Pulmonary oxygen toxicity in chickens and rabbits

Chickens exposed to hyperbaric oxygen (3 to 5 ATA) or to 100% oxygen at atmospheric pressure for prolonged periods showed no pathologic pulmonary damage, although hydrogen peroxide did accumulate in their airways. Superoxide dismutase in the peripheral nucleated red blood cells and the rate of oxidation of specifically labeled glucose were increased in chickens exposed to hyperbaric oxygen for three hours. Superoxide dismutase increased in the lung lavage of the rabbits and in the peripheral nucleated red blood cells. Glucose oxidation was unchanged. The difference in superoxide dismutase is probably the result of the desquamated, damaged cells found in the rabbit lung lavage. That only rabbit bronchi are lined with oxidant-sensitive ciliated cells suggests that the absence of these ciliated cells in fowl may well be responsible for the observed resistance of these birds to oxidant damage by oxygen.     

核因子-kB在高脂饮食兔颈总动脉球囊损伤后的动态变化及其与内膜增生的关系

目的观察高脂饮食兔颈总动脉球囊损伤后核因子kB（NF-kB）表达的变化及其与动脉内膜增生的关系。方法对高脂饮食兔颈总动脉球囊损伤后不同时间段的颈总动脉标本采用组织形态学方法检测内膜增生；采用原位杂交方法检测损伤血管NF-kB mRNA的表达。结果（1）球囊损伤后，内膜面积随时间逐步增生，中层各时段均未见明显变化，内膜／中层比率随时间逐步增长。对照侧内膜轻度增生但明显较损伤侧轻（P〈0．05）。（2）球囊损伤后6h即可见NF-kB表达，并于2周达高峰，4周仍有较强表达。NF-kB在损伤侧表达均强于对照侧（P〈0．05）。结论高脂饮食免颈总动脉球囊损伤后，NF-kB被激活，从而引起炎症反应，导致内膜增生可能是再狭窄发生的重要机制之一。     

核因子-κB在高脂饮食兔颈总动脉球囊损伤后的动态变化及其与内膜增生的关系

目的观察高脂饮食兔颈总动脉球囊损伤后核因子κB(NF-κB)表达的变化及其与动脉内膜增生的关系。方法对高脂饮食兔颈总动脉球囊损伤后不同时间段的颈总动脉标本采用组织形态学方法检测内膜增生;采用原位杂交方法检测损伤血管NF-κB mRNA的表达。结果⑴球囊损伤后,内膜面积随时间逐步增生,中层各时段均未见明显变化,内膜/中层比率随时间逐步增长。对照侧内膜轻度增生但明显较损伤侧轻(P<0.05)。⑵球囊损伤后6 h即可见NF-κB表达,并于2周达高峰,4周仍有较强表达。NF-κB在损伤侧表达均强于对照侧(P<0.05)。结论高脂饮食兔颈总动脉球囊损伤后,NF-κB被激活,从而引起炎症反应,导致内膜增生可能是再狭窄发生的重要机制之一。     

Pulmonary effects of inhaled zinc oxide in human subjects, guinea pigs, rats, and rabbits.

Occupational exposure to freshly formed zinc oxide (ZnO) particles (less than 1.0 micron aerodynamic diameter) produces a well-characterized response known as metal fume fever. An 8-hr threshold limit value (TLV) of 5 mg/m3 has been established to prevent adverse health effects because of exposure to ZnO fumes. Because animal toxicity studies have demonstrated pulmonary effects near the current TLV, the present study examined the time course and dose-response of the pulmonary injury produced by inhaled ZnO in guinea pigs, rats, rabbits, and human volunteers. The test animals were exposed to 0, 2.5, or 5.0 mg/m3 ZnO for up to 3 hr and their lungs lavaged. Both the lavage fluid and recovered cells were examined for evidence of inflammation or altered cell function. The lavage fluid from guinea pigs and rats exposed to 5 mg/m3 had significant increases in total cells, lactate dehydrogenase, beta-glucuronidase, and protein content. These changes were greatest 24 hr after exposure. Guinea pig alveolar macrophage function was depressed as evidenced by in vitro phagocytosis of opsonized latex beads. Significant changes in lavage fluid parameters were also observed in guinea pigs and rats exposed to 2.5 mg/m3 ZnO. In contrast, rabbits showed no increase in biochemical or cellular parameters following a 2-hr exposure to 5 mg/m3 ZnO. Differences in total lung burden of ZnO, as determined in additional animals by atomic absorption spectroscopy, appeared to account for the observed differences in species responses. Although the lungs of guinea pigs and rats retained approximately 20% and 12% of the inhaled dose, respectively, rabbits retained only 5%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Naltrexone prevents ethanol-induced changes in rat thymus

Ethanol is known to suppress the immune response, but the underlying mechanism accounting for the immunosuppression is not clearly elucidated yet. The purpose of this study was to investigate the effect of a single dose of ethanol on relative proportion of the four major rat thymocyte subsets and possible mechanism of its action. To this end, adult female AO rats were treated with: a) ethanol (2 or 4 g/kg, IP), b) naltrexone (5 mg/kg, IP) followed 45 min later by ethanol (2 or 4 g/kg, IP), c) naltrexone (5 mg/kg, IP), or d) only saline. Twenty hours later the rats were sacrificed and the proportion of the four major thymocyte populations defined by expression of CD4 and CD8 molecules was analyzed. Flow cytometric analysis revealed that ethanol evoked a decrease in the percentage of double-positive CD4+CD8+ thymocytes followed by a proportional increase in the percentage of single-positive CD4+CD8− cells. Naltrexone pretreatment prevented the ethanol-induced alterations in thymocyte subsets. The results clearly indicate that ethanol affects the process of intrathymic T-cell maturation. It seems that this effect might be mediated by an opioid-dependent mechanism.     

Pituitary hyperplasia

Pituitary hyperplasia is rare, difficult to diagnose and sometimes controversial. The hyperplasia could be physiologic which is usually reversible, or pathologic which varies in presentation from incidental to tumor like lesion with and without hormonal disturbance. Any pituitary cell is capable of undergoing hyperplasia in the presence of the right stimuli. In this article we summarize the various pathologic and morphologic features of each subtype of pituitary hyperplasia, give an account of the molecular, hormonal and cellular basis of this condition and outline its clinical significance, differential diagnosis and prognosis.     

Pituitary hyperplasia in primary hypothyroidism

One case of primary hypothyroidism with hyperplasia of the pituitary gland was reported. This enlargement was decreased after hormone replacement therapy. Pituitary hyperplasia occurs secondarily to primary endocrine gland failure. Reactive enlargement of the pituitary gland must be differentiated from primary pituitary abnormalities in order to avoid unnecessary surgery.