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Biomedical subjects

J V Hurley

Publications and source records attributed to J V Hurley.

16 recordsLinked to original sources
PubMed1992

Wound healing in foetal sheep: a histological and electron microscope study.

A study was made of the healing of excised, unsutured and sutured skin wounds in foetal sheep of 75, 90 and 120 days gestation and of wounds in newborn lambs and adult ewes. Foetal and postnatal wounds were found to heal in a very similar way. At each stage of development studied, excised wounds contract rapidly and histological and electron microscope examination demonstrates formation of granulation tissue and its maturation to scar tissue in all types of wound. Examination of polyvinyl sponges 7 and 14 days after subcutaneous implantation confirms the ability of foetal sheep to form vascularised scar tissue. The cellular inflammatory response to wounding is much less prominent in foetal than in postnatal sheep, the number and type of extravascular cells reflecting the changes in blood leucocyte content during development. From a very early stage foetal sheep react to insoluble irritants by the formation of multinucleate giant cells.

Actins↗
PubMed1992

The response of the rabbit rectus femoris muscle to ischemia and reperfusion.

The rectus femoris muscle of the rabbit is perfused by a single artery and vein and is a valuable new model for study of ischemia-reperfusion injury of skeletal muscle. The consequences of increasing duration of ischemia to the rectus femoris have been examined. Postischemic muscle survival (means +/- SEM), as measured by Nitro blue tetrazolium (NBT) staining 24 hr after ischemia, was 90.5 +/- 1.5% after 2 hr normothermic ischemia, 77.1 +/- 7.7% after 3 hr, 41.8 +/- 7.6% after 3 1/2 hr, and 10.7 +/- 8.7% after 4 hr. Histology confirmed the NBT findings at 24 hr and showed considerable regeneration of muscle fibers 1-2 weeks after injury. The injury caused by 3 1/2 hr normothermic ischemia is the most suitable baseline for study of the effects of pharmacological agents in ischemic muscle injury. Further study of the effects of 3 1/2 hr ischemia by a quantitative Evan's blue method revealed a rapid increase in vascular permeability commencing at the start of reperfusion and lasting for 5-6 hr. Vascular labeling with saccharated ferric oxide showed widespread labeling of venules within the injured muscle and electron microscopic examination showed severe injury to both leaking and nonleaking small blood vessels. However, increased vascular permeability accounted for only a small part of the increase in weight of ischemic muscle.

Animals↗
PubMed1979

Chemotaxis.

Explore the source record for details and available documents.

Chemotactic Factors↗
PubMed1978

Current views on the mechanisms of pulmonary oedema.

Understanding of the causes of pulmonary oedema must be based on knowledge of the mechanism responsible for fluid exchange between the several compartments of the normal lung. Recent physiological studies have clarified the main features of these mechanisms. However in three areas knowledge is still incomplete--the magnitude of the hydrostatic and oncotic forces responsible for fluid movement within the lung, the means by which protein leaks across the wall of small pulmonary vessels and the routes by which fluid and protein pass between the interstitial tissues of the lung and the alveolar space. Further work is needed in these areas. On the basis of this physiological knowledge the mode of development of hydrostatic oedema, the role of lymphatics in pulmonary oedema, and the several stages of pulmonary oedema development that may culminate in alveolar flooding are now clearly understood. Knowledge is less complete about oedema due to increased vascular permeability. In some experimental models, such as alloxan, leakage is due to irreversible injury to the alveolar wall; in other models, including ANTU, oedema formation has been shown to depend upon minor and reversible changes in pulmonary vascular endothelium similar to those that cause exudate formation in areas of acute inflammation. In no instance is detailed information available of both the rate and magnitude of protein leakage and of the morphological basis of increased vascular permeability. Further work is required in this area. Present knowledge allows an adequate explanation of the changes that occur in many clinically important types of pulmonary oedema, including cardiac failure and neurogenic pulmonary oedema. Other types of oedema, notably that which may complicate traumatic shock or extrapulmonary sepsis and high altitude pulmonary oedema, are more complex and the details of their pathogenesis are still obscure.

Animals↗
PubMed1978

The no-reflow phenomenon in experimental free flaps.

The no-reflow phenomenon was studied following reconstitution of blood flow by microvascular anastomosis in an ischemic and denervated free epigastric flap in the rabbit. Microscopic, histological, angiographic, and hematological studies demonstrated the progressive nature of this obstruction to the peripheral blood flow after increasing periods of ischemia. This obstruction reached a point of irreversibility after 12 hours of ischemia, leading to ultimate death of these flaps. These results are consistent with the hypothesis that an ischemia-induced no-reflow phenomenon is caused by cellular swelling, intravascular aggregation, and the leakage of intravascular fluid into the interstitial space. Similarities between these experimental findings and human observations are made. The clinical importance of early diagnosis and treatment of ischemic tissues is emphasized.

Animals↗
PubMed1978

The effects of the perfusion of various solutions on the no-reflow phenomenon in experimental free flaps.

The effects of solution perfusion in the free epigastric flap of the rabbit, after normothermic ischemic periods of 8 hours or 12 hours, have been examined by operative microscopic and histological methods. A smaller group of animals was also studied in which the perfusion was done before the ischemic insult. An ischemia-related obstruction to the peripheral blood flow occurred in the absence of stagnant ischemic blood in this model. Although the 3 perfusion fluids studied were shown to penetrate to all levels of a flap after such an ischemic period, none of them had a beneficial effect on skin survival. However, the solution containing mannitol did have a protective effect on fat survival. Analogies between these experimental findings and the clinical situation are made, and the importance of the early diagnosis and treatment of ischemia in a flap is emphasized.

Abdominal Muscles↗
PubMed1978

Relationship between lymphocyte emigration and vascular endothelium in chronic inflammation.

