Fluorocarbon emulsions

Abstract

Perfluorocarbon emulsions have been the topic of intense investigation for many years and presently there are still no absolute indications for their use in clinical practice. The relatively disappointing results of the early clinical studies, as a consequence of using low concentrations of a relatively underdeveloped emulsion, have been responsible for a largely negative impression and it is now essential that the newer second generation emulsions should be judged individually with regard to their efficacy and toxicity under different circumstances. Technological advancement in the fields of chemistry and detergent/emulsifier research will continue and new formulations are being developed which which will require to be tested in models in the laboratory. In the future, this class of drugs will continue to be the topic of intense investigation and their mechanisms of action, which are undoubtedly more complex than the simple carriage of dissolved gases in solution, will be clarified. However, whether fluorocarbon emulsions will ever be used as a 'blood substitute' as was originally anticipated is doubtful.

Use of Perfluorocarbon based Blood Substitute Perftoran in Correction of Hypoxia During Acute Anemia in Animals

“…The pathological condition of organism with a decrease in the total amount of red blood cells (RBCs) and hemoglobin in the volume of blood is called anemia. The etiological factors of anemia are diverse; they can be congenital, acquired, but regardless of the cause and pathogenesis, the common result of anemia is the decrease in the total amount of hemoglobin and RBCs in the volume of blood and as a consequence -the decrease of oxygen-carrying function of RBCs and the development of hypoxemia and hypoxia (1)(2)(3)(4).…”

“…The first is a stage of collapse and it occurs immediately after the blood loss and lasts approximately one day after the bleeding ceases. At this stage the clinical picture is dominated by the symptoms of collapse, whereas the picture of peripheral blood has almost no deviation from the norm, because with rapid massive blood loss the decrease in hemoglobin and RBCs is only due to the decrease of CBV (1)(2)(3)(4)(5). Compensatory factor in this stage is peripheral vascular spasm.…”

“…Compensatory factor in this stage is peripheral vascular spasm. The second is a hydremic stage in which decrease in CBV leads to the activation of mechanisms directed towards restoring the amount of fluid circulating in the vascular system: the tissue fluid passes into the vessels; the resulting thirst stimulates the flow of water into the body, which, along with a decrease in dieresis, which develops as a result of both the spasm of kidney vessels and the delay of sodium in organism under the influence of aldosterone released by adrenal glands, leads to an increase in the amount of water in vascular bed (2)(3)(4)(5)(6)(7). At the same time the release of RBCs from depots to blood occurs.…”

“…As a result of the processes developed in the stage of reticulocyte crisis the hemoglobinization of RBCs is normalized, the color index is restored. Together with erythropoiesis, leukopoiesis is also stimulated, which is manifested in a slight leukocytosis (3)(4)(5)(6)(7)(8)10).…”