A significant percentage of cancer patients develop secondary lymphedema after surgery or radiotherapy. The preferred treatment of secondary lymphedema is complex physical therapy. Pharmacotherapy, for example with diuretics, has received little attention, because they were not effective and only offered short-term solutions. Sodium selenite showed promise as a cost-effective, nontoxic anti-inflammatory agent. Treatment with sodium selenite lowers reactive oxygen species (ROS) production, causes a spontaneous reduction in lymphedema volume, increases the efficacy of physical therapy for lymphedema, and reduces the incidence of erysipelas infections in patients with chronic lymphedema. Besides biological effects in reducing excessive production of ROS, sodium selenite also displays various pharmacological effects. So far the exact mechanisms of these pharmacological effects are mostly unknown, but probably include inhibition of adhesion protein expression.

The effects of the H1-receptor antagonist dimethpyrindene and the H2-receptor antagonist burimamide on circulatory and respiratory parameters and on plasma histamine levels were tested in 21 mongrel dogs. Both drugs released histamine. The incidence for this effect was 10/11 in the case of dimethpyrindene and 5/10 in the case of burimamide. Following dimethpyrindene all animals showed arterial hypotension, pulmonal hypertension, decrease in peripheral resistance and hyperventilation. The portal venous pressure was increased in dogs reacting by a histamine release. Following burimamide both an initial arterial hypertension and a subsequent hypotension were observed the latter being more pronounced in the group with histamine release. In this group the portal venous pressure raised considerably. In the non-reacting animals cardiac output was elevated, probably due to a release of catecholamines. It seemed remarkable that the effect of exogenous histamine on portal venous pressure was completely blocked by dimethpyrindene, but not the action of histamine released by the drug itself. It is concluded that the effects of anti-histaminic drugs on possibly histamine-induced physiological and pathophysiological processes should be interpreted very carefully as far as their specificity is concerned.

The effects of histamine on the circulatory system have been the subject of a great number of investigations [1]. There was a wide range in doses of histamine applied, in methods used for determining circulatory parameters and in laboratory animals involved, and the results obtained were often contradictory. In order to contribute to the main problem whether endogenous histamine is involved in pathophysiological or clinical stituations it was the aim of the present study to answer the following questions:(1) Do the effects of histamine in the circulatory system depend on the actual histamine levels?(2) How do H1-and H2-receptor antagonists influence the histamine actions? (3) Do H1-and Ha-receptor antagonists alter the actual plasma histamine levels? MethodsThe experiments were carried out in 23 mongrel dogs (both sexes, 14-28 kg body weight) which were anaesthesized with pentobarbitone and breathed room air spontaneously. The acid-base balance and the body temperature were controlled.Aortal plasma histamine concentration was measured by a specific ftuorometric test [2,3]. Blood pressure was recorded in aorta, pulmonal artery, portal vein and inferior caval vein by Statham strain gauges and was determined at end exspiration. Blood flow in the superior mesenteric artery and hepatic artery was estimated using electromagnetic flow meters (Statham). Cardiac output was calculated with the thermodilution method [4,5]. Resistance in several regions of the vascular bed was calculated from the equation R = Ap/Q 9 kg body weight [6]. Pulse rate and breath rate were counted from the blood pressure curves recorded.The experiments were started 30 minutes after completing the operation (laparotomy, insertion of catheters, flow probes and the thermistors, calibrations).Only one dose of histamine (10 ~g/kg histamine dihydrochloride corresponding to 6 ~g/kg histamine base) was injected into the inferior caval vein. 30 minutes later 5 mg/kg dimethpyrindene (Zyma-Blaes, Munich) or 10 mg/kg burimamide (SK & F, Welwyn Garden, UK) were administered into the same vein. 10 minutes later on again 6 ~-g/kg histamine base were applied. Blood samples for plasma histamine assay were taken immediately before and 30 seconds after the injection of histamine. Results(a) Effects of a single dose of histamine (6 sg/kg on plasma histamine levels and circulatory parameters (Table 1) The plasma histamine concentration increased by about 6000% though the dose of histamine applied (about 120 ~g/animal) by no means was life-threatening or even fatal to the dogs.Cardiac output and pulse rate were not altered, but arterial and central venous pressures as well as total systemic resistance decreased considerably. Since arterial pressure and total systemic resistance decreased to the same extent the effect of this dose of histamine on the mean aortal pressure was mainly caused by peripheral vasodilatation and not by negative inotropic action of histamine on the heart.At the time of maximum aortal hypotension there was no increase in pulmonal arterial pressur...

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Several studies have shown an impressive reduction in swelling as a result of compression, and inelastic bandages have become widely accepted as a part of lymphatic decongestive therapy for managing lymphoedema.Lymphoedema bandaging is indicated to reduce swelling, improve limb shape, skinand tissue-condition and to ameliorate symptoms such as discomfort. Compression therapy for lymphoedema is based mainly on the use of inelastic, short-stretch bandages with high compression, usually protecting the skin with polyurethane foam bandages. In this preliminary report it is shown that completely rigid material like zinc paste applied without padding provides a good level of efficacy.