Perfluamin

/LABORATORY ANIMALS: Acute Exposure/ Using the hepatic macrophage system of the rat, cell alteration was examined by magnetometry after intravenous application of various perfluorochemicals (emulsified perfluorodecalin (C10F18), perfluorooctane (C8F17Br) and Fluosol-DA (corresponding to a 20% emulsion of 70% perfluorodecalin and 30% perfluorotripropylamine, C9F21N)). After administration of high doses, all perfluorochemicals led to cytoskeleton alteration. This alteration, expressed as retardation of the relaxation period of ferromagnetic iron oxide particles, was most pronounced after administration of Fluosol-DA.

/LABORATORY ANIMALS: Acute Exposure/ The effect of an emulsion of perfluorochemicals (PFC) (7 parts perfluorodecalin and 3 parts perfluorotripropylamine, 4.4 g PFC/kg bw) on organ function was determined. Whereas maximal storage of PFC was reached in the spleen as early as 12 hr after PFC administration, the liver attained a maximal PFC content only after 2 days. The increase in weight also differed: a maximum occurred in the spleen on the 4th day, in the liver on the 8th day. Indocyanine green (ICG) clearance showed a small decrease, statistically significant after 12 and 24 hr. Colloidal carbon clearance, used as a measure of the function of the reticuloendothelial system (RES) decreased instantly after PFC to less than half the control value; after full recovery a second decrease was seen which lasted till the 4th day after PFC. Pretreatment with C 48/80 or with increasing doses of E. coli endotoxin could largely obviate the depressive effect of PFC-loading on carbon clearance. Serum transaminases increased to about twice the control levels but were normal by the 2nd day, and thereafter. Alkaline phosphatase showed a 2.5 fold increase but returned to control level after the 2nd day. It is concluded that while a severe disturbance of liver function did not occur, the reduction in the capacity of the RES can become a serious factor in the defense against a simultaneously appearing infection if not compensated by activating the RES. /Perfluoro chemical emulsion/

/LABORATORY ANIMALS: Acute Exposure/ Because of uncertainty about the mechanism by which fluorocarbons ameliorate myocardial ischemia, the effects of a fluorocarbon emulsion, perfluorodecalin and perfluorotripropylamine (Fluosol-DA 20% TM) with and without 100% O2 inhalation, on cardiac hemodynamics and energetics were studied in the anesthetized dog. Left ventricular (LV) intramural partial pressure of oxygen (PmO2) was measured by before and after iv infusion of Fluosol-DA 20% (40 ml/kg), and was compared with measurements made in another group of dogs receiving the volume expander dextran (36 ml/kg). Both groups of dogs were then ventilated with 100% O2 and repeat measurements were performed. In the 11 animals receiving fluorocarbons, there were increases in left atrial pressure, LV myocardial blood flow, and LV myocardial O2 consumption (MVO2) compatible with volume expansion. After 100% O2, LV MVO2 decreased to control values, while PmO2 increased to 127 +/- 48 mm Hg (p<0.001). There were no significant changes in heart rate, arterial pressure or first derivative of LV pressure (dP/dt) during the study. In 10 dogs treated with dextran there was no change in heart rate or dP/dt, but arterial and left atrial pressures were higher after dextran infusion and remained elevated after 100% O2 inhalation. LV MVO2 increased with volume expansion, and remained increased after 100% O2. PmO2 (66 +/- 18 mm Hg) after 100% O2 was lower (p<0.02) than in the fluorocarbon-treated dogs after O2 inhalation.

/LABORATORY ANIMALS: Acute Exposure/ IV administration of emulsions of some perfluorochemicals (PFCs) are followed by lung gas-exchange alterations, lung inflation and animal death. The emulsion toxicity can be caused by both low aggregation stability of the emulsion in the blood stream and appearance of the additional gas pressure in alveoli as a result of difference in the rates of alveolar gas and PFC vapor diffusion. Theoretical and experimental analysis shows that absence of emulsion particle aggregation into blood stream, low pressure of saturated vapors of PFC phase and relatively low rate of PFC expiration from the organism are essential conditions for the creation of a safe fluorocarbon blood substitutes.

For more Non-Human Toxicity Excerpts (Complete) data for PERFLUAMINE (6 total), please visit the HSDB record page.

Basic treatment: Establish a patent airway. Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poison A and B/

Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in respiratory arrest. Positive pressure ventilation techniques with a bag valve mask device may be beneficial. Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start an IV with D5W /SRP: "To keep open", minimal flow rate/. Use lactated Ringer's if signs of hypovolemia are present. Watch for signs of fluid overload. Consider drug therapy for pulmonary edema ... . For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam (Valium) ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poison A and B/