RESUMO
A preliminary study was conducted on prevention and treatment of adrenaline induced pulmonary edema in rat with anisodamine. An animal model of rat fatal pulmonary edema close to clinical neurogenic edema was made by intravenous injection of adrenaline. It is a kind of mixed pulmonary edema with both an increase in pulmonary capillary pressure and in permeability of pulmoary microvasculature. Anisodamine showed a pretty good preventive and therapeutic effect.The observation under eletron microscope:(1) In the group of edema: It showed that protein-rich fluid accumulated in the alveolar and interstitial space. The endothelial cells and epithelial cells were swollen and degenerated. Some of the basement membrance was lost and disintegrated.(2) In the group with anisodamine prevention and treatment: It revealed that all of the pathological changes diminished. The epithelium and endothelium were normal, edema disappeared. The interstitial space widen and alveolar septal thicken which was due to the repair of the inflammation resulting in proliferation of connective tissue. The results showed that anisodamine cart inhibit the pulmonary microvascular and alveolar permeability as well.
RESUMO
Electron microscopic changes about the effect of gossypol acetic acid ongastrocnemius muscles of male monkeys,rats and guinea pigs were studied.The resultsare as follows:The ultrastructure of gastrocnemius muscles of adult male Rhesus monkeys afteradministration of gossypol orally with a daily dose of 4mg/kg for 2 years showedapparently normal in appearance,except some nuclear condensation and dissociationof nuclear membrance seen in individual animal.After oral aministration of gossypol in adult male Wistar rats with an antifertilitydosage,i.e 20mg or 30mg/kg/day for 30 days,no obvious difference was seen betweenthe experimented and control groups.Except mild distension of the smooth endoplasmicreticulum and dissociation of nuclear membrane sometimes seen in some of theexperiment animals.Similar results was obtained in the male guinea pigs.After a heavy dose(60mg/kg/day)of gossypol given to rats for 37 days,mostof the myofibrils still keep their normal periodic structures,each fiber is maintainingtheir transversly arranged pattern of dark A-bands and light I-bands alternativelyalong the whole length of the fiber.But some myofibrils had lost their normal striation.The width of the I-band increased and the breaking down or lysis precessesin few or even an individual myofibril had begun.There were no obvious pathologicalchanges seen in the mitochondria.Persistent oral administration of gossypol in ratewith a dosage of(60mg/kg/day)for 55 days,the pathological changes became moreobvious.The mitochondria became disordered in arrangement.Concomitant with thesschanges,the myofibrils appeared dystropic and fragmented.It indicated the presenceof myofibrillar degeneration.If the daily dose are increased to 60mg/kg for 25 days in guinea pigs.Theremight be no significant pathological changes in the myofibrils in them.Nevertheless,some mitochondria were swollen in various extents and the cristae became fragmentedor dissolved,which was known as mitochondrial necrosis.The relationship between hypokalemic paralysis and the present results inducedby toxic effect of gossypol were analysed and discussed.