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Biomedical subjects

D Heath

Publications and source records attributed to D Heath.

At least 145 records · Page 8Linked to original sources
PubMed1979

Electron microscopy of the plexiform lesion.

Pulmonary arteries from a case of plexogenic pulmonary arteriopathy were studied with the electron microscope. Many muscular pulmonary arteries showed intimal fibrosis of concentric or "onion-skin" type. The cells embedded within this fibrosis resembled smooth muscle but since they also possessed some features of fibroblasts we refer to them as myofibroblasts. Myofibroblasts also occurred in plexiform lesions together with fibroblasts and "fibrillary cells". These fibrillary cells contained numerous, prominent filaments with a random orientation. They lined the vascular channels of the plexiform lesions as well as being present within the stroma. They appeared to phagocytose fibrin and then to organise the plexiform lesion into a fibrous scar. Fibrillary cells closely resemble vasoformative reserve cells and the cells of the cardiac myxoma and so-called "papillary tumour" of heart valves. They may, therefore, be primitive multipotential cells found throughout the entire cardiovascular system.

Adult↗
PubMed1979

The pulmonary endothelial cell.

The surface of the endothelial cells of the pulmonary trunk of the Wistar albino rat was studied by means of silver preparations and by scanning and transmission electron microscopy. This surface is the site of cytoplasmic projections and the opening of caveolae which together appear to be features associated with the active metabolic rôle of the pulmonary endothelial cell.

Animals↗
PubMed1979

Observations on some ultrastructural features of normal pulmonary blood vessels in collapsed and distended lungs.

In this paper we describe certain special features of the pulmonary vasculature of rats from both distended and collapsed lungs. Evaginations of medial smooth muscle cells are a generalised response to contraction and are absent from distended lungs. They form at surfaces of low tissue pressure, such as the intima of veins and the adventitia of arteries. Contacts between endothelium and smooth muscle are common, particularly in veins, and often terminate in tight junctions. We also describe a variety of cystic spaces. Those between the endothelium and elastic lamina of pulmonary arteries are probably a fixation artefact. Those within the endothelium, except discoid bodies, are all extracellular spaces, and are not vacuoles as they may seem to be at first sight.

Animals↗
PubMed1978

Evagination of vascular smooth muscle cells during the early stages of Crotalaria pulmonary hypertension.

Fifteen adult female Wistar albino rats were fed on a diet containing powdered Crotalaria spectabilis seeds for periods of up to 5 wk. Electron microscopic studies were carried out on the lungs of these animals and also of three control rats. Both groups of animals showed protuberances of smooth muscle cells. In the control rats such protuberances were small and filled out spaces created by undulation of the internal elastic lamina produced by collapse of the vessel. These protuberances could be prevented by fixing the lung in distension. Evaginations of smooth muscle cells in the test rats were larger, devoid of myofilaments and organelles and arose from the parent cell between dense attachment points on the sarcolemma. Frequently they arose through a narrow cytoplasmic isthmus and had such electron-lucent contents as to resemble a cyst within the endothelium. In fact they pressed onto the undersurface of endothelial cells which fitted over them like a cap. Such evaginations are thought to arise as a result of sustained vasoconstriction.

Animals↗
PubMed1978

The ultrastructural effects of acute decompression on the lung of rats: the influence of frusemide.

Rats were placed in a decompression chamber and the chamber and the pressure reduced to 265 mm Hg over a period of 1 hr. Other rats were subjected to the same treatment after having been given an injection of frusemide. An ultrastructural study of the lungs of these rats showed that acute decompression of this magnitude can cause swelling and disintegration of type I alveolar epithelial cells. Although capillary endothelial cells showed only minor cytoplasmic damage many capillaries were ruptured with diapedesis of red cells. This is believed to be caused by gross capillary dilatation associated with pulmonary congestion. Pretreatment with frusemide prevented capillary rupture and reduced the degree of epithelial degeneration. However, frusemide induced swelling of capillary endothelial cells which was unassociated with acute decompression.

Acute Disease↗
PubMed1978

The pulmonary vasculature in haematite lung.

