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Biomedical subjects

J M Kay

Publications and source records attributed to J M Kay.

At least 55 records · Page 3Linked to original sources
PubMed1984

Amiodarone pulmonary toxicity.

Numerous cytoplasmic lamellar bodies were seen in many cell types in an open lung biopsy from a patient on amiodarone therapy. These membrane-bound lamellar bodies were characterized by distinct, concentric parallel membranes and peripheral granular densities. Their morphology and distribution suggest a metabolic disorder of phospholipid degradation induced by this drug. The differential diagnosis of lamellar body accumulation in the lung is discussed. This case emphasizes the desirability for ultrastructural study of lung biopsies in such potentially reversible lung disease.

Amiodarone↗
PubMed1983

Ultrastructure of lung in pulmonary veno-occlusive disease.

A 17-year-old boy died of severe pulmonary hypertension due to pulmonary veno-occlusive disease. The condition was diagnosed in a lung biopsy specimen and confirmed at necropsy. The lung specimen was studied by electron microscopy and immunofluorescence microscopy. The occluded pulmonary veins were lined by intact endothelial cells, beneath which was a haphazard proliferation of collagen fibrils and smooth muscle cells. The alveolar capillaries showed thickening of the endothelial cell basement membrane with an increase in the number of cytoplasmic processes of pericytes. Electron-dense deposits were located within the thickened basement membrane. These deposits were considered to represent disintegrating extravasated erythrocytes rather than immune complexes because immunofluorescence microscopy showed no immunoglobulin or complement deposition within the lung.

Adolescent↗
PubMed1983

Comparative morphologic features of the pulmonary vasculature in mammals.

The ratio of right to left ventricular weight (0.3), and the ratio of the medial thickness of the pulmonary trunk to that of the aorta (0.4 to 0.7) are similar in humans and other mammals for which data are available. There are interspecies differences in quantity and arrangement of collagen, smooth muscle, and elastic tissue in the pulmonary trunk. The medial thickness of muscular pulmonary arteries is similar in man, baboon, ferret, goat, llama, and monkey. In most other mammals these vessels are more muscular than those in humans. The goat is similar to man because the muscular pulmonary arteries terminate at an external diameter of 100 microns. In most other mammals, smooth muscle is present in much smaller pulmonary arterial vessels. There is pronounced interspecies variation in the course and structure of the pulmonary veins. The cat, civet, dog, ferret, fox, goat, horse, monkey, and rabbit have pulmonary veins with thin fibrous walls such as occur in humans. However, the pulmonary veins are muscular in the cow, guinea pig, llama, pig, and rat.

Animals↗
PubMed1982

Failure to show decrease in small pulmonary blood vessels in rats with experimental pulmonary hypertension.

We induced chronic pulmonary hypertension in one group of rats by exposing them to chronic hypobaric hypoxia (380 mm Hg for three weeks) and in another group by administering a single subcutaneous dose of monocrotaline (60 mg/kg body weight). Both groups of rats showed increase of the right ventricular mean systolic blood pressure and right ventricular hypertrophy. We measured the surface area of histological sections of the left or right lungs and counted all small blood vessels with an external diameter of less than 50 microns and with a definite elastic coat lying distal to respiratory bronchioles. In the 10 rats with chronic hypoxic pulmonary hypertension the mean total number of small pulmonary blood vessels was 428.8 +/- 96.9 (SD) compared with 337.8 +/- 91.9 in 10 untreated control rats. The number of small pulmonary blood vessels per mm2 of lung tissue was 4.0 +/- 1.3 in the chronically hypoxic rats compared with 3.8 +/- 1.2 in the controls. The mean total number of small pulmonary blood vessels in nine rats with monocrotaline-induced pulmonary hypertension was 396.8 +/- 61.7 compared with 384 +/- 55.4 in three control rats. The number of small pulmonary blood vessels per mm2 lung tissue was 3.3 +/- 0.6 in the rats treated with monocrotaline compared with 3.6 +/- 0.6 in the control group. We conclude that the number of small pulmonary blood vessels is not reduced in rats with pulmonary hypertension induced by chronic hypoxia or monocrotaline.

Animals↗
PubMed1982

Angiotensin converting enzyme activity and evolution of pulmonary vascular disease in rats with monocrotaline pulmonary hypertension.

