Evidence that halothane anaesthesia induces intracellular translocation of surface coat and Golgi response in equine pulmonary intravascular macrophages.

The pulmonary intravascular macrophages (PIMs) of horse contain a unique electron-dense globular surface-coat which is arranged in a linear fashion in conformity with the contours of the cell membrane. The coat is sensitive to heparin treatment and to the digestive effect of lipolytic lipase, suggesting that the coat is predominantly composed of lipoproteins. During the present study, ultrastructural features of PIMs were analysed after exposing horses to halothane inhalation which was chosen as the model agent of lipid-soluble anaesthetic. The surface-coat showed acute sensitivity to halothane by disappearing almost completely from the surface after 1-2 h of exposure. The cell membranes were thrown into extraordinary arrays of lamellipods, pseudopods and veils. Concurrently, the globular units of the coat were translocated into the endosomal-lysosomal system, most probably via receptor-mediated endocytosis. There was a high profile of the expanded Golgi apparatus especially the trans Golgi network (TGN) in close association with the centrioles and microtubules. Cytochemistry revealed an enrichment of the Golgi complex with acid phosphatase activity. On the other hand, halothane showed an inhibitory effect on the lysosomal acid phosphatase of the PIMs. It is proposed that the Golgi response occurred as an obligatory concomitant of internalization of the surface-coat and its subsequent passage through endosomal-lysosomal system. The acid phosphatase activity as a marker enzyme of the expanded Golgi is correlated with metabolic effects of the internalized coat which is unique to the pulmonary intravascular macrophages. Furthermore, the intense expression of acid phosphatase at the Golgi level of the PIMs may signify a component of secretory phenotype in order to produce vasoactive mediators at the onset of stressful stimuli triggered by the halothane anesthesia.