Search

We measured the carotid body volume of rats treated with chronic hypoxia alone and chronic hypoxia together with a single neonatal injection of N-ethyl-N-nitrosourea (10 mg/kg). All the animals so treated showed enlargement of their carotid bodies, but no carotid body chemodectomas occurred.

We studied the ultrastructure of the carotid body of three normal rats and three rats living in a hypobaric chamber at a pressure of 460 mm Hg for 27, 28 and 35 days respectively. The type I cells of the carotid bodies of our hypoxic rats were enlarged due to an increase in the volume of their cytoplasm. Many of their dense core vesicles were vacuolated and the core was displaced eccentrically to become adherent to the limiting membrane of the vesicle. The concentration and distribution of dense core vesicles remained unaltered and there were no obvious changes in the mitochondria, ribosomes or Golgi apparatus. There was pronounced capillary dilatation in the carotid bodies of all three rats exposed to chronic hypoxia. This change was accompanied by attenuation of capillary endothelial cells and increased frequency of endothelial fenestrations. There were no structural changes in the type II cells.

A quantitative histological study was carried out on the carotid bodies of 10 normal rats and 10 rats living in a hypobaric chamber at a pressure of 460 mm Hg from 25 to 96 days. In the chronically hypoxic rats there was a four-fold increase in the mean combined volume of the carotid bodies. Morphometric analysis disclosed a three-fold increase in the mean volume of specialised glomic cells and a ten-fold increase in the mean volume of capillaries, although the proportion of glomic cells was actually significantly decreased. In all our hypoxic rats there was evidence of both right and left ventricular hypertrophy. However, there was no linear relation between total carotid body volume or volume of glomic cells on one hand and the right and left ventricular weight, on the other hand. Although there was no linear relation between combined total carotid body volume and duration of hypoxia, the linear relation between glomic cell volume and duration of hypoxia was significant at the 5 per cent. level. The increase in vascularity of the hypoxic carotid body may be a mechanism to increase blood flow and thus oxygen transport to a hypoxic organ with increased metabolic activity. Small quantities of an amorphous hyaline material of unknown nature were found in relation to capillaries and type I cells in all the hypoxic rats.

We measured the number and nuclear diameter of type I cells in the carotid bodies of 10 normal rats and in 10 rats living in a hypobaric chamber at a pressure of 460 mm Hg for 25 to 96 days. In normal rats, the number of type I rats, the number ranged from 15.92 to 30.77 times 10-3 with a mean of 40.79 times 10-3 which differed significantly from that in the control group. In 5 hypoxic rats the number of type I cells was less than the highest figure in the control group. The mean diameter of the nuclei of type I cells of hypoxic rats (5.5 mu) was greater than that of the controls (5.0 mu). The largest type I nuclei were seen in those rats which had been subjected to hypoxia for the shortest time.