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Biomedical subjects

L Reid

Publications and source records attributed to L Reid.

At least 91 records · Page 5Linked to original sources
PubMed1981

The effect of chronic hypoxia on pulmonary arteries in young rats.

The effect of hypoxia on the postnatal development of rat lung from 8 days of life and continuing for 3, 7, 14, 21 and 28 days is described, with particular emphasis on the pulmonary arterial circulation. In hypoxic rats, absolute lung volume and body weight increases more slowly than in age-matched controls but lung volume relative to body weight is greater. After three days hypoxia intra-acinar arterial concentration is reduced and medial thickness of small arteries increased but by Day 7, both features return to "normal" values. By Day 14, right ventricular hypertrophy is apparent as is reduction in lumen diameter of preacinar arteries. From Day 21, muscle is seen in smaller and more peripheral arteries than normal: By Day 28 arteries of all sizes show increased medial thickness, and arterial and alveolar concentration is reduced. Compared with adult rats the growing lung seems to be somewhat "protected" in that the hypoxia-induced changes occur slowly although ultimately their severity is similar. At the end of the exposure period, however, the young lung is small for age suggesting that the changes are more severe than in the adult.

Animals↗
PubMed1981

Smooth muscle myosin in precursor and mature smooth muscle cells in normal pulmonary arteries and the effect of hypoxia.

Exposure to hypoxia increases pulmonary arterial muscularity-in the intra-acinar arteries "new" muscle appears in the normally nonmuscular regions and in the preacinar arteries, medial thickness increases. In the present study by immunofluorescence techniques, the myosin content of the pulmonary arterial walls at two levels of the circulation (intra-acinar and preacinar) were studied in control rats and those exposed to hypobaric hypoxia of 380 torr for 3,7, 10, or 14 days. In control animals, we show that the precursor smooth muscle cells, pericytes and intermediate cells normally present in the nonmuscular regions of the intra-acinar arteries, contain smooth muscle myosin. With exposure to hypoxia, smooth muscle myosin in the intra-acinar arteries increases to Day 10, both in area of staining and fluorescent intensity. This is in contrast to the preacinar arteries were only the area of myosin increases. Antihuman platelet (non-muscle) myosin shows a little faint staining in both control and hypoxic animals. Adaptations to hypoxia by the intra-acinar precursor and preacinar mature smooth muscle cells is different, and suggests that the functions subserved by the myosin filaments at each of the two levels differs.

Animals↗
PubMed1981

Mitotic activity of airway epithelium after short exposure to tobacco smoke and the effect of the anti-inflammatory agent phenylmethyloxadiazole.

Mitotic activity of extra- and intra-pulmonary airway epithelium has been studied in male rats exposed to tobacco smoke for 1, 2, 3, 7 or 14 days, with and without addition of the anti-inflammatory agent phenylmethyloxadiazole (PMO) to the tobacco. In both control and exposed animals the mitotic index is greater in extrapulmonary regions than intrapulmonary ones. A single exposure to tobacco smoke significantly increases mitotic activity in both airway regions. This initial level of mitotic response is not maintained but is rapidly restored by 1 day free from tobacco exposure: the second peak is as high as the first. Exposure to tobacco + PMO modifies timing and amplitude of the mitotic response. The effect of PMO is somewhat paradoxical since the first peak occurs later, i.e. after 2 days of exposure, but the increase is almost twice that seen after tobacco alone. The timing of the second peak is the same as after tobacco alone, but its amplitude is only half. In each experimental group the mitogenic effect is exerted on an intact epithelium. In animals exposed to tobacco alone, or tobacco + PMO, in extrapulmonary airways mitoses are located mainly in the basal region of the epithelium, whereas in intrapulmonary airways they are located mainly at the mid or superficial level.

Animals↗
PubMed1980

Mode of regulation of natural killer cell activity by interferon.