Small blood vessels within areas of chronic inflammation which contain large numbers of lymphocytes develop unusually thick walls. Combined histological and electron microscope study shows that the thickening is due to hypertrophy of endothelial cells which come to resemble the endothelium of post-capillary venules in lymphoid tissue. Vessels of this type have been found in experimental granulomas induced by injection of Freund's adjuvant or killed tubercle bacilli and in human biopsy material from cases of rheumatoid arthritis and Hashimoto's disease of the thyroid. Comparison with the developing Peyer's patch in young rats shows that the unusual vessels in granulomas are very similar in endothelial cell size, pattern of distribution, extent of lymphocyte migration and degree of carbon leakage to post-capillary venules of the immature Peyer's patch. Study of the time at which lymphocytes appear in large numbers within the granuloma or developing Peyer's patch and the time at which thickened vessels are first seen suggest tha the endothelial changes are a consequence and not a cause of lymphocyte emigration. The stimulus to endothelial hyperthrophy appears to be massive sustained migration of lymphocytes, but the functional significance of this change in vascular structure is not clear.

Animals↗
PubMed1977

The mechanism of escape of plasma protein from small blood vessels in the mucosa of the small intestine of the rat.

A study has been made in rats of the relative rates of escape of plasma protein, measured by accumulation of Evans Blue, and of the large marker particle, HgS, into uninjured small bowel and into an area of intradermal injection of histamine. The rate of escape of Evans Blue, per unit mass of tissue, into small bowel and into an area of histamine-stimulated skin were found to be almost the same, but leakage of HgS into the bowel was only about 1/10 of leakage of the same tracer into a site of intradermal histamine injection. If it be assumed, as is generally accepted, that all the protein that leaks from histamine-stimulated vessels does so via gaps in vascular endothelium that are large enough to allow escape of large marker particles like HgS, these findings show that only a small fraction of the protein that leaks into normal intestinal mucosa can escape via gaps, and that most of the leakage must occur by a route not permeable to particles of HgS. The findings give no indication of the nature of the alternative route for escape of protein.

Animals↗
PubMed1976

Delayed and prolonged vascular leakage in inflammation: the effects of dehydromonocrotaline on blood vessels in the rat cremaster.

Local application of dehydromonocrotaline to the rat cremaster produces a delayed prolonged increase in vascular permeability with a time course similar to that of the pulmonary oedema seen after intravenous injection of the same substance. Study of the injured area by the carbon labelling technique and by electron microscopy shows that the increased permeability involves both capillaries and venules of all sizes within the region exposed to dehydromonocrotaline. The vascular leakage appears to be due to a direct effect on the endothelium of small blood vessels. Carbon deposition in labelled capillaries and venules is predominantly intramural and indicative of increased vascular permeability. Accumulation of carbon within the lumen of capillaries is uncommon, and accounts for only a small fraction of total capillary labelling. The findings indicate that capillaries are a major source of inflammatory exudate in this type of injury and suggest that the importance of leakage from capillaries has been underestimated in other types of delayed prolonged increase in vascular permeability.

Animals↗
PubMed1975

Reaction to Kveim test material in sarcoidosis and other diseases.

81 patients, 24 with sarcoidosis and the remainder with various other diseases, were tested with three batches of Kveim material prepared from the same spleen. Positive Kveim tests were observed in sarcoidosis, tuberculosis, Hodgkin's disease, ulcerative colitis, rheumatoid arthritis, and Weber-Christian disease. These results show that a positive Kveim reaction to the material under test was not specific to sarcoidosis.

Arthritis, Rheumatoid↗
PubMed1975

Primary epithelial tumour in the right atrium of the heart and inferior vena cava in NZR/gd inbred rats; pathology of 18 cases.

In NZR/Gd inbred albino rats, tumours occurred in the right atrium or inferior vena cava of approximately 20 per cent. of untreated animals, of both sexes, over the age of 1 yr. The tumours were centred in the wall of the right atrium in 15 cases, and in the inferior vena cava in another three cases; they appeared to be primary in these sites. The tumours were slowly growing, but eventually malignant. Light- and electron-microscopic study showed the tumours were composed of epithelial alveoli imbedded in a collagenous connective tissue containing spindle cells and thin-walled blood capillaries. The epithelium varied from flat to low columnar, and often secreted mucoid material into the lumina, or sometimes into surrounding tissue. This tumour, for which the name atrio-caval epithelial mesothelioma is suggested, very closely resembles a rare epithelial tumour of the right atrium previously described in humans under a variety of names. An underlying embryological anomaly had been postulated in these tumours in humans, and the occurrence of pathologically similar lesions in high incidence in hearts of NZR/Gd inbred rats should help test the hypothesis of genetic and developmental causes in the genesis of this rare cardiac neoplasm.

Animals↗
PubMed1975

Pulmonary oedema in rats given dehydromonocrotaline: a topographic and electron-microscope study.

Study of cleared, histological and electron-microscope specimens shows that increased vascular permeability plays a major role in the formation of the pulmonary oedema and pleural effusions that occur in rats following the intravenous injection of a large dose of dehydromonocrotaline. There is a latent interval of 6-8 hr between injection of the dehydroalkaloid and the start of increased permeability which appears to be due to a direct damaging effect of the toxin on the endothelium of pulmonary capillaries and small venules. The endothelial injury does not cause permanent disruption of small blood vessels, and 2 days after injury all vessels are patent and lined by a complete layer of endothelium. Large numbers of mononuclear cells are present in the interstitial tissues of the lung 44 hr after injury. These cells appear to be emigrated blood monocytes but the cause of their emigration and their role in the subsequent progression of this type of injury to the lung are not clear.

Animals↗