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Biomedical subjects

D Heath

Publications and source records attributed to D Heath.

At least 19 recordsLinked to original sources
PubMed1992

The ultrastructure of pulmonary arteries and arterioles in emphysema.

The lungs from three cases of pulmonary emphysema obtained at heart-lung transplantation were examined by electron microscopy to determine the origin of intimal longitudinal muscle and the formation of muscular tubes in small pulmonary arteries and arterioles. The earliest change consisted of migration of mature smooth muscle cells from the media of small pulmonary arteries, through gaps in the internal elastic lamina, into the subendothelial space. Most of these cells then adopted a longitudinal orientation, maintained a muscular phenotype, and became enmeshed in a web of elastic fibres. A small minority, immediately subjacent to the endothelium, were orientated circularly and, in some vessels, were enclosed by rudimentary internal and external elastic laminae to form early muscular tubes. Pulmonary arterioles, which are normally devoid of a media, contained several layers of circularly orientated smooth muscle cells, some of which also formed muscular tubes. It is postulated that the limited migration of mature smooth muscle cells seen in states of chronic hypoxia is mediated by a different stimulus from that causing the florid invasion of the intima by immature smooth muscle, with subsequent transformation into myofibroblasts, which characterize plexogenic pulmonary arteriopathy.

Adult↗
PubMed1992

Mast cells in the human lung at high altitude.

Mast cell densities in the lung were measured in five native highlanders of La Paz (3600 m) and in one lowlander dying from high-altitude pulmonary oedema (HAPO) at 3440 m. Two of the highlanders were Mestizos with normal pulmonary arteries and the others were Aymara Indians with muscular remodelling of their pulmonary vasculature. The aim of the investigation was to determine if accumulation of mast cells in the lung at high altitude (HA) is related to alveolar hypoxia alone, to a combination of hypoxia and muscularization of the pulmonary arterial tree, or to oedema of the lung. The lungs of four lowlanders were used as normoxic controls. The results showed that the mast cell density of the two Mestizos was in the normal range of lowlanders (0.6-8.8 cells/mm2). In the Aymara Indians the mast cell counts were raised (25.6-26.0 cells/mm2). In the lowlander dying from HAPO the mast cell count was greatly raised to 70.1 cells/mm2 lung tissue. The results show that in native highlanders an accumulation of mast cells in the lung is not related to hypoxia alone but to a combination of hypoxia and muscular remodelling of the pulmonary arteries. However, the most potent cause of increased mast cell density in the lung at high altitude appears to be high-altitude pulmonary oedema.

Adult↗
PubMed1992

Nodules resembling arachnoid villi in pulmonary venules in plexogenic pulmonary arteriopathy.

We have found nodules histologically resembling arachnoid villi adjacent to pulmonary venules in a woman of 30 years with primary pulmonary hypertension. Such lesions have been reported previously in cases of mitral stenosis and pulmonary thromboembolism and we believe them to absorb excess water from the interstitial tissues of the alveolar walls, thus protecting the lung from the development of edema. In this way they seem to have a similar function to that of cerebral arachnoid villi and granulations which transport cerebrospinal fluid into the dural sinuses.

Adult↗
PubMed1992

The rat is a poor animal model for the study of human pulmonary hypertension.

The pulmonary circulation of the rat is widely used as an animal model for studies of human pulmonary hypertension. It is not difficult to understand its appeal. The species is a small laboratory animal which is readily accommodated in decompression chambers for studies for simulated high altitude. It is also very susceptible to the action of the metabolites of pyrrolizidine alkaloids which rapidly lead to severe pulmonary vascular disease in the absence of intrinsic heart and lung disease, thus suggesting its value as an animal model of primary pulmonary hypertension. However, these obvious advantages of the rat pulmonary circulation are outweighed by the fact that its pathological reactions to hypoxia and noxious dietary agents differ significantly from those found in human disease. This can lead to erroneous conclusions as to the nature of the remodelling of the human pulmonary vasculature in pulmonary hypertension.

Animals↗
PubMed1991

Morphological changes in the pituitary-adrenocortical axis in natives of La Paz.

Increased activity of the hypothalamic-pituitary-adrenocortical axis is part of the response to the stress of initial exposure to hypoxia, but there is evidence to suggest that it persists after homeostatic stability has been regained and acclimatization achieved. The adrenal glands of five lifelong residents of La Paz, Bolivia, who had lived at altitudes in the range 3600-3800 m, were significantly larger than those in age-matched controls from sea level (15.3 g vs 10.4 g; P less than 0.001) and appeared hyperplastic. The pituitary glands of the highlanders were not significantly different in size from those of the controls (0.67 g vs 0.51 g), but contained larger populations of corticotrophs expressed in terms of the total cell population of their anterior lobes (25.6% vs 19.4%; P less than 0.001). In conjunction with other studies of this endocrine axis in man and animals exposed to a hypoxic environment, these data suggest that greater amounts of adrenocorticotrophic hormone (ACTH) are required to maintain normal adrenocortical function under such circumstances, probably as a result of hypoxic inhibition of adrenocortical sensitivity to stimulation. Physiological hyperplasia of the adrenal cortex may be common in people living at high altitude.

