Suction-tip dissecting scissors for pelvic surgery.
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Biomedical subjects
Publications and source records attributed to G D Angelini.
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Postoperative spasm of the internal mammary artery graft can cause morbidity and mortality after myocardial revascularization. To our knowledge, the ability of systemic vasodilators to overcome internal mammary artery spasm has not been studied clinically. In 50 patients in whom the left internal mammary artery was used for myocardial revascularization, we have investigated the effect of five agents on internal mammary artery free flow: normal saline, dobutamine, glyceryl trinitrate, sodium nitroprusside, and enoximone, a phosphodiesterase III inhibitor. After the internal mammary artery was harvested, free flow was measured under controlled hemodynamic conditions before any pharmacologic intervention (flow 1) and a mean of 18.5 +/- 3 (standard deviation) minutes after a systemic infusion of one of the five agents was begun (flow 2). The increase in free flow expressed as a percentage of initial flow was greater for enoximone (94% +/- 24%) than for normal saline (18% +/- 11%), dobutamine (40% +/- 27%), and glyceryl trinitrate (52% +/- 36%) (all three p < 0.01). The increase in flow for sodium nitroprusside (78% +/- 37%) was greater than for normal saline and dobutamine (both p < 0.05). We therefore recommend the systemic use of enoximone and sodium nitroprusside, in rank order, to prevent and treat postoperative spasm of the internal mammary artery.
Intimal smooth muscle cell proliferation and superimposed atheroma are the main causes of late failure of saphenous vein bypass grafts. It has been suggested that these reactions are caused by the production of growth factors from the cells of the vessel wall. To test this hypothesis, we cultured segments of pig venous arterial grafts, removed 1 and 4 weeks after implantation, in serum-free medium for 24 hours. Tissue viability as assessed by adenosine triphosphate concentration was maintained throughout the 24-hour culture period (239 +/- 21 nmol/gm wet weight [standard error of the mean], n = 26, 0 hours; 240 +/- 24 nmol/gm wet weight, n = 17, 24 hours). Cell proliferation occurred and autoradiography showed proliferating cells to be located in the neointimal and medial layers. These cells were identified as smooth muscle cells by means of a monoclonal antibody to alpha-actin. Graft-conditioned media were tested for mitogenic activity by means of a fibroblast proliferation assay. Media conditioned for 24 hours produced significant stimulation of cell growth (284% +/- 30%, n = 17) above that obtained in culture medium alone (100%). This mitogenic activity was inhibited by 61% +/- 9%, n = 8, with a polyclonal-neutralizing antibody to platelet-derived growth factor. Reverse-transcription polymerase chain reaction analysis and Northern blots demonstrated platelet-derived growth factor B messenger ribonucleic acid (mRNA) in vein grafts but not in ungrafted vein. Analysis of graft tissue sections by in situ hybridization demonstrated an abundance of platelet-derived growth factor B mRNA positive cells in the endothelial and neointimal layers, as well as in the endothelial cells of the adventitial vessels. These data constitute direct evidence for active growth factor production within the cells of the vein graft. They also suggest that endogenously produced platelet-derived growth factor may play a role in regulating smooth muscle cell proliferation in this model.
Pericardial closure early after open heart surgery has been shown to consistently lower cardiac output and stroke volume, while mean arterial blood pressure is maintