Alteration of chemoreceptor responses and ultrastructural features of ischemic carotid body of the cat.

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Abstract
Effects of short-term ischemia on chemoreceptor responses to various stimuli and ultrastructural features of the carotid body of the cat were examined. Total occlusion of the arteries supplying the carotid body induced an increase in chemoreceptor discharges. After 1 h ischemia, chemoreceptor responses to NaCN and asphyxia were markedly depressed to 10-40% of the control, while those to ACh and HCl were not greatly affected. Prolonged ischemia (2-3 h) produced a marked decrease in responsiveness to all stimuli. Ischemia (1 h) induced changes in the ultrastructural appearance of the glomus cell, including a decrease in the number of dense-cored vesicles, the appearance of swollen or vacuolated mitochondria and amorphous substances, while the nerve ending showed a relatively well-preserved appearance. Prolonged ischemia (2-3 h) produced dengenerative changes both in the glomus cell and nerve ending; vacuolation, a marked decrease in electron density of cytoplasmic matrix of the glomus cell and nerve ending, and marginal shrinkage of the nuclei. The markedly depressed responses to NaCN and asphyxia after 1 h ischemia are due to dysfunction of the glomus cell, while ACh and HCl, acting directly on the nerve ending which was not greatly affected by ischemia, evoked well-preserved responses in the chemoreceptors.