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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because of reports of fluroxene toxicity in man, the effect of phenobarbital treatment on the toxicity and metabolism of fluroxene was studied in 9 rhesus monkeys. Six monkeys that were exposed to a mean calculated alveolar fluroxene concentration of 5.8% for 4-hr periods up to a total of 16 hr showed no evidence of toxicity. Two animals were sacrificed after a single 4-hr exposure to obtain control measures of fluroxene metabolites in tissues. Four monkeys that had previously survived received exposures to fluroxene and 3 monkeys that had no exposure to fluroxene died during fluroxene anesthesia after treatment with phenobarbital (mean time, 3 hr). Toxicity was manifested by arterial hypotension, pulmonary edema, and arterial hypoxemia. Phenobarbital treatment enhanced production of fluroxene metabolites, including the highly toxic trifluoroethanol. Concentrations of trifluoroethanol in mixed-expired gas, blood, and urine, and of total nonvolatile fluorine in blood, urine, and tissues of animals treated with phenobarbital were 2 to 10 times as in control animals. The results suggest that the rhesus monkey is a valuable model for the study of fluroxene pharmacology and that inclusion of an enzyme-inducing challenge in the evaluation of potential toxicity of other anesthetics seems warranted.
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PMID:Fluroxene toxicity induced by phenobarbital. 0 Nov 68

The production of hydrofluoric acid (HF) and its use have increased remarkably due to the rapid development of the electronic and petrochemical industries. HF has a highly corrosive and penetrating action when it comes in contact with organic material, including body tissue. When burns are caused by a high concentration of HF, fatal cases have been reported, even when the contact with HF is only for a short time or on a small area of the body. The causes of death have been reported to be lung edema, mineral disturbance and systemic injury. But no pathological experiments have been reported. In the present study, experiments of HF burns using mice (d.d.Y., 6w, male) were performed, mainly histopathologically and ultramicroscopically. Histological examination revealed that thrombosis occurred in the lung, and that the group in which mice had more thrombi showed a higher death rate. Thrombosis in the lung may be one of the main causes of death by hydrofluoric acid burns. Other organs showed no significant change. Ultrastructural examination of the lungs, revealed that the thrombi were seen in the capillary of the alveolar septa much more than in the pulmonary arteries and were mainly composed of platelets. The endothelial cells in the lungs were injured and had condensed cytoplasm, intracellular edema, or dilation of the intercellular gap. The basement membrane of the capillary was sometimes bared between the strongly condensed endothelial cells, but no platelets directly touched the membrane. Moreover, that no platelets directly touched the subendothelial tissue and the mechanism of the platelet aggregation is interesting. Platelet aggregation was thought to have resulted from the unbalance between thrombogenic factors and antithrombogenic factors in the blood above the surface of endothelial cells caused by endothelial injury. Endothelial cells in the lungs were assumed to be injured by fluoride, directly or indirectly, because the group which showed higher fluorine contents in the lungs showed more severe injury to the endothelial cells and because the fluorine contents in the lung increased much more than that in the other organs which had no thrombi.
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PMID:[Hydrofluoric acid burn: particulars on multiple pulmonary thrombi]. 260 38

The use of fluorine compounds in various areas of medicine, particularly in dentistry, as well as in agriculture and industry became very popular in the second half of the 20th century. Fluorine owed this widespread acceptance to observations that its compounds stimulate ossification processes and reduce the prevalence of caries. Unfortunately, growing expectations overshadowed the truth regarding interactions of fluoride on the molecular level. The fact was often ignored that fluoride is toxic, even though laboratory data stood for a careful approach to the benefits of usage. Excessive exposure to fluoride may lead to acute poisoning, hyperemia, cerebral edema, and degeneration of the liver and kidneys. Acute intoxication through the airways produces coughing, choking, and chills, followed by fever and pulmonary edema. Concentrated solutions of fluorine compounds produce difficult to heal necrotic lesions. In spite of these dramatic symptoms, acute intoxications are relatively rare; the more common finding is chronic intoxication attributable to the universal presence of fluorine compounds in the environment. The first noticeable signs of excessive exposure to fluoride in contaminated water, air, and food products include discolorations of the enamel. Dental fluorosis during tooth growth and loss of dentition in adulthood are two consequences of chronic intoxication with fluorine compounds. Abnormalities in mineralization processes affect by and large the osteoarticular system and are associated with changes in the density and structure of the bone presenting as irregular mineralization of the osteoid. Fluorine compounds also act on the organic part of supporting tissues, including collagen and other proteins, and on cells of the connective tissue. These interactions reduce the content of collagen proteins, modify the structure and regularity of collagen fibers, and induce mineralization of collagen. Interactions with cells produce transient activation of osteoblasts, stimulate fibroblasts to produce collagenase, and trigger toxic reactions in osteocytes and chondrocytes of trabecular bone. Growing deformations of the skeleton reduce mobility and result in permanent crippling of the patient. Fluoride increases the mass of non-collagen proteins such as proteoglycans and glucosaminoglycans, accelerating skin aging even though protein biosynthesis is generally suppressed. The final outcome includes progressive vascular lesions and disorders of energy metabolism in muscles. In conclusions, the use of fluoride, particularly by dentists and pediatricians, must be controlled and adapted to individual needs. It is worth remembering that fluoride: is the cause of disability due to bone deformations and abnormalities in the musculoskeletal system; reduces the incidence of caries but do not protect against tooth loss; exerts an adverse effect of metabolic processes in the skin; accelerates calcification of vessels and thus reduces their elasticity; inhibits bioenergetic reactions, in particular oxidative phosphorylation, reducing physical activity of muscles. These findings suggest that fluorine may be yet another factor in accelerated aging and revive the dispute started more than two and half thousand years ago whether aging is a physiologic or pathologic process. The understanding of factors modifying the process of aging is the basis for preventive measures aimed at extending life and maintaining full psychosocial activity.
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PMID:[Fluorine as a factor in premature aging]. 1689 76

The present investigation was conducted to evaluate the teratogenic and developmental toxicity of fluoride and endosulfan alone and in combination in pregnant Swiss albino mice exposed during the organogenetic period (5-14 days) of gestation. Fluoride (25.1 mg/kg body weight in water) and endosulfan (1.8 mg/kg bw by oral intubation) when administered alone and in combination (fluoride 25.1 mg/kg bw + endosulfan 1.8 mg/kg bw) to pregnant mice caused significant teratogenic effects in developing fetuses. There was no maternal mortality but significant decreases in maternal weight gain and numbers of live fetuses and significant increases in numbers of fetal resorption were recorded in the treated groups. The fetal body weight and litter size also decreased significantly in all treated groups. No external malformations were observed in any of the fetuses. The percent of visceral and skeletal anomalies increased in the fetuses of all treated groups. The fetal malformations observed were internal hydrocephaly, microphthalmia, anophthalmia, pulmonary edema, subcutaneous edema, reduced ossification of skull bones, widened cranial sutures, rib anomalies (short, wavy, partially ossified, or absent ribs), and reduced ossification of phalanges. The occurrence of visceral and skeletal malformations was more severe in the combination group, suggesting additive interaction of fluoride and endosulfan in inducing developmental toxicity in Swiss albino mice.
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PMID:Combination of fluoride and endosulfan induced teratogenicity and developmental toxicity in Swiss albino mice exposed during organogenesis. 3159 77