Adrenocorticotropic Hormone↗
PubMed1991

Pulmonary vascular remodelling in a high-altitude Aymara Indian.

A histological study of the pulmonary vasculature in a young male high-altitude Aymara Indian revealed four aspects of interest. There was muscularization of the terminal portion of the pulmonary arterial tree to involve pulmonary arterioles as small as 15 microns in diameter, thus forming a basis for the slightly increased pulmonary vascular resistance of native highlanders. Intimal longitudinal muscle was found in pulmonary arteries and arterioles and though to be due to chronic alveolar hypoxia. Inner muscular tubes similar to those found in chronic obstructive lung disease were present. Pulmonary veins and venules also showed intimal muscularization suggesting that alveolar hypoxia affects vascular smooth muscle cells per se irrespective of their situation. The nature of the remodelling in a pulmonary blood vessel depends on a combination of hypoxia and haemodynamics.

Adult↗
PubMed1991

Lung mast cells in plexogenic pulmonary arteriopathy.

The numbers of mast cells/mm2 of lung parenchyma were counted in four controls, 15 cases of primary plexogenic pulmonary arteriopathy (PPA), and 17 cases in which the arteriopathy was secondary to congenital heart disease, to determine if increased numbers occur in PPA and with what stage of disease they might be associated. Considerable accumulations of lung mast cells may occur in this disease, but these are not closely related to any particular histological stage in the development of the arteriopathy. It is postulated that while mast cells could conceivably exert a vasodilatory effect on constricted small pulmonary arteries, it seems more likely that they are part of the parenchymal changes that commonly develop in this disease.

Adolescent↗
PubMed1991

Pulmonary peptides, norepinephrine and endocrine cells in monocrotaline pulmonary hypertension.

The concentrations of norepinephrine and of the peptides bombesin, calcitonin gene-related peptide and neurotensin were measured in rats with monocrotaline pulmonary hypertension. The numbers of pulmonary endocrine cells showing positive immunoreactivity for calcitonin, calcitonin gene-related peptide, protein gene product 9.5 and bombesin were counted in a second group of rats with monocrotaline pulmonary hypertension. The concentration of norepinephrine in the lungs decreased significantly in the test rats but this could be attributed to dilution by an increased mass of tissue. The pulmonary concentration of all three peptides showed a decrease in the rats treated with monocrotaline but this was highly significant only in the case of bombesin. The pulmonary content of bombesin showed a substantial and significant decrease in the test rats. No neuroendocrine cells immunopositive for bombesin were identified in any of the control or test rats. There was no difference between the control and test rats with respect to the form or distribution of the cells immunoreactive for the other three The lack of pulmonary endocrine cells showing immunoreactivity for bombesin may be related to the absence of intimal proliferation in the pulmonary arteries in this species. This is in striking contrast to what occurs in plexogenic pulmonary arteriopathy in man and suggests that monocrotaline-induced pulmonary hypertension in rats is not a good animal model for this disease.

Animals↗
PubMed1990

The occurrence and distribution of certain polypeptides within the human carotid body.

Both carotid bodies from 26 patients coming to necropsy were fixed in 10% neutral buffered formalin and sections 4 microns thick were stained for various peptides by use of the immunogold technique. The results show that the human carotid body contains met- and leu-enkephalin, substance P, vasoactive intestinal peptide (VIP), neurotensin and bombesin. The distribution of these six peptides within the carotid body differs. Thus met- and leu-enkephalin are both present predominantly within glomic chief cells but with a marked tendency to favour the dark variant of these cells. Substance P and VIP both show a weak immunoreactivity in comparison to the enkephalins and are present in all three variants of chief cell. Neurotensin shows the weakest immunoreactivity of all and is restricted to a few glomic chief cells in a minority of cases. Bombesin also shows a weak immunoreactivity in glomic chief cells but a strong reaction in glomic arteries and arterioles. In these vessels bombesin appears to be confined to smooth muscle cells in the media but we cannot say whether it is secreted by them or merely bound to receptor sites on their membranes. These findings are related to quantitative data on the concentration of peptides in the human carotid body from a previous paper with which we were associated.

Bombesin↗
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↗