A histological study was made of the pulmonary vasculature in two cases of haematite lung. Between fibrotic nodules in the lung the muscular pulmonary arteries showed the development of longitudinal muscle in the intima, a change thought to be associated with stretch and distortion of these vessels. In some arteries this muscular layer in the intima showed secondary fibrosis. No muscularized pulmonary arterioles were seen, indicating an absence of constriction of the terminal portions of the pulmonary arterial tree. Pulmonary arteries in fibrotic areas had become progressively engulfed by the fibrous tissue. The occlusive and obliterative vascular changes in 'haematite lung' are in reality those of silicosis which are brought about by the inhalation of silica particles with the iron sesquioxide. The only feature peculiar to haematite lung is the intense accumulation of iron-containing dust in and around the pulmonary blood vessels.

Humans↗
PubMed1978

Evagination of smooth muscle cells in the hypoxic pulmonary trunk.

Six female Wistar albino rats were exposed to the hypoxia of a simulated altitude of 5500 m, three for a period of one week and three for a month. They developed ultrastructural changes in the pulmonary trunk consisting of evaginations of muscle cells of its media through gaps in the internal elastic lamina to press into the underlying endothelial cells. Such evaginations were usually devoid of myofilaments and organelles. Some appeared so electron-lucent as to be unrecognisable as muscle apart from the unequivocal connection with the parent smooth muscle cells. Elsewhere we have demonstrated that muscular evaginations in normal pulmonary blood vessels are an artefact brought about by collapse of lung tissue and that they can be avoided by distending the lung. Hence in the present investigation, in which the pulmonary trunk was fixed in distension, the evaginations are interpreted as indicating contraction of the muscle cells able to overcome the distending force. We interpret them as evidence of constriction of muscle cells in the media of the pulmonary trunk in response to hypoxia.

Animals↗
PubMed1978

The electron microscopy of "fibrinoid necrosis" in pulmonary arteries.

Fibrinoid necrosis was induced in the pulmonary arteries of five male Wistar albino rats by feeding them on a diet adulterated by the addition of 0.07% ground Crotalaria spectabilis seeds by weight. Electron microscopy of the arteries affected by the process showed fibrin in the thrombus occluding their lumens and in the arterial intima, held up from further penetration of the media by the inner elastic lamina. Naturally occurring gaps in this lamina were found, and it is postulated that they determine the characteristic histological configuration of fibrinous vasculosis. The smooth muscle cells of the media of the pulmonary veins showed clear evaginations, devoid of myofilaments and organells, indicative of sustained constriction compatible with viability of the cells. In contrast, the smooth muscle cells of the media of the pulmonary arteries showed loss of myofilaments leading to frank necrosis. Other cells seen in the media include fibrocytes and "vasoformative reserve cells." The authors consider that the latter have considerable and varied potential. Once liberated during the process of fibrinoid necrosis in the arterial media they may play an important part in pulmonary vascular pathology as, for example, in the formation of the plexiform lesion.

Animals↗
PubMed1977

Ultrastructure of hypoxic hypertensive pulmonary vascular disease.

Ten adult female Wistar albino rats were subjected to a sub-atmospheric pressure of 380 mm Hg for periods up to 35 days. Five control rats were also studied. The rats exposed to chronic hypoxia developed right-ventricular hypertrophy secondary to hypoxic hypertensive pulmonary vascular disease. Electron microscopy of control rats revealed individual smooth muscle cells immediately beneath the endothelium of pulmonary arterioles. On exposure to chronic hypoxia there was a hyperplasia of immature smooth muscle cells to form a distinct media between external and internal elastic laminae. The external lamina is thick and represents the original single lamina of the normal pulmonary arteriole. The inner lamina is thin and is newly formed internal to the smooth muscle cells. In hypoxic hypertensive pulmonary vascular disease there is no form of intimal proliferation so that the associated pulmonary hypertension is reversible.

Animals↗
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↗
PubMed1977

Pulmonary calcinosis.

The clinical and pathological features are described of a case of pulmonary calcinosis complicating cystic disease of the renal medulla. A histopathological study of the lung revealed calcification in the alveolar walls and in the blood vessels, predominantly in the pulmonary veins and venules. The calcified deposits were also studied by electron microscopy, and appearances suggestive of active growth of the deposits were recognised. Chemical analysis of the lung revealed a calcium content some 55 times greater than that of a normal lung. There was a five-fold increase in magnesium content. Reference is made to the literature demonstrating that the chemical composition of metastic calcification differs according to whether it is visceral or non-visceral in type.

Adult↗