Whereas xenogeneic tumors such as baby hamster kidney or HeLa cells grow in nude mice, the same cells persistently infected with a variety of viruses are rejected. Spleen cells from normal nude mice were found to be induced to produce interferon and to exert natural killer (NK) activity on virus persistently infected (PI) tumor cells, and not on uninfected parental cells in vitro. The phenotype of the interferon-producing cells and the NK effector cells was found to be the same namely, Qa 5(+), Ly 5(+), ganglio-N- tetraosylceramide, with 35 percent of the NK cells also expressing Thy 1.2. NK activity against virus PI tumor cell lines could be nonspecifically augmented both in vivo and in vitro by prior contact with virus PI tumor cells. It was unambiguously demonstrated with chemically homogeneous mouse interferon that interferon, and not a contaminant, was responsible for the augmentation of NK activity in vitro. Studies on the mode of interferon action in augmenting NK activity revealed that the target cell for interferon action was serologically distinct from the NK effector cell. Anti-Ly 5 + complement (C)-treated spleen cells were depleted of NK activity and the ability to produce interferon, but, upon incubation with interferon for 1-3 h, regained both NK activity and susceptibility to anti-Ly 5 + C. Treatment with anti-Qa 5 + C eliminated NK activity, which could not be restored by the addition of interferon. We conclude that interferon produced by Ly 5(+) cells in response to virus PI tumor cells acts on Ly 5(-) precursor cells and induces their differentiation into functional Ly 5(+) NK effector cells.

Animals↗
PubMed1980

Hypoxia and pulmonary vascular endothelium.

The steady development of pulmonary hypertension in the rat between Days 1 and 14 of exposure to hypoxia is based largely on structural remodelling of the pulmonary arterial circulation. The changes induced by hypobaric hypoxia (380 Torr; PaO2 of 40 mmHg) are different in the pre-acinar muscular arteries from the intra-acinar (alveolar wall) arteries, including the effect on the endothelial cell. Quantitative analysis of normal lungs has revealed structural features peculiar to the pulmonary microcirculation. The precapillary arterial unit that lies within the alveolar region includes (i) a non-muscular region and (ii) a partially muscular region as well as (iii) a muscular region. The endothelial cells in these segments or 'compartments' appear different from each other in the normal animal and behave differently in disease. In the various segments the endothelial cell has different neighbours and there are differences in its boundary markers (the basement membrane and elastic lamina). In the normal precapillary arterial unit the neighbour may be a pericyte, intermediate cell or smooth muscle cell. The pericyte and intermediate cell are precursor smooth muscle cells that under the influence of hypoxia develop into mature muscle.

Animals↗
PubMed1980

Polyalveolar lobe: anatomic and physiologic parameters and their relationship to congenital lobar emphysema.

Polyalveolar lobe is one of the recently described pathological entities that can give rise to congenital lobar emphysema (CLE). In polyalveolar lobe, the total alveolar number as determined by microscopic point-counting of randomly taken lung sections is increased three to fivefold. The airways and arteries are normal for age in number, size and structure. Follow-up over 10-20 yr of patients operated upon for congenital lobar emphysema, including those of polyalveolar lobe etiology shows that these patients do well clinically. All patients have some pulmonary function abnormalities, specifically a decrease in airway conductance, and forced expiratory volume. It is not possible to distinguish patients with polyalveolar lobes from other CLE patients on the basis of pulmonary function data. All patients had normal lung volumes and vital capacities, despite losing 8%-20% of their pulmonary parenchyma. Based on compensatory lung growth, it may be preferable to operate earlier, rather than later in these cases.

Child, Preschool↗
PubMed1980

Development of Crotalaria pulmonary hypertension: hemodynamic and structural study.

In awake rats with indwelling catheters, the development of pulmonary hypertension after feeding Crotalaria spectabilis seeds is followed. Hypoxemia is excluded as a factor. Other hemodynamic changes are found before hypertension. After 7 days, pulmonary artery pressure (Ppa) is normal, 17.17 +/- 0.30 (SE) mmHg and from 14 days significantly increased (P < 0.01). Oxygen consumption (Vo2) is significantly increased by day 7 (control 22.72 +/- 2.13 ml . min-1 . kg-1; Crotalaria 42.47 +/- 2.95; P < 0.001). and cardiac index (CI) is significantly above normal after 7, 14, and 21 days (control 350 +/- 31 ml . min-1 . kg-1; 7 days Crotalaria 476 +/- 28; P < 0.02); pulmonary vascular resistance (PVR) increases to six times normal at day 33 (control 0.033 +/- 0.003 U/kg; 33 days Crotalaria 0.194 +/- 0.020; P < 0.001). The pulmonary arteries of these same rats were studied by quantitative morphometric techniques. The first change, muscle in smaller and more peripheral arteries than normal, is detected when Vo2 and CI are increased. Increased medial thickness of arteries < 200 micrometer diameter follows with Ppa rises. Even later, the larger arteries increase their media as the number of peripheral arteries falls and right ventricular hypertrophy becomes apparent, and hypertension and increased PVR are well established.

