RESUMEN
The ability to assess the activity of gonadotropin-releasing hormone (GnRH) neurons has been greatly enhanced by transgenic animal models with targeted expression of green fluorescent protein (GFP). However, it has yet to be demonstrated that the GnRH system continues to exhibit a full range of normal physiological functions in the presence of such genetic manipulation. Accordingly, we have used repetitive blood sampling via indwelling venous catheters to define LH secretory patterns in normal and transgenic mice. Transgenic females proved to be reproductively competent as defined by fecundity, appropriate cyclic changes in vaginal cytology in intact adult females, and spontaneous LH surges as well as surges in response to steroid or mating stimuli. The expression of c-fos following such steroid treatment and mating in ovariectomized transgenics was similar to the expression previously reported in nontransgenic mice. Likewise, the percentage of retrogradely labeled GnRH neurons was similar to that reported in nontransgenic mice. However, episodic LH secretion, an index of GnRH pulse generator activity, was dramatically compromised in ovariectomized female transgenics compared with C57BL6 controls of both sexes and castrated transgenic males. Taken together, these findings suggest that the GnRH pulse generator is selectively impaired in ovariectomized females in which GnRH neurons express GFP.
Asunto(s)
Hormona Liberadora de Gonadotropina/fisiología , Hipotálamo/fisiología , Hormona Luteinizante/metabolismo , Neuronas/fisiología , Proteínas Proto-Oncogénicas c-fos/fisiología , Animales , Femenino , Proteínas Fluorescentes Verdes/análisis , Proteínas Fluorescentes Verdes/genética , Hormona Luteinizante/sangre , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Transgénicos , Microscopía Fluorescente , Orquiectomía , OvariectomíaRESUMEN
BACKGROUND: Chronically implanted catheters often become covered with a thin, white adherent covering of tissue that has been referred to as a fibrin sheath. This tissue often interferes with catheter function. METHODS: To chronicle the development of this sheath, rats were implanted with silicone rubber central venous catheters. Five rats were euthanized at 3,7, and 60 days postimplantation so that gross necropsy and histology could be performed on the catheterized vessels. RESULTS: The coating that developed around the external portion of the catheter started as a dark red thrombus containing fibrin and progressed into vascularized, fibrous connective tissue. CONCLUSIONS: The translucent to white sheath that forms around chronically implanted catheters is not composed of fibrin and is therefore not likely to be dissolved by fibrinolytic agents such as urokinase, streptokinase, or tissue plasminogen activator.
Asunto(s)
Cateterismo Venoso Central/efectos adversos , Venas Yugulares/patología , Trombosis/patología , Animales , Colágeno/análisis , Colorantes , Femenino , Fibrina/análisis , Hematoxilina , Histocitoquímica , Venas Yugulares/química , Masculino , Ácido Fosfotúngstico , Ratas , Ratas Sprague-DawleyRESUMEN
Hexoses infused slowly into the duodenum or hepatic-portal vein reduce feeding. However, hexoses can increase food intake following rapid infusion via either of these two routes. Insulin responses and resultant glycemic changes differ following fast and slow duodenal glucose infusion. This is unlikely to be the primary explanation, because fructose affects feeding but is not a secretagogue of insulin under our testing conditions. In follow-up studies, we infused glucose or fructose into the hepatic-portal vein at the fast or the slow rate, and measured 14C incorporation into liver mitochondria and glycogen, and tritiated water uptake into hepatic lipids. Fast infusion of glucose or fructose increased lipid formation, reducing mitochondrial uptake and glycogen formation, and was associated with hunger enhancement. Slow hexose infusion was associated with substrate uptake into mitochondria and glycogen, with reduced uptake into hepatic fat. These findings all are consistent with the previously observed positive correlation seen between mitochondrial oxidation and satiety (28).