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Biomedical subjects

A J Bryan

Publications and source records attributed to A J Bryan.

At least 91 records · Page 5Linked to original sources

Surgical preparation induces injury and promotes smooth muscle cell proliferation in a culture of human saphenous vein.

OBJECTIVE: The aim was to investigate the influence of vessel wall injury, incurred during routine vein preparation, on smooth muscle cell proliferation. METHODS: A newly developed quantitative organ culture was used, in which segments of human saphenous vein were cultured in medium containing 30% fetal bovine serum and 1 microCi.ml-1 of [3H]thymidine for up to 14 d. Endothelial integrity was measured by scanning electron microscopy and medial cell viability by adenine nucleotide concentrations. Cell proliferation was measured by DNA concentration, global incorporation of [3H]thymidine, and by counting labelled cells in autoradiographs of transverse sections. RESULTS: Surgical preparation led to endothelial injury and reduced adenine triphosphate concentration by 60%. Surgically prepared veins also suffered a significant decline in DNA concentration during culture, which implied that injury led to cell necrosis. Surgically prepared veins showed 2.1- and 2.7-fold greater global incorporation of [3H]thymidine than freshly isolated veins after 7 and 14 d in culture, respectively, which corresponded with a 23-fold and 11-fold greater abundance of thymidine labelled cells in the medial layer. Intimal thickening and the numbers of total and thymidine labelled cells in the intimal layer were similar. CONCLUSIONS: The data show that injury incurred during routine surgical preparation is associated with enhanced medial smooth muscle cell proliferation. The effect of injury was most probably to permit an increased response of medial smooth muscle cells to serum derived mitogens.

Adenosine Triphosphate↗

A surgical technique that preserves human saphenous vein functional integrity.

We investigated the effect of a novel surgical preparative technique for human saphenous vein by using the concentration of adenosine triphosphate and the adenosine triphosphate/diphosphate ratio to quantify medial integrity and by using stimulated rates of prostacyclin production to quantify endothelial function. Freshly isolated vein had an adenosine triphosphate concentration of 358 +/- 54 nmol.g-1 wet weight and an adenosine triphosphate/diphosphate ratio of 2.89 +/- 0.13 (n = 12); it produced prostacyclin in response to fluid shear at a rate of 14.3 +/- 2.0 pg.min-1.mg-1 wet weight (n = 12). Surgically prepared vein obtained on completion of the last proximal anastomosis had been distended with the patient's own arterial pressure using a side-arm connected to the aortic cannula. This vein had an adenosine triphosphate concentration of 413 +/- 70 nmol.g-1 wet weight and an adenosine triphosphate/diphosphate ratio of 2.74 +/- 0.44 (n = 11), and it produced prostacyclin at a rate of 13.1 +/- 0.2 pg.min-1.mg-1 wet weight (n = 12). All values were indistinguishable from those in freshly isolated vein. The results demonstrate that this simple technique for distention at arterial pressure preserved medial and endothelial function.

Adenosine Diphosphate↗

Pleural effusions: is thoracoscopy a reliable investigation? A retrospective review.

In this paper, we consider the results of thoracoscopy in a busy thoracic unit where the referring physicians place their greatest emphasis upon simple standard investigation of pleural disease. Between 1985 and 1989 620 patients with a pleural effusion of unknown aetiology were referred to our thoracic medical unit. Initial investigations included aspiration of pleural fluid for cytology and culture, and blind pleural biopsy for histological examination. Recourse to thoracoscopy was only taken in the absence of a diagnosis or non-resolution of the patients symptoms and signs. Of these 620 patients only 48 (8%) remained without a diagnosis and were referred for thoracoscopy. Histological assessment of biopsies obtained at thoracoscopy revealed malignancy in 24 patients (50%) and benign conditions in 16 patients (33%). In eight patients (17%) no conclusive diagnosis was established; in this latter group, six patients continued with their symptoms and further invasive investigations revealed malignancy. In this setting where thoracoscopy was used as a last resort, the sensitivity for thoracoscopy was 83% and the specificity was 100% with a predictive value of a negative result being 25%. In conclusion, from our experience, the majority of pleural disease may be diagnosed using simple techniques but thoracoscopy can be very helpful in the more complex cases. Moreover, inconclusive histology following thoracoscopy is an indication for further investigation if the condition does not improve.

Adult↗

Median sternotomy wound dehiscence: a retrospective case control study of risk factors and outcome.

Over a 5-year period from 1985 to 1989, 2760 patients underwent open heart surgery at the University Hospital of Wales. Of these, 44 (1.6%, 35 men, mean age 61 years) developed median sternotomy dehiscence 2-40 (median 9) days after surgery. Infection was an associated factor in 18 patients (41%) and Staphylococcus aureus the predominant isolate in seven of those. Thirty-seven patients underwent rewiring of the sternotomy wound and seven patients underwent debridement, removal of wires and delayed closure. In those undergoing rewiring, sternal stability was maintained in 34 patients (92%). There were seven deaths (16%), of which two were considered to be wound-related. Median hospital stay of survivors was 34 (range 16-84) days. Comparison with 88 matched controls by univariate analysis showed preoperative chronic obstructive airways disease, reduced FEV1/FVC ratio (both P < 0.001) and smoking (P < 0.05) were all more common in the dehiscence group. In addition, reoperation for bleeding (P < 0.05), prolonged bypass time, postoperative ventilation period and length of stay in the intensive care unit (all P < 0.001) were more common in the study group.

Cardiac Surgical Procedures↗

Time-course of medial and intimal thickening in pig venous arterial grafts: relationship to endothelial injury and cholesterol accumulation.