Animals↗
PubMed1980

Low lung capacity and hypoxemia in children with thalassemia major.

We evaluated lung function in 17 children with thalassemia major in stable condition receiving blood transfusions at regular intervals and subcutaneous desferoxamine daily. Total lung capacity (TLC) was below 2 SD of normal values for height in 7 of the 17 children and arterialized capillary PO2 was below the normal range in 15. We studied lung mechanics in 4 children with reduced TLC and found static and dynamic compliance below 2 SD of normal values for height in 3, and lung recoil at TLC above normal values and specific upstream conductance (Gus/TLC) above 2 SD of normal values in all 4. Although these alterations in lung function have been described in patients with pulmonary fibrosis, we found no fibrosis in autopsy specimens of lung from 8 other patients with thalassemia. The rate constant of carbon monoxide diffusion (kCO) was above the predicted mean in 14 of 15 children. These findings can be explained by a decrease in the growth of airspace relative to the vascular bed and major airways during childhood.

Adolescent↗
PubMed1980

Endothelial and subintimal changes in rat hilar pulmonary artery during recovery from hypoxia. A quantitative ultrastructural study.

Whereas hypoxia is known to cause an increase in thickness of both the medial and adventitial layers of the muscular pulmonary arteries, little is known of its effect on the endothelial cell and rest of the intima. The present study describes the ultrastructural changes in the intima of the hilar intrapulmonary muscular artery of the rat after exposure to hypobaric hypoxia of 380 torr for 10 days and their resolution during recovery periods of between 3 and 70 days in room air. After 10 days of hypoxia, the intima is 3 times thicker than the controls (control = 1.81 micrometers. +/- 0.13 standard error (S.E.); hypoxia = 5.59 micrometers. +/- 1.14 S.E.; p less than 0.05). The thickness of the endothelial cell layer doubles (control = 1.57 +/- 0.12 S.E.; hypoxia = 3.29 micrometer. +/- 0.23 S.E.; p less than 0.001) and point-counting the cytoplasm of these cells reveal significant relative increase in areal proportions, and hence most marked hypertrophy, of ribosomes, rough endoplasmic reticulum, and Golgi apparatus. An increase in number of endothelial cells is also apparent. The increase in thickness of the subendothelial layer is due to appearance of edema. In addition, microfibrillar basement membrane-like material is found focally within the subendothelial layer. In some sections, approximately 50 per cent of the endothelial associated basement membrane is absent. During recovery periods, there is regression of all the hypoxia-induced changes, save that the amount of subendothelial elastin increases to day 28 recovery, thereby altering the structure of the wall. The presence of elastin, collagen fibers, and microfibrils on the luminal side of the endothelial basement membrane, in control and experimental animals, points to their synthesis by the endothelial cell.

Air↗
PubMed1980

Hypoxia-induced structural changes in the media and adventitia of the rat hilar pulmonary artery and their regression.

