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Biomedical subjects

D Heath

Publications and source records attributed to D Heath.

At least 127 records · Page 7Linked to original sources

Altitude-related deaths in seven trekkers in the Himalayas.

The clinical features and necropsy findings are described for seven trekkers in the Himalayas whose deaths were related to high altitude. The fatal outcome was due to serious pulmonary and cerebral disease. Oedema of the lungs and brain was prominent but so was thrombosis and haemorrhage, features of acute mountain sickness that have received insufficient recognition in the past. Most of the men were middle aged. Some began their trekking soon after flying to high altitude before becoming acclimatised and some remained at high altitude or climbed even higher despite the development of vomiting, breathlessness, and exhaustion. In one case death occurred despite prompt recognition and treatment of symptoms by administration of oxygen and swift evacuation to low altitude.

Adult↗

Electron microscopy of hypertensive pulmonary vascular disease.

Hypertensive pulmonary vascular disease secondary to chronic alveolar hypoxia is the result of vasoconstriction and then muscularization of the terminal portions of the pulmonary arterial tree. Ultrastructurally these two phases are characterized respectively by muscular evaginations and the hyperplasia of smooth muscle cells. Plexogenic pulmonary arteriopathy secondary to congenital cardiac shunts, primary pulmonary hypertension or rare cases of cirrhosis of the liver are characterized by concentric-laminar proliferation of myofibroblasts. Later there is a development of plexiform lesions which consist of vascular channels separated by a matrix of proteoglycan containing fibrillary cells and myofibroblasts. Fibrinoid necrosis results from the passage of fibrinogen from the vascular lumen into the arterial wall.

Adult↗

Endothelial pavement patterns in human arteries.

The endothelium of the carotid arteries, pulmonary trunk and aorta from twelve human subjects aged between 42 and 86 yr was examined en face after staining of the cell borders with a silver nitrate solution. The three vessels each showed similar features with a background pattern of fusiform, mononuclear cells oriented in the longitudinal axis of the vessel. Superimposed on this was a highly variable pattern of small and large polygonal cells and, less commonly, giant cells. Many examples of an abrupt transition from one pattern to another were observed. Preparations which were also stained with haematoxylin showed that large polygonal cells and giant cells contained many nuclei, often arranged into one or more nuclear clusters. The endothelial pattern was related to the underlying intimal structure by taking transverse sections of selected arterial segments. Although a specific endothelial pattern could not be related to a particular intimal morphology, there was a tendency for increasing intimal fibrous thickening and lipid deposition to be associated with more disorganised endothelial patterns and with the presence of large, multinucleate endothelial cells.

Adult↗

Anatomical variation and quantitative histology of the normal and enlarged carotid body.

The carotid bodies from 150 consecutive cases coming to necropsy were examined to determine the degree of anatomical variation of the organ. Single, double and bilobed variants were found. The origin of the carotid body was variable, the angle of the carotid bifurcation being the most typical, but a minority were encountered on the internal or external carotid arteries, the common carotid artery and the ascending pharyngeal artery. Carotid bodies which were enlarged had no preferred site or origin, but some showed early or pronounced nodularity. Both carotid bodies from 100 of these cases were subjected to detailed qualitative and quantitative histological study. From these measurements we were able to define hyperplasia of the organ as a differential sustentacular cell count in excess of 47 per cent., a lobular diameter over 565 micrometers, and a combined carotid body weight over 30 mg. Carotid body hyperplasia occurred in cases of myocardial hypertrophy secondary to both hypoxaemia and systemic hypertension.

Aged↗

Hyperplasia of the carotid body.

The histopathology of hyperplasia of the carotid bodies was studied in 6 cases of hypoxaemia and right ventricular hypertrophy secondary to pan-acinar emphysema, and in five cases of systemic hypertension with left ventricular hypertrophy. The features of the hyperplasia were the same in the two groups. There was proliferation of sustentacular (type II) cells and compression of central cores of chief (type I) cells. It is speculated that the hyperplasia of sustentacular cells is associated in some way with the prevention of retention of sodium ions and water which characterises hypoxic cor pulmonale in "blue bloaters", systemic hypertension, and ascent to high altitude with the complications of acute mountain sickness, and pulmonary and cerebral oedema.

Aged↗

Structure of the glomic arteries.

The structure of the arteries which supply blood tp the carotid bodies was examined in five cases in which the weights of the cardiac ventricles were normal and in which hypoxaemia due to emphysema or systemic hypertension were absent. The right glomic arteries were studied by light microscopy, and the left by electron microscopy. A sixth case, also free from myocardial hypertrophy, was used solely for an examination of the common carotid artery, the carotid sinus and the internal carotid artery by light and electron microscopy. The glomic arteries resembled the carotid sinus in being highly elastic with a rich supply of non-myelinated nerve fibres and thus had a structure consistent with having a baroreceptor function.

Adult↗

Pulmonary circulation of the llama at high and low altitudes.

We have studied the pulmonary circulation of three closely related animals, the llama, alpaca, and guanaco. The mean pulmonary arterial pressure of 12 llamas and one alpaca indigenous to high altitude in the Andes was found to be slightly but significantly higher than that of three llamas and three guanacos born and bred at low altitude in England. On the other hand, the medial thickness of the muscular pulmonary arteries and the relative weights of the two ventricles were the same in three llamas and one alpaca at high altitude as they were in one llama and two guanacos at low altitude. It is concluded that the pulmonary vasoconstrictive response to hypoxia, while present, is greatly reduced in this species and it is suggested that this may have taken place by evolutionary adaptation.