With use of an established model of pig saphenous vein grafts in the carotid artery, the time-course of the following changes was related: (1) medial and intimal size by morphometry of transverse sections, (2) cell number by deoxyribonucleic acid concentration, (3) cell density by deoxyribonucleic acid concentration per milligram wet weight and by counting nuclei in transverse sections, (4) endothelial morphology by scanning electron microscopy, and (5) cholesterol concentration. In the first week after grafting, medial and intimal thickening occurred associated with an increase in cell number. Between 1 and 4 weeks after grafting, further rapid medial and intimal thickening occurred with no further increase in cell number but with a reduction in cell density, which suggested that cell migration, hypertrophy, and the laying down of extracellular matrix were responsible. Between 4 and 39 weeks after grafting, a slower increase in medial and intimal size occurred, associated with a parallel increase in cell number and no further change in cell density. The endothelium of grafts showed only localized abnormalities, including loss of cells and leukocyte adhesion, either 1 or 4 weeks after grafting. Cholesterol concentration was slightly elevated 1 week after grafting but returned to values similar to those in vein by 4 weeks after grafting. Distention to 600 mm Hg during surgical preparation of vein for grafting resulted in lower graft patency after either 1 or 4 weeks and caused significant medial and endothelial injury. Distention did not, however, affect changes in medial or intimal size, deoxyribonucleic acid, or cholesterol concentration caused by grafting. We conclude that three processes contribute to medial and intimal thickening, namely: (1) an initial phase of rapid smooth muscle cell proliferation, (2) smooth muscle cell migration, hypertrophy, and synthesis of extracellular matrix, and (3) a late phase of slower smooth muscle cell proliferation. The incomplete late suppression of smooth muscle cell proliferation occurs despite regeneration of a morphologically intact endothelium and in the absence of progressive cholesterol accumulation.

Anastomosis, Surgical↗

Intimal proliferation in an organ culture of human saphenous vein.

This study investigated whether intimal proliferation, the characteristic feature of the response of human saphenous vein to arterial implantation, also occurs in organ culture. Vein segments were maintained for 14 days in medium supplemented with 30% fetal bovine serum. Tissue viability (measured by adenosine triphosphate [ATP] concentration) decreased only 20% from 280 +/- 20 to 220 +/- 20 nmol/g wet weight. In veins prepared for culturing, endothelial loss (approximately 20%) was confined to near the cut edges. Cultured veins retained an endothelial layer in the initially undamaged areas, while the initially injured areas became covered by a mixture of endothelial and vascular smooth muscle cells. Autoradiography in conjunction with scanning electron microscopy showed the presence of proliferating cells on the intimal surface. Transverse sections of cultured veins showed the development of a new intima containing vascular smooth muscle cells identified by immunocytochemistry with anti-alpha-actin. There were also endothelial cells identified with Ulex europaeus lectin arranged in capillarylike structures. Pulse or continuous labeling of cultures with [3H]thymidine showed that proliferating cells were confined to the new intima and suggested that the smooth muscle cells in this layer arose from both immigration and proliferation. The results demonstrate that intimal proliferation occurs in organ culture of human saphenous veins.

Adult↗

Distention promotes platelet and leukocyte adhesion and reduces short-term patency in pig arteriovenous bypass grafts.

A pig model of autologous saphenous vein to common carotid artery bypass grafting was developed. An end-to-end anastomotic technique led to lower middle graft and distal turbulence. Saphenous veins were surgically prepared with or without distention at 600 mm Hg, implanted into the arterial circulation, and removed 2 hours later. Medial integrity was then assessed by adenosine triphosphate/adenosine diphosphate concentration ratio, and endothelial integrity, leukocyte and platelet adhesion by scanning electron microscopy. In grafts made with undistended vein adenosine triphosphate/adenosine diphosphate concentration ratio was not significantly lower (3.0 +/- 0.1, n = 32) than in freshly isolated vein (3.3 +/- 0.1, n = 26), endothelial cover was 98% +/- 1%, n = 6, and there was little platelet or leukocyte adhesion. In distended grafts adenosine triphosphate/adenosine diphosphate concentration ratio was reduced to 2.2 +/- 0.2 (n = 7, p less than 0.005), endothelial cover was reduced to 38% +/- 14% (n = 6, p less than 0.001), and there was extensive platelet and leukocyte adhesion to exposed subendothelium. In separate experiments graft patency measured at 1 to 5 weeks was significantly greater (96%, n = 25) when undistended vein was used than when distended vein was used (64%, n = 25, p less than 0.005). The data show that distention leads to medial and endothelial damage and that this is associated with increased platelet and leukocyte adhesion and with reduced early patency.

Adenosine Diphosphate↗

Late postoperative cardiac tamponade presenting as dysphagia.

A case of late cardiac tamponade seen with progressive dysphagia 15 days after aortic valve replacement is reported. The diagnosis was confirmed echocardiographically and successful pericardiocentesis was followed by immediate alleviation of the dysphagia.

Aortic Valve↗

Surgical preparation impairs release of endothelium-derived relaxing factor from human saphenous vein.

Release of endothelium-derived relaxing factor was measured from freshly isolated human saphenous vein and from vein subject to routine surgical preparation for coronary artery bypass grafting. Surgical preparation led to a significant decline in endothelium-derived relaxing factor release as compared with freshly isolated vein, and these changes were associated with loss of endothelial coverage. Storage of freshly isolated vein in blood but not in Hartmann's solution also resulted in a decline in maximally stimulated endothelium-derived relaxing factor release that was not associated with loss of endothelium. Reduced production of endothelium-derived relaxing factor, a potent vasodilator and inhibitor of platelet adhesion and aggregation, may be implicated in the etiology of early vein graft thrombosis.

Animals↗