Chronic hypobaric hypoxia induces structural features characteristic of pulmonary hypertension, but little is known of their reversal. In the present study, rats have been exposed to hypobaric hypoxia for 10 days and subsequently allowed to recover in room air for 3, 14, 28, or 70 days. With the use of 1-mu sections and electron-microscopic and point-counting techniques, the regression of the medial and adventitial changes in the rat hilar intrapulmonary artery has been followed. In the media, 10-day hypoxia causes more than a doubling in thickness due to 1) hypertrophy of smooth muscle cells, particularly of rough sarcoplasmic reticulum and Golgi apparatus; 2) an increase in extracellular connective tissue, microfibrils, collagen fibers, and elastin, and 3) edemalike fluid. In addition, the elestic laminas are doubled in thickness, and myofilamentous processes of the hypertrophied smooth muscle cells contact them. After just 3 days' recovery, some cells have already returned to normal diameter, although medial thickening is unchanged. By Day 14 and at Days 28 and 70 of recovery, medial thickness and cell diameter are within the normal range, and by recovery Day 70, there is a significant increase in the relative areal proportion of extracellular collagen fibers and a decrease in elastin (P less than 0.001). Hypoxia also produces a more than twofold increase in adventitial thickness. Hypertrophy of fibroblasts and an increase in their number contribute to the thickening, as does as increase in collagen fibers. During 3-70 days of recovery, thickness is gradually reduced to normal levels, although it is still significantly above normal at Days 3, 14, and 28. The increases in thickness at these times are due mainly to the accumulation of collagen fibers, which are still apparent after 70 days of recovery. Thus, hypoxia causes a doubling in thickness of the medial and adventitial coats of the hilar muscular pulmonary artery, which with recovery regain near normal thickness but whose structure is altered. The increase in collagen fibers contributes to contracture and reduced distensibility in these vessels, which is apparent in arteriograms as narrowed lumen diameter.

Animals↗
PubMed1980

Ultrastructural findings in lung biopsy material from children with congenital heart defects.

The ultrastructural features of pulmonary arteries are described in lung biopsy material from 6 children with congenital heart defects. Right ventricular hypertrophy was found in all 6 children and increased pulmonary artery pressure in all but one. The presence of muscle in smaller and more peripheral arteries than expected for the age of the child was detected in all cases. Ultrastructural examination of the peripheral arteries revealed, for the first time, in the nonmuscular regions of human arterial walls, pericytes and intermediate cells (previously shown to be precursor smooth-muscle cells); in addition, new arterial muscle was found in the normally nonmuscular region. In the 4 cases where medial thickness of the normally muscular arteries was increased, the smooth-muscle cells were hypertrophied and the extracellular connective tissue increased. In all cases, junctions between endothelial cells and smooth-muscle cells, intermediate cells, or pericytes were found. These changes are similar to those described in the rat with hypoxia-induced pulmonary hypertension. In addition, in 2 of the 6 cases, bundles of nerve axons in Schwann cell sheaths were found in adventitial layer of small, intraacinar muscular arteries (not previously demonstrated ultrastructurally at this site in the human lung); varicosities with agranular and granular vesicles, probably adrenergic, were also identified.

Axons↗
PubMed1979

Ultrastructural features of the distended pulmonary arteries of the normal rat.

Detailed study has been made of the structure of the normal pulmonary artery of rat by both light (1-micrometer sections) and electron microscopy. After tying the pulmonary veins at the hilum, the lungs were fixed by simultaneous injection of glutaraldehyde into the pulmonary trunk and trachea. Study of distended arteries allows precise measurement and assessment of normal lung structure. Four regions of the pulmonary artery can be identified by wall structure and are described here--muscular, partially muscular, non-muscular and the newly described thick-walled oblique muscular. Electron microscopid examination has demonstrated in the non-muscular regions of the partially muscular arteries, an "intermediate" cell and in the non-muscular arteries, a pericyte. The intermediate cell lies internal to the single elastic lamina but external to the endothelial cell, is surrounded by its own basement membrane and contains filaments mainly along the adluminal region of the cell. The pericyte also lies internal to the single elastic lamina, is within the basement membrane of the adjacent endothelial cell and has previously been reported in the lung only in the walls of alveolar capillaries. The structure of the intermediate cell and its position suggest it is a transitional stage between the pericyte and smooth muscle cell.

Animals↗
PubMed1979

Unusual vascular anomalies causing persistent pulmonary hypertension in a newborn.

A unique case of pulmonary vascular anomalies causing persistent pulmonary hypertension in a newborn is described. The child died 3 days after birth. Necropsy revealed marked hypoplasia of the right and left pulmonary arteries with a normal main pulmonary artery, patent ductus arteriosus, bilateral systemic arteries to the lungs from the abdominal aorta, and partial anomalous pulmonary venous connection. Quantitative morphometric techniques demonstrated slight abnormalities of alveolar development and severe arterial medial hypertrophy with abnormal extension of muscle into small peripheral arteries. Bronchopulmonary development appeared relatively normal in spite of the vascular abnormalities.

Angiocardiography↗