Os. Atwal et al., EVIDENCE THAT HALOTHANE ANESTHESIA INDUCES INTRACELLULAR TRANSLOCATION OF SURFACE-COAT AND GOLGI RESPONSE IN EQUINE PULMONARY INTRAVASCULARMACROPHAGES, Journal of submicroscopic cytology and pathology, 26(3), 1994, pp. 369-386
The pulmonary intravascular macrophages (PIMs) of horse contain a uniq
ue 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 lipo
lytic lipase, suggesting that the coat is predominantly composed of li
poproteins. 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-c
oat showed acute sensitivity to halothane by disappearing almost compl
etely from the surface after 1-2 h of exposure. The cell membranes wer
e thrown into extraordinary arrays of lamellipods, pseudopods and veil
s. Concurrently, the globular units of the coat were translocated into
the endosomal-lysosomal system, most probably via receptor-mediated e
ndocytosis. There was a high profile of the expanded Golgi apparatus e
specially the trans Golgi network (TGN) in close association with the
centrioles and microtubules. Cytochemistry revealed an enrichment of t
he Golgi complex with acid phosphatase activity. On the other hand, ha
lothane showed an inhibitory effect on the lysosomal acid phosphatase
of the PIMs. It is proposed that the Golgi response occurred as an obl
igatory concomitant of internalization of the surface-coat and its sub
sequent passage through endosomal-lysosomal system. The acid phosphata
se activity as a marker enzyme of the expanded Golgi is correlated wit
h metabolic effects of the internalized coat which is unique to the pu
lmonary intravascular macrophages. Furthermore, the intense expression
of acid phosphatase at the Golgi level of the PIMs may signify a comp
onent of secretory phenotype in order to produce vasoactive mediators
at the onset of stressful stimuli triggered by the halothane anesthesi
a.