The influence of chronically hypoxemic states on human carotid body structure and cardiac hypertrophy.
Quantitative and qualitative changes in the human carotid body morphology, and their relationship to changes in the weight of right and left ventricles were investigated in 10 patients with a history of chronic hypoxemia. 5 patients without a history of cardiac, pulmonary or cerebral respiratory failure served as the control group. In the chronically hypoxemic group, a 2.67-fold increase in the total specific glomus cell volume was found. Up to a critical volume this increase is due to hypertrophy, beyond that it is due to hyperplasia. The course of the morphologic changes under the influence of slowly progressive chronic hypoxemia is discussed in a frame work of three stages (stage I - hypertrophy, stage II = nodular hyperplasia, stage III = atrophy). Plasmacellular infiltrates are constant though sometimes sparse. They are mostly perineural in location, less often intralobular and if so almost exclusively periglomoidal. In one case, we found an increase of Schwann cells in the interstitial and periglomoidal space without demonstrable degeneration of the nerve fibres themselves. Our hypothesis suggests that degeneration of special nerve terminals of the reciprocal type occurs in afferent nerve fibers. The increase of right ventricular weight (by a factor of 2.05) is significant, in contrast to that of the left. A linear correlation between the increase of right ventricular weight and the increased total glomus cell volume was not established. In 4 cases, however, we found pulmonary hypertensive vascular changes, which might be responsible for the disparity in the linear relationship.
D000368:Aged; D001284:Atrophy; D006332:Cardiomegaly / Q000473:pathology*; D002344:Carotid Body / Q000473:pathology*; D002908:Chronic Disease; D005260:Female; D006801:Humans; D006965:Hyperplasia; D006976:Hypertension, Pulmonary / Q000473:pathology; D000860:Hypoxia / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D010950:Plasma Cells; D011660:Pulmonary Heart Disease / Q000473:pathology; D012583:Schwann Cells