Fibrosis hepatica y progesterona

Con el fin de estudiar la acción de la Prog sobre la fibrosis hepática, fue inducida esta alteración por medio de la ingesta de C14C y etanol, en 55 conejos, entre 1 y 2 años, raza New Zealand; desarrolando la fibrosis en 6 meses. El grupo de animales tratados con Prog, ya sea desde el comienzo o después de 180 días de recibir el tóxico, presentaba disminución o menos fibrosis; así como protección del hepatocito, que se evidenciaba por la nobalonización o vacuolización de las células, no infiltrado inflamatorio, ni tampoco metamorfosis grasa. Si algunas de estas alterraciones habían aparecido, al iniciar el tratamiento con Prog disminuían gradualmente hasta desaparecer. Los datos de laboratorio tuvieron una diferencia altamente significativa a los 60 y 180 días entre los grupos que recibían el tóxico y los que revibían Prog, ya sea desde el comienzo o diferida. La Prog, como se ha visto en cultivos de fibroblastos fetales y en el tratamiento de tumores desmoides o adhesiones quirúrgicas, destruye los fibroblastos y por consiguiente disminuye el tamaño de estos tumores y la cohesión de las adherencias. La razón de no haberse hallado una resolución total de la cirrosis (aunque si una disminución manifiesta de la fibrosis) puede deberse a la actividad de miofibroblastos que provocan la retracción del tejido hepático dañado

Fibrosis hepatica y progesterona

Con el fin de estudiar la acción de la Prog sobre la fibrosis hepática, fue inducida esta alteración por medio de la ingesta de C14C y etanol, en 55 conejos, entre 1 y 2 años, raza New Zealand; desarrolando la fibrosis en 6 meses. El grupo de animales tratados con Prog, ya sea desde el comienzo o después de 180 días de recibir el tóxico, presentaba disminución o menos fibrosis; así como protección del hepatocito, que se evidenciaba por la nobalonización o vacuolización de las células, no infiltrado inflamatorio, ni tampoco metamorfosis grasa. Si algunas de estas alterraciones habían aparecido, al iniciar el tratamiento con Prog disminuían gradualmente hasta desaparecer. Los datos de laboratorio tuvieron una diferencia altamente significativa a los 60 y 180 días entre los grupos que recibían el tóxico y los que revibían Prog, ya sea desde el comienzo o diferida. La Prog, como se ha visto en cultivos de fibroblastos fetales y en el tratamiento de tumores desmoides o adhesiones quirúrgicas, destruye los fibroblastos y por consiguiente disminuye el tamaño de estos tumores y la cohesión de las adherencias. La razón de no haberse hallado una resolución total de la cirrosis (aunque si una disminución manifiesta de la fibrosis) puede deberse a la actividad de miofibroblastos que provocan la retracción del tejido hepático dañado (AU)

[Hepatic fibrosis and progesterone]. / Fibrosis hepática y progesterona.

To study the progesterone (Prog.) action on the hepatic fibrosis, we produced fibrosis on 55 New Zealand male rabbits, by oral ingestion of carbon tetrachloride (Cl4C) and ethanol. They developed it in six months. All the animals received the toxic. A group of these animals also received the Prog since the onset (0.66 mg/3 times a week, IM) and the rest received it 180 days after the beginning of the experiment. We could see in the biopsies of the animals who received Prog since the beginning or after 180 days: protection of the hepatocytes, no vacuolization of the cell, no inflammatory infiltrate, no fat metamorphosis, very thin fibrous hands. If one of these alterations had appeared with the toxic, the Prog action would have diminished it gradually until its disappearance. Between the groups who received only toxic and the groups that received th Prog (at the beginning or deferred), the laboratory results showed a high significative difference (p less than o.01) especially in the transferases (ASAT-ALAT) in the 60-180 days period. The Prog in the fibroblasts culture and in the treatment of desmoid tumours, on operative adhesions, destroy the fibroblasts and for this action diminished the volume of the tumour and the adhesions. Perhaps the incomplete resolution of the cirrhosis (though the hands of fibrosis diminished considerably) could be explained by the activity of another kind of fibroblast (the myofibroblast), which provokes the retraction of cirrhotic hepatic tissue.

