RESUMEN
This study tests whether exposure to cigarette smoke alone or combined with cellophane wrapping of the pancreas increases the development of microscopic abnormalities in the pancreas of Syrian golden hamsters. Ninety hamsters were randomly divided into 4 groups. Thirty-five hamsters were exposed to 3 continuous hours of cigarette smoke daily for 3 months following celiotomy to cellophane wrap the gastric lobe of the pancreas (group 1). Thirty-two hamsters were not exposed to continuous cigarette smoke and had the wrap surgery alone (group 2). Twelve hamsters were exposed to cigarette smoke and had no surgery (group 3). Eleven hamsters had no exposure to cigarette smoke and no surgery (group 4). All of the hamsters were sacrificed after 3 months. The gastric (wrapped) and splenic (unwrapped) lobes of the pancreas were reviewed grossly and histologically. In all 4 groups, there were no gross abnormalities in either lobe of the pancreas. Histopathologic evaluation of the gastric lobes from group 1 showed that 13 of 35 lobes (37%) had pancreatitis (11 chronic, 1 acute, and 1 both). In group 2, 12 of 32 (38%) gastric lobes had pancreatitis (10 chronic, 2 acute). The incidence of pancreatitis in groups 1 and 2 was significantly higher than in groups 3 (0/12; p < 0.04) and 4 (0/11; p < 0.03), respectively. A significantly lower incidence of pancreatitis was found in the splenic lobes of all 4 groups when compared to gastric lobes in groups 1 and 2. Three of the 67 cellophane-wrapped glands had ductal hyperplasia. The effects of cellophane wrapping of the pancreas, both in the wrapped and unwrapped areas, induced changes of pancreatitis and hyperplasia that may be preneoplastic. Cigarette smoking, alone or combined with cellophane wrapping, did not cause these changes. Longer exposure to cigarette smoke may be needed to cause premalignant changes in the hamster pancreas.
Asunto(s)
Celofán , Páncreas/patología , Pancreatitis/patología , Humo/efectos adversos , Fumar/patología , Animales , Celofán/toxicidad , Enfermedad Crónica , Cricetinae , Modelos Animales de Enfermedad , Hiperplasia , Masculino , Mesocricetus , Páncreas/efectos de los fármacosRESUMEN
Neutrophil activation for adherent and nonadherent cells, as measured by flow cytometry, was not strongly dependent on material surface chemistry. We had hypothesized that material-induced neutrophil activation was an important parameter associated with material failure. All materials tested [cellophane, an acrylonitrile copolymer (AN69), Pellethane, nylon, polyethylene terephthalate, low density polyethylene, and polydimethylsiloxane] activated isolated human neutrophils, which were resuspended in plasma or serum, to similar extents based on L-selectin shedding, CD11b upregulation, and stimulation of the oxidative burst after 30-min exposure. Inhibition of complement activation by sCR1 unexpectedly had little effect if any on nonadherent neutrophils. However, neutrophil adhesion, but not the level of activation of the adherent cells, was strongly dependent on complement activation. Pretreatment with albumin did not inhibit adhesion or reduce neutrophil activation, but plasma pretreatment resulted in increased activation for nonadherent and adherent cells. More adhesion and a higher level of activation of adherent cells was observed following pretreatment with fibrinogen, a ligand of CD11b. Taken together these results suggest that upon contact with a material, neutrophil activation may occur though mechanisms that are not mediated by complement. For example, the presence of plasma proteins such as fibrinogen at the interface may trigger activation and the release of other activating agents. Although the material differences are small, the extent of activation may be significant and warrant further study of the mechanism and consequences of that activation.
Asunto(s)
Materiales Biocompatibles/farmacología , Citometría de Flujo , Reacción a Cuerpo Extraño/etiología , Neutrófilos/efectos de los fármacos , Estallido Respiratorio/efectos de los fármacos , Resinas Acrílicas/farmacología , Resinas Acrílicas/toxicidad , Acrilonitrilo/análogos & derivados , Acrilonitrilo/farmacología , Acrilonitrilo/toxicidad , Adsorción , Materiales Biocompatibles/toxicidad , Adhesión Celular/efectos de los fármacos , Celofán/farmacología , Celofán/toxicidad , Materiales Biocompatibles Revestidos/farmacología , Materiales Biocompatibles Revestidos/toxicidad , Activación de Complemento , Dimetilpolisiloxanos/farmacología , Dimetilpolisiloxanos/toxicidad , Fibrinógeno , Humanos , Antígeno de Macrófago-1/fisiología , Neutrófilos/fisiología , Nylons/farmacología , Nylons/toxicidad , Plasma , Polietileno/farmacología , Polietileno/toxicidad , Tereftalatos Polietilenos/farmacología , Tereftalatos Polietilenos/toxicidad , Poliuretanos/farmacología , Poliuretanos/toxicidad , Albúmina Sérica Bovina/química , Siliconas/farmacología , Siliconas/toxicidadRESUMEN
There are no differences in the multinucleate cell formation in normal and athymic mice after the subcutaneous implantation of a cellophane strip. The number of Ia+ epitheloid cells and multinucleate foreign body giant cells was lower and the number of epitheloid cells sharing the marker of activated macrophages (M 57) was higher in athymic compared to normal mice. The epitheloid cells of athymic and euthymic animals exhibited no difference in the expression of Mac-2 molecule. The difference of the expression of surface markers between athymic and euthymic animals does not influence the foreign body giant cell formation.