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Biomedical subjects

B Meyrick

Publications and source records attributed to B Meyrick.

At least 91 records · Page 5Linked to original sources
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

Development of pulmonary arterial changes in rats fed Crotalaria spectabilis.

The early changes in pulmonary artery structure and the timing and development of right ventricular hypertrophy were examined in rats after ingestion of Crotalaria spectabilis; the arteries were distended with a Micropaque--gelatin mixture. The earliest change, detected at Day 3, is the appearance of new muscle in normally nonmuscular arteries. Increased medial wall thickness of the normally muscular arteries is apparent from Day 7, reaching significance in the smaller arteries from Day 10 and in the larger arteries from Day 14. A reduction in number of small, filled peripheral arteries is apparent at Day 14 and is significant at Day 21 as is the increase in the ratio of alveoli to arteries per unit area of section. Right ventricular hypertrophy is detected and significant at Day 21 and, like all the arterial changes, continues to increase to Day 35. Hypoxia produces similar changes to those described above, although without the inflammation seen after Crotalaria ingestion, but the time table is different. New muscle appears in both models at the same time, but the other changes appear more slowly after ingestion of Crotalaria spectabilis.

Animals↗
PubMed1979

Hypoxia and incorporation of 3H-thymidine by cells of the rat pulmonary arteries and alveolar wall.

In the pulmonary arterial circulation hypoxia produces increase in thickness of the medial muscle coat as well as of the adventitia; in addition muscle appears in smaller arteries than is normal and the number of small arteries that fill on Micropaque-gelatin injection is reduced. To assess the role of hyperplasia in these changes, the uptake of 3H-thymidine by the cells of the pulmonary arterial wall has been studied in rats exposed to hypobaric hypoxia (exposure to 380 torr) after 1, 3, 5, 7, 10, and 14 days. Using autoradiographs of 1-micron sections, the glutaraldehyde-distended intrapulmonary hilar muscular artery, the peripheral, intraacinar arteries less than 100 micron in external diameter, and the alveolar wall had different patterns of uptake. In the hilar pulmonary artery, after 24 hours of exposure, the labeling index for adventitial fibroblasts is increased eightfold over the control value, and for endothelial cells, threefold, while for medial smooth muscle cells, there is a gradual and small increase to Day 14. Newly muscularized intraacinar arteries are first apparent at Day 3, when they comprise 40% of the intraacinar arteries, increasing to 80% at Day 7. No decrease in density of arteries is found. Uptake of 3H-thymidine by new muscle cells is not apparent until Day 5 when labeling is maximum. The endothelial cells of the newly muscularized arteries show an increased labeling index only at Days 7 and 10. The veins and normally muscular arteries do not show these changes. In the alveolar walls, the concentration of labeled cells is significantly above the control value at Days 3, 5, and 7 and significantly below, at Day 14. At this level, the interstitial, epithelial, and endothelial cells contribute to the increase.

Animals↗
PubMed1978

The effect of continued hypoxia on rat pulmonary arterial circulation. An ultrastructural study.

Hypoxia is known to cause pulmonary hypertension with an increase in arterial muscle-both hypertrophy of the medial coat of the normally muscular arteries and development of new muscle more peripherally than is normal--and a decrease in the number of small arteries. The present study descirbes the ultrastructural features of these changes. Pulmonary arteries less than 100 microgram. in diameter after distension and including alveolar capillaries and the muscular arter at the hilum were examined after exposure to 380 torr for between 1 and 52 days. The earliest change, detected from day 2, is the appearance of new muscle in the nonmuscular regions of artery. The position of the new muscle internal to the single elastic lamina and immediately subjacent to endothelium distinguished it from normal muscle. Ultrastructural examination shows not an "extension" of muscle along a pathway, but differentiation to form new muscle, by preexisting cells--by the pericyte in the nonmuscular arteries and by the intermediate cell in the partially muscular. The veins are spared. Endothelial cells also change significantly from day 3. In the normally nonmuscular regions of artery and in the alveolar capillaries, they are thickened. In the nonmuscular regions of artery, although the endothelial cells appear edematous, the number of Weibel-Palade bodies is increased and new muscle appears subjacent. Elsewhere the Weibel-Palade bodies show normal distribution. The extreme narrowing of the lumen caused by thickened endothelial cells and by encroachment of new muscle as well as the finding of capillaries that are no longer patent doubtless explain the reduction in small peripheral areteries.

