Effects of ischemia on the function and structure of the cat carotid body.
Interrupting the blood supply to the carotid body by ligating arteries of its vascular peduncle altered the chemoreceptive properties of the carotid nerve and produced structural changes in parenchymal (glomus and sustentacular) cells. The onset of ischemia was marked by an increase in the discharge of both A (myelinated) and C (unmyelinated) sensory fibers followed by depression and finally by receptor silence. The discharge of A-fibers disappeared after 30-50 min and that of C-fibers after 60-90 min. During ischemia of 15-60 min duration the threshold to pharmacological (NaCN, ACh) and 'natural' (hypoxic) stimuli progressively increased and was accompanied by reversible changes in the structure of parenchymal cells and nerve endings. Ischemia for 2 h or longer produced irreversible functional damage and disappearance of glomus and sustentacular cells from the carotid body. Following ischemic injury, nerve fibers regenerated and all responded to mechanical stimuli but only a few were stimulated by natural or pharmacological agents. Thus, parenchymal cells of the carotid body appear to be most important in transduction by allowing sensory fibers to respond to chemical stimuli.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D002545:Brain Ischemia / Q000503:physiopathology*; D002344:Carotid Body / Q000098:blood supply* / Q000503:physiopathology / Q000648:ultrastructure; D002415:Cats; D002628:Chemoreceptor Cells / Q000187:drug effects / Q000502:physiology; D004553:Electric Conductivity / Q000187:drug effects; D008854:Microscopy, Electron
D000109:Acetylcholine