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Biomedical subjects

J M Kay

Publications and source records attributed to J M Kay.

At least 73 records · Page 4Linked to original sources
PubMed1977

Unexplained pulmonary hypertension with pulmonary arteritis in rheumatoid disease.

The case is described of a 24-year-old woman who died after suffering from rheumatoid arthritis for eight years. During the last four months of her life there was clinical evidence of pulmonary hypertension. At necropsy the heart showed right ventricular hypertrophy but no congenital defect. Microscopic examination of the lungs disclosed evidence of hypertensive pulmonary vascular disease with medial hypertrophy and intimal fibrosis of muscular pulmonary arteries together with hypertensive changes in the pulmonary arterioles. Some of the muscular pulmonary arteries also showed fibrinoid necrosis of their media and acute arteritis. It was concluded that the fibrinoid necrosis was a minifestation of severe hypertensive pulmonary vascular disease rather than being a primary rheumatoid arteritis of the lung.

Adult↗
PubMed1976

Effects of phenobarbitone, cinnarizine, and zoxazolamine on the development of right ventricular hypertrophy and hypertensive pulmonary vascular disease in rats treated with monocrotaline.

The results of this experiment suggest that the addition of zoxazolamine to the diet may prolong the survival and reduce the incidence of right ventricular hypertrophy and hypertensive pulmonary vascular disease in male rats given a single subcutaneous injection of monocrotaline. Phenobarbitone and cinnarizine were ineffective.

Animals↗
PubMed1975

A quantitative morphological study of the carotid bodies of rats living at a simulated altitude of 4300 metres.

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.

Adaptation, Physiological↗
PubMed1975

The effect of chronic hypoxia on the number and nuclear diameter of type I cells in the carotid bodies of 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.

Animals↗