Animals↗
PubMed1978

Pulmonary arteries of the normal rat: the thick walled oblique muscle segment.

The structure and certain metrical features of the pulmonary arterial tree in the normal rat have been studied in detail by both light and electron microscopy after its distension by injection. In the parts of the tree where the muscle wall is complete a segment with oblique muscle has been identified. The wall of this segment is thick, and is composed largely of obliquely orientated, closely packed smooth muscle cells with little intervening connective tissue, while it lacks a complete external elastic lamina. Both the axial pathway and its side branches have such oblique segments. Proximal and distal to an oblique segment there are transitional regions where obliquely arranged muscle fibres spiral external to the circularly arranged fibres usually described in muscular arteries. The existence of thick walled oblique muscle segments in the pulmonary arterial tree of the normal rat is important since this animal is frequently used in experimental studies, and the thick segments could be taken as evidence of induced hypertrophy.

Animals↗
PubMed1975

In vitro incorporation of (3H)threonine and (3H)glucose by the mucous and serous cells of the human bronchial submucosal gland. A quantitative electron microscope study.

Incorporation of [3H]threonine and [3H]glucose by the mucous and serous cells of the human bronchial submucosal gland has been studied over 8 h using, for the first time in vitro pulse labeling and electron microscope autoradiography. In assessing the autoradiographs, two methods were compared, the circle analysis and the recently described hypothetical grain analysis. Preliminary studies showed formaldehyde to be the most suitable fixative. Chemical analysis of tissue revealed that [3H]threonine was incorporated into the polypeptide moiety of the bronchial gland product and that metabolites of [3H]-glucose were incorporated into the carbohydrate. Tritiated threonine was first localized in the endoplasmic reticulum of both mucous and serous cells and later migrated to the Golgi apparatus, while metabolites of [3H]glucose localized first mainly in the Golgi apparatus. From here, both radioactive precursors were next identified in vacuoles and, finally, in secretory granules. The mucous cell incorporated strikingly more of both radioactive precursors than the serous cell. Thus, it seems that oligosaccharides of mucous and serous cell glycoproteins are synthesized mainly in the Golgi apparatus and added there to the polypeptide core which is synthesized in the endoplasmic reticulum. The relationship of the mucous cell to the serous cell is discussed. It seems that under "normal" conditions each cell represents a different line but that injury may transform a serous cell into a mucous cell.

Autoradiography↗
PubMed1975

The effect of in utero decapitation on the morphological and physiological development of the fetal rabbit lung.

A study has been made of the consequences of in utero decapitation on the morphological and physiological development of the fetal lung. Fetal rabbits were decapitated in situ at 22 days, without losing any amniotic fluid, and allowed to continue their development with their undamaged littermates as controls. Such decapitation, of course, removes the pituitary and so interferes with adrenal cortical development. Morphological studies showed an interference with lung development in that, although the number of alveolar saccules increased normally, their walls failed to thin. In the decapitated fetuses, a reduction in the number of lamellated bodies per Type II pneumonocyte was found at each age studied; while dense, homogeneous bodies were more numerous. The normal disappearance of glycogen in the Type II pneumonocytes of the decapitated fetuses was retarded. Physiological studies supported these findings. In control fetuses allowed to breathe for a while the Bubble Stability Ratio increased rapidly from day 26 to reach a maximum at 28 days; whereas, in the decapitated ones, bubble stability was not apparent before day 28 and by the 29th day had reached a maximum which was lower than that of the controls. In the control fetuses, lecithin was detected in lung fluid from 26 days on, and in stomach fluid from 29 days. It is argued that lung development must be, at least in part, under the control of the fetus' own pituitary-adrenal axis.

Animals↗