In vivo interaction of pulmonary intravascular macrophages with activated platelets in microvessels of equine lung after multiple exposures to halothane, isoflurane, and thiamylal: A comparative ultrastructural and cytochemical study

Abstract

The pulmonary intravascular macrophages (PIMs) of equines contain a unique electron-dense surface coat that is predominantly composed of lipoproteins. A single exposure of inhalatory halothane causes mobilization of the surface coat into the endocytotic system of the PIMs, followed by expansion of the Golgi apparatus and its enrichment with acid phosphatase. Simultaneously, the cells of the lymphocytic series show hyperplasia in the form of mitotic changes inside the microvascular compartment of the lung. Halothane is known to cause acute and chronic hepatotoxicity because of its biotransformation into trifluoroacytelated polypeptides. The present study was designed to examine the comparative effects of reexposures of inhalatory doses of halothane, isoflurane, and the intravenous barbiturate thiamylal sodium in ponies to evoke a stronger response in the PIMs after four exposures at increasing intervals of 1, 2, and 6 weeks. Ultrastructural and cytochemical evidence is presented that halothane induced translocation of the surface coat into the vacuolar system of the PIMs, followed by expansion of the Golgi apparatus and its enrichment with acid phosphatase. The cell membrane was thrown into extraordinary lamellipodial extensions, which enabled the PIMs to interact with platelets within the narrow confines of the pulmonary capillaries. The relationship between PIMs and platelets developed into large platelet aggregates. Isoflurane and thiamylal sodium did not affect the circulating platelets, although the surface coat was translocated into the endolysosomes in both situations. Although isoflurane is a lipid-soluble inhalant anesthetic similar to halothane, it is subject to very little biotransformation after use and in the present model demonstrates no immune response.

The immune response to anesthesia: Part 2 sedatives, opioids, and injectable anesthetic agents

“…In ponies anesthetized with halothane, isoflurane, or thiamylal IV and administered oxygen, structural changes in PIMs resulted in platelet trapping (Atwal & McDonell ). These changes also occurred with thiamylal suggesting that either thiamylal exerted effects on the lung despite IV administration, or more likely, that inhaling oxygen has an effect on the pulmonary immune response.…”

“…These changes also occurred with thiamylal suggesting that either thiamylal exerted effects on the lung despite IV administration, or more likely, that inhaling oxygen has an effect on the pulmonary immune response. The clinical significance of these structural changes is unknown, but the authors of that study proposed that the PIMs activated the platelets as part of the inflammatory cascade (Atwal & McDonell ). To the authors' knowledge, no other studies designed to assess the pulmonary or systemic immune response to anesthetics have been performed in horses.…”