations may be linked to the formation of adrenochrome from abnormally high catecholamine levels in blood. Furthermore, results presented here also suggest that the reduction in the mortality rate of patients on sulfinpyrazone therapy may involve an antiarrhythmic property of the drug.

Ventricular dysfunction and necrosis produced by adrenochrome metabolite of epinephrine: relation to pathogenesis of catecholamine cardiomyopathy.

We have examined the effects of adrenochrome and other metabolites of epinephrine on the ultrastructure and contractile activity of isolated rat hearts perfused under conditions in which the heart rate and coronary flow were controlled. Perfusion of hearts with epinephrine or metanephrine significantly increased contractile force; vanillylmandelic acid and dihydroxymandelic acid did not alter contractile force development, whereas adrenochrome (50 mg/L) declined contractile force with epinephrine (50 mg/L) was associated with increased resting tension and maximum rates of force development and relaxation, and decreased time for peak tension development and 1/2 relaxation. On the other hand, hearts perfused with adrenochrome showed early decline followed by steady increase in resting tension; maximum rates of force development and relaxation were reduced and times for peak tension development and 1/2 relaxation were increased. Hearts perfused or 10 minutes or more with adrenochrome (50 mg/L), but not epinephrine, metanephrine, dihydroxymandelic acid or vanillylmandelic aicd, showed ultrastructural damage. Adrenochrome concentrations of 10 or 25 mg/L altered the appearance of mitochondria after 30 minutes of perfusion. Infusion of epinephrine (1 mg/L) during perfusion with adrenochrome partially maintained contractile force during the first 15 minutes of perfusion but did not alter the severity of ultrastructural changes due to adrenochrome. These results are consistent with the concept that oxidation products of catecholamines such as adrenochrome are partly responsible for inducing myocardial necrosis and failure following massive catecholamine injections in intact animals.