We have investigated the role of angiotensin converting enzyme (ACE) in the development of pulmonary hypertension, right ventricular hypertrophy, and pulmonary vascular disease in rats given a single subcutaneous injection of the pyrrolizidine alkaloid monocrotaline. Thirty-six young female Wistar rats were divided into a test group of 27 animals and a control group of nine animals. Each test rat was given a single subcutaneous injection of monocrotaline (60 mg/kg body weight). On the first, third, fifth, seventh, tenth, twelfth, fourteenth, seventeenth, and twenty-second days after the injection of monocrotaline the mean right ventricular systolic blood pressure was measured in one control and three test rats. The animals were then killed and we measured the specific activity of ACE in serum and lung homogenate. We also evaluated muscularisation of pulmonary arterioles, medial hypertrophy of muscular pulmonary arteries, and right ventricular hypertrophy. The sequence of changes was as follows: muscularisation of pulmonary arterioles and medial hypertrophy of muscular pulmonary arteries were apparent seven days after administration of monocrotaline; pulmonary hypertension and reduced lung ACE activity occurred after 10 days; right ventricular hypertrophy was detected after 12 days. Serum ACE activity was unchanged. It is concluded that the reduction in lung ACE activity is a result rather than a cause of the pulmonary hypertension. This reduction in lung ACE activity may be a protective mechanism designed to limit the elevation of the pulmonary arterial pressure.

Animals↗
PubMed1982

Lung angiotensin converting enzyme activity in rats with pulmonary hypertension.

We have studied serum and lung tissue angiotensin converting enzyme (ACE) activity in female Wistar rats with pulmonary hypertension induced by two different methods. Chronic pulmonary hypertension was produced in one group of 10 rats (CH) by confinement in a hypobaric chamber (380 mmHg) for three weeks, and in another group fo 10 rats (M) by a single subcutaneous injection of monocrotaline (60 mg/kg body weight). In these two groups of tests rats and in 20 untreated controls (C), we evaluated right ventricular mean systolic blood pressure (Prvs mmHg), right ventricular hypertrophy, and serum ACE (n mol/ml/min). In lung tissue homogenate, we measured the specific activity of ACE (n mol/mg protein/min), alkaline phosphatase (AP) (IU/mg protein) and lactic dehydrogenase (LDH) (IU/mg protein). The Prvs in groups, C, CH, and M was 25 +/- 7 SD, 41 +/- 7, and 51 +/- 5, respectively. The ratio of right ot left ventricular weight (RV/(LV + S)%) in groups, C, CH, and M was 29 +/- 4, 52 +/- 5, and 56 +/- 7, respectively. The lung tissue ACE in groups C, CH, and M was 85 +/- 11, 65 +/- 20, and 22 +/- 5, respectively. In groups CH, and M the Prvs and RV/(LV + S)% were significantly elevated above control values while lung ACE was significant decreased (p less than 0.05). There was a significant inverse relationship between lung ACE on one hand, and Prvs (r = - 0.73) and RV/(LV + S)% (r = - 0.71) on the other hand. Serum ACE and lung AP were unchanged. In group M there was a slight but significant reduction in lung LDH. Chronic pulmonary hypertension, irrespective of its method of production, is associated with decreased lung ACE. The reduction in lung ACE is inversely proportional to the severity of pulmonary hypertension and right ventricular hypertrophy.

Alkaline Phosphatase↗
PubMed1981

Myocardial ultrastructure and the development of atrioventricular block in Kearns-Sayre syndrome.

A right ventricular endomyocardial biopsy specimen from a 30-year-old male with chromic progressive external ophthalmoplegia, retinal pigmentation and complete atrioventricular block (Kearns-Sayre syndrome) was examined in the electron microscope. There was a proliferation of mitochondria between the myofibrils and beneath the sarcolemma. Many of the mitochondria showed morphologic abnormalities not previously described in this condition. There were associated accumulations of glycogen. A similarly affected female with left anterior hemiblock developed complete atrioventricular block at age 26 years, Despite the ultrastructural changes, clinically detectable myocardial disease is not a feature of Kearns-Sayre syndrome. However, intraventricular conduction defects show an unusually rapid progression to potentially fatal complete atrioventricular block and are an indication for prophylactic cardiac pacing.

Adult↗
PubMed1981

Effect of intermittent normoxia on muscularization of pulmonary arterioles induced by chronic hypoxia in rats.

We studied the effect of continuous and intermittent normoxia for 6 and 20 wk on the muscularization of pulmonary arterioles in rats with chronic hypoxic hypertension. After 4 wk in a hypobaric chamber (380 mm Hg) the proportion of small pulmonary blood vessels with 2 elastic laminae (PVTEL) was 21.57 +/- 14.86% (SD) (n = 10) compared with 3.66 +/- 1.86% in 10 untreated control animals. Recovery using continuous normoxia and intermittent normoxia 16 h/day for 6 wk caused a reduction in PVTEL to 8.45 +/- 4.09% (n = 6) and 7.16 +/- 6.96% (n = 6), respectively. Right ventricular hypertrophy (RVH) was reversed by recovery using continuous normoxia for 6 wk but was unaffected by intermittent normoxia (16 h/day). Intermittent normoxia 8 h/day for 6 wk did not reduce the PVTEL or RVH. Continuous normoxia for 20 wk reversed the muscularization of small pulmonary vessels (PVTEL, 3.86 +/- 3.57%; n = 4) and RVH. Intermittent normoxia (16 h/day) for 20 wk significantly diminished the PVTEL to 7.39 +/- 3.73% (n = 5) but did not reduce RVH. Prolonged continuous normoxia slowly reversed the pulmonary hypertension, RVH, pulmonary vascular lesions, and polycythemia induced by chronic hypoxia. Intermittent normoxia (16 h/day) diminished the pulmonary vascular lesions but not the pulmonary hypertension, RVH, and polycythemia. Intermittent normoxia (8 h/day) was ineffective.

Animals↗
PubMed1980

Effect of intermittent normoxia on chronic hypoxic pulmonary hypertension, right ventricular hypertrophy, and polycythemia in rats.

The effect of continuous and intermittent normoxia on chronic hypoxic pulmonary hypertension, right ventricular hypertrophy, and polycythemia was studied in rats. After 4 wk in a hypobaric chamber (380 mmHg), the mean right ventricular blood pressure (Prv) was 29.2 +/- 1.8 (SEM) mmHg (n = 10) compared with 11.1 +/- 1.1 mmHg in 10 untreated control animals. After recovery in room air (24 h/day) for 6 wk, the Prv was significantly reduced to 21.2 +/- 3.5 mmHg (n = 6). Recovery using intermittent normoxia (8 and 16 h/day) for 6 wk did not reduce Prv. In 10 control rats, the ratio of right to left ventricular weight (RV/(LV + S) was 28.8 +/- 1.1%. After 4 wk of chronic hypoxia the RV/(LV + S) was 48.5 +/- 2.4% (n = 10). Recovery using complete normoxia for 6 wk significantly reduced the RV/(LV + S) to 32.8 +/- 1.9% (n = 6). Intermittent normoxia (8 and 16 h/day) did not reduce RV/(LV + S). Chronic hypoxia (380 mmHg) for 4 wk elevated the hematocrit from 35 to 66%. The polycythemia was reversed by recovery using continuous normoxia for 6 wk. Intermittent normoxia (8 and 16 h/day) was ineffective.

Animals↗
PubMed1978

Ultrastructure of carotid body in rats living at a simulated altitude of 4300 metres.

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.

Altitude↗
PubMed1977

Lung mast cells in rats exposed to acute hypoxia, and chronic hypoxia with recovery.

Exposure to acute hypoxia (barometric pressure 263 mmHg) for 8 hours did not lead to increased numbers of mast cells in the lungs of rats. In contrast, in adult rats kept for 35 days at a barometric pressure of 380 mmHg there was a proliferation of mast cells around the pulmonary blood vessels and in the alveolar septa. This hyperplasia of lung mast cells in response to chronic hypoxia was reversible on removal of the hypoxic stimulus. There was a correlation between the logarithm of the perivascular lung mast cell density (defined in the paper) and the logarithm of the right ventricular weight. There was no increase in the mast cells in the carotid bodies of the hypoxic rats. Young male, old male, young female, and old female rats which had been subjected for 39 days to a barometric pressure of 380 mmHg showed a proliferation of mast cells around the pulmonary blood vessels and in the alveolar walls. This response was greatest in the adult animals and independent of their sex. In the age and sex experiment there was a correlation between the perivascular lung mast cell density and the medial thickness of the muscular pulmonary arteries. Since mast cell hyperplasia has been reported as preceding right ventricular hypertrophy, it is conceivable that mast cell proliferation in the lung may be a defence mechanism to limit the severity of hypoxic pulmonary hypertension rather than to mediate it.

Age Factors↗