To assess the manifestation and location of airway inflammation in smokers with chronic bronchitis (CB) or chronic obstructive pulmonary disease (COPD), we lavaged the airways of 12 smokers with CB and 11 smokers with COPD and coexisting CB (OCB). For comparison, the airways of 5 asymptomatic smokers (AS) and 10 healthy nonsmokers (HNS) were lavaged. In all cases, the first lavage aliquot, labeled "bronchial lavage" (BL), was processed separately from the four subsequent aliquots, which were combined and labeled "bronchoalveolar lavage" (BAL). The composition of BL and BAL fluids indicate an ongoing inflammatory process in the airways of all three groups of smokers. CB patients with obstruction had significantly lower concentrations of inflammatory cells in the BL and BAL fluids compared with subjects with nonobstructed CB. Furthermore, airway obstruction, indicated by a reduced FEV1, was significantly correlated with the concentrations of glutathione (p < 0.001), myeloperoxidase (MPO; p < 0.01), and eosinophil cationic protein (ECP; p < 0.01) in BAL fluids. Taken together, these findings suggest that the manifestations of inflammation present in the airways of smokers with CB are different in those who have developed obstruction compared with those who have not.

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In the thrombogenic theory of the pathogenesis of arteriosclerotic lesions, parietal fibrin deposits in the arteries play a primary role. In an effort to elucidate the hemostatic system in the arterial wall, the thromboplastic activity and the fibrinolytic activity (estimated as plasminogen activator) in the layers of the human aorta have been estimated. The simultaneous presence of high thromboplastic activity and little or no fibrinolytic activity found in the intima and the media suggest that fibrin can easily he deposited after tissue injury and that its eventual removal depends upon the humoral fibrinolytic system in the circulating blood. The observations apparently support the thrombogenic theory.

Felding JU, Rasmussen JB, Lildholdt T. Gas composition of the normal and the ventilated middle ear cavity. Scand J Clin Invest 1987; 47, Suppl 186 31-41.ABSTRACT Epidemiologic and controlled studies indicate that late minimal hearing impairment is a sequelae after the use ofa ventilation tube in early childhood. The patho-physiology is unknown, but abnormal middle eargas composition might be important. Therefore it is mandatory to measure middle ear gas composition in order to understand the gas exchange in the normal middle ear, as well as the,change in gas composition associated with ventilation tubes.Accordingly, the aim ofthis study was to measure middle ear gas composition both in the physiologic state and in artificial ventilation by a transtympanic tube. Employing puncture of the typanic membrane, through a liquid seal, we aspirated 300 microliters of middle ear gas. The procedure was carried out under the otomicroscope on adults without any anaesthesia. A total of 58 normals participated, along with 10 persons with unilateral ventilation tubes and 1 with a patent Eustachian tube.The mean values of physiologic state were: Partial pressure of oxygen in the middle ear cavity= 39 mm Hg, and partial pressure of carbondioxide in the middle ear cavity = 48 mm Hg. The mean values of artificially ventilated ears were: Partial pressure of oxygen in the middle ear cavity = 138 mm Hg, and partial pressure of carbondioxid in the middle ear cavity = 15 mm Hg. The total imprecision was 4,2/4,4 mm Hg and the accuracy seems fair,especially because we found a quasi equilibrium to the "most probable value", the venous blood gasses.It is concluded that artificial ventilation of the middle ear cavity, with a ventilation tube increases the oxygen content of the middle ear cavity with a factor 3.2. This constitutes a relative hyperoxic atmosphere with a subsequent possibility for a toxic tissue damage.The middle ear cavity has been described as an open, non ventilated gas pocket [I]. However, due to the minimal elasticity of the tympanic membrane, the middle ear cavity acts as a rigid box with a virtual opening via the Eustachian tube. If closed, a negative pressure develops which gradually leads to formation of fluid, i.e. secretory otitis media (SOM). Consequently, SOM is defined as fluid behind an 31 Scand J Clin Lab Invest Downloaded from informahealthcare.com by McMaster University on 12/01/14 For personal use only. I 1 FIG. 7. Model of the normal middle ear and relevant surroundings. The steady state refers to a constant middle ear pressure; this is due to a balance between diffusion from the cavity into venous blood, and the flow microvolumes ofair (1-2 p1/2 min.) through the Eustachian tube. Scand J Clin Lab Invest Downloaded from informahealthcare.com by McMaster University on 12/01/14 For personal use only.

No abstract