Altitude↗

Pulmonary mast cells in cattle and ilamas at high altitude.

The density of mast cells in various anatomical locations within the lung were measured in a peruvian Andean llama, a Peruvian Andean cow and a sea-level-cow. These densities were determined separately around pulmonary arteries, pulmonary veins, pulmonary arterioles and venules, in the alveolar septa, and around bronchi. The total mast cell density did not differ significantly between the three animals and there were more periarteriolar and perivenular mast cells in the llama than in either of the two cows. These data do not support the hypothesis that the perivascular mast cell is responsible for initiating the vasopressor response to hypoxia. In fact it can be argued that they actually inhibit this response since a high mast cell density was found in the llama, and animal which does not develop pulmonary hypertension at high altitude.

Altitude↗

Small pulmonary arteries in some natives of La Paz, Bolivia.

A histological study was made of the small pulmonary blood vessels in pieces of lung obtained at necropsy from 19 long-term residents of La Paz, Bolivia (3800 m). There was variation in the response of the pulmonary vasculature of these subjects to the chronic hypoxia of high altitude. The most characteristic finding, seen in seven of the 16 cases beyond infancy, was distal extension of vascular smooth muscle into pulmonary arterioles as small as 20 micrometer in diameter. Medial hypertrophy of the muscular pulmonary arteries occurred in only three of these seven subjects. Intimal fibrosis was seen in eight of the 19 cases and was ascribed to age; such fibrotic proliferation may affect the reversibility of hypoxic pulmonary hypertension and associated vascular changes in highlanders.

Adult↗

The ultrastructure of age-associated intimal fibrosis in pulmonary blood vessels.

The pulmonary blood vessels were examined from five human lungs surgically resected for bronchial carcinoma. Age-associated intimal fibrosis in these vessels was acellular in veins but more cellular in muscular pulmonary arteries. In both classes of vessel the cell involved in the production of this fibrosis was the myofibroblast, a cell which shares the properties of fibroblast and smooth muscle. The endothelial cells of pulmonary arteries contained numerous, uniform filaments with a random orientation but such filaments were rare in veins.

Aged↗

Observations on the rare association between portal and pulmonary hypertension.

Pulmonary arterial hypertension with severe pulmonary vascular disease is a rare association of portal hypertension in man, be it the result of cirrhosis of the liver or obstruction of the portal vein. We induced portal hypertension in 23 rats by partially ligating the portal vein or by totally occluding it in two stages. The rats were killed between one and 15 months after operation. A collateral circulation of varicose, anastomotic vessels was established, and in six animals well-marked oesophageal varices developed. Despite this evidence of sustained portal hypertension, hypertrophy did not develop in the right ventricle or in the media of the pulmonary trunk or muscular pulmonary arteries in any of the animals. This suggests that mechanical obstruction of the portal vein per se is not responsible for the development of pulmonary hypertension. Other factors, perhaps of a humoral nature, appear to be required to induce this rare association of portal hypertension but we have been unable to identify these. In particular, blood levels of oestrogen were not raised after ligation of the portal vein.

Animals↗

Pulmonary endothelial pavement patterns.

The appearance of the endothelial pavement pattern was studied in the pulmonary trunk, pulmonary veins, aorta, and inferior vena cava of the rat by means of silver staining of the cell borders. The endothelial cell in each of the four blood vessels was found to have its own distinctive shape, fusiform and pointed in the direction of blood flow in the case of the aorta and larger and more rectangular in the pulmonary trunk and pulmonary veins. Detailed quantitation of the dimensions and surface area of the endothelial cells in each blood vessel was carried out by a photographic technique. Pulmonary hypertension was induced in one group of rats by feeding them on Crotalaria spectabilis seeds. The endothelial pavement pattern in their pulmonary trunks became disrupted with many of the cells assuming a fusiform shape reminiscent of aortic endothelium. Many small, new endothelial cells formed in the pulmonary trunk suggesting division of cells to line the enlarging blood vessels. In contrast the endothelial cells of the inferior vena cava merely increased in size to cope with the dilatation of this vein.

Animals↗

Endothelial cell pavement pattern in the pulmonary trunk in rats in chronic hypoxia.

Right ventricular hypertrophy, and by inference pulmonary arterial hypertension, were induced in female Wistar Albino rats by subjecting them to a barometric pressure of 380 mmHg for four weeks. A control group was kept at normal barometric pressure for a similar period of time. The cell boundaries of the endothelial lining of the aorta, pulmonary trunk and inferior vena cava were stained in situ by a modified silver method of Poole et al. (1958). Photomicrographs of the intimal surfaces of these blood vessels at a standard magnification were used to determine the length, breadth and area of the cells. In the control rats the endothelial cells were found to have a characteristic shape and size in each of the three vessels studied. Those of the aorta were small and elongated in the direction of blood flow with tapering ends. The endothelial cells of the inferior vena cava were rectangular. Those of the pulmonary trunk were polygonal and had tessellated borders. In the test rats with right ventricular hypertrophy induced by chronic hypoxia the endothelial cell pavement pattern of the pulmonary trunk changed to resemble that of the aorta. It is considered that this was an expression of the acquired pulmonary hypertension, the fusiform shape appearing appropriate for an elevated pressure.

Animals↗