Fibrosis hepática y progesterona. / [Hepatic fibrosis and progesterone]

To study the progesterone (Prog.) action on the hepatic fibrosis, we produced fibrosis on 55 New Zealand male rabbits, by oral ingestion of carbon tetrachloride (Cl4C) and ethanol. They developed it in six months. All the animals received the toxic. A group of these animals also received the Prog since the onset (0.66 mg/3 times a week, IM) and the rest received it 180 days after the beginning of the experiment. We could see in the biopsies of the animals who received Prog since the beginning or after 180 days: protection of the hepatocytes, no vacuolization of the cell, no inflammatory infiltrate, no fat metamorphosis, very thin fibrous hands. If one of these alterations had appeared with the toxic, the Prog action would have diminished it gradually until its disappearance. Between the groups who received only toxic and the groups that received th Prog (at the beginning or deferred), the laboratory results showed a high significative difference (p less than o.01) especially in the transferases (ASAT-ALAT) in the 60-180 days period. The Prog in the fibroblasts culture and in the treatment of desmoid tumours, on operative adhesions, destroy the fibroblasts and for this action diminished the volume of the tumour and the adhesions. Perhaps the incomplete resolution of the cirrhosis (though the hands of fibrosis diminished considerably) could be explained by the activity of another kind of fibroblast (the myofibroblast), which provokes the retraction of cirrhotic hepatic tissue.

Respiratory changes after intraarterial acetylcholine and abdominal concussion.

In 50 dogs anesthetized with chloralose the respiratory changes produced by intraarterial acetylcholine (ACh) and after an abdominal blow, were studied. Intraarterial ACh produced expiratory apnea when it was injected in the superior and inferior mesenteric artery, splenic and left gastric artery. This apnea disappeared when the splanchnic nerves were severed and disappeared or decreased after atropine sulfate was injected. The duration of the apnea coincides with the contraction of the gut smooth muscle recorded, with a small balloon placed in the jejunum or in the ileum. The ACh did not produce respiratory changes when it was injected in the hepatic artery and pulmonary trunk. In the peripheral arteries, especially in the subclavian, ACh injection produced a respiratory stimulation which could be caused by the pain which accompanied the muscular contraction. After a blow in the abdominal wall, an expiratory apnea was also obtained, similar to that observed by the injection of ACh in the gastrointestinal arteries. This apnea disappeared when splanchnic nerves were severed or when atropine sulfate was injected. Smooth muscle contraction was also observed, suggesting that the expiratory apnea was originated in the smooth muscle receptors.

Respiratory changes after intraarterial acetylcholine and abdominal concussion.

In 50 dogs anesthetized with chloralose the respiratory changes produced by intraarterial acetylcholine (ACh) and after an abdominal blow, were studied. Intraarterial ACh produced expiratory apnea when it was injected in the superior and inferior mesenteric artery, splenic and left gastric artery. This apnea disappeared when the splanchnic nerves were severed and disappeared or decreased after atropine sulfate was injected. The duration of the apnea coincides with the contraction of the gut smooth muscle recorded, with a small balloon placed in the jejunum or in the ileum. The ACh did not produce respiratory changes when it was injected in the hepatic artery and pulmonary trunk. In the peripheral arteries, especially in the subclavian, ACh injection produced a respiratory stimulation which could be caused by the pain which accompanied the muscular contraction. After a blow in the abdominal wall, an expiratory apnea was also obtained, similar to that observed by the injection of ACh in the gastrointestinal arteries. This apnea disappeared when splanchnic nerves were severed or when atropine sulfate was injected. Smooth muscle contraction was also observed, suggesting that the expiratory apnea was originated in the smooth muscle receptors.