Browsing by Subject "Pulmonary"

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    Oxygen toxicity in the infant rhesus monkey lung. Light microscopic and ultrastructural studies
    (Murcia : F. Hernández, 1986) Ainsworthl, Dorothy M.; Keithl, lngegerd; Lobas, Jeffrey G.; Farrel, Philip M.; Eicker, W.
    Eight monkeys were anesthetized with ketamine hydrochloride and positive pressure ventilated with >95% oxygen (tests) or room air (controls) for 24 hours. Two test monkeys and one control were treated with E. col; endotoxin (500 pg/kg) 1V at the start of the study and after 12 hours. Histopathological changes in the lung parenchyma were evaluated using light and electron microscopy. Interstitial edema was detected as early as 24 hours after the onset of hyperoxia but there was no significant increase in the alveolar-capillary distance (blood-air barrier). Morphologic signs of oxygen toxicity further included swelling and disruption of vascular endothelium, and swelling of alveolar Type I1 pneumocytes. There was no difference in the number of macrophages per high power field between the four groups but significant differences were observed in the number of neuroepithelial bodies (NEBs) per cmL and mast cells per high power field at the light microscopic level. Treatment with endotoxin did not protect against oxygen toxicity and was associated with an exacerbation of the morphological alterations in the lung parenchyma and swelling of alveolar Type 1 pneumocytes.
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    Remote lung injury after experimental intestinal ischemia-reperfusion in horses
    (F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2014) Montgomery, Julia B.; Hamblin, Brie; Suri, Sarabjeet Singh; Johnson, Laura E.; New, Dallas; Johnston, Jennifer; Kelly, Jenny; Wilson, David G.; Singh, Baljit
    Ischemia followed by reperfusion leads to release of toxic molecules into the circulation, and these molecules may cause injury in remote organs such as the lung. Horses commonly suffer from episodes of intestinal ischemia-reperfusion (IR) due to intestinal twisting/strangulation followed by repair. Because there is no evidence of lung injury associated with IR in horses, we designed a study to characterize the intestinal IR-associated lung inflammation and determine the effect of lidocaine on lung inflammation in IR horses. Lung tissues were collected from non-anesthetized (n=4) and anesthetized (n=4) control horses and horses (n=12) after 70 minutes of ischemia followed by 60 minutes of reperfusion. Horses in IR groups received Lactated Ringer’s Solution (LRS; n=6) or lidocaine (n=6) intravenously. Control lungs had normal histology but lungs from IR horses showed moderate accumulation of neutrophils in blood vessels and airways. We found increased staining for TLR4, IL-8, TLR9, and von Willebrand factor (vWF) along with aggregates of vWFpositive platelets in lung vessels of IR horses compared to the controls. Lung TNFα was significantly increased in IR horses compared to the control horses (P<0.05). Neutrophil numbers, but not MPO concentrations, were significantly lower, while macrophage numbers were higher in the IR group receiving lidocaine compared to the LRS horses (P<0.05). We conclude that intestinal IR leads to remote lung injury characterized by recruitment of inflammatory cells and expression of inflammatory molecules in horses, and lidocaine may ameliorate lung inflammation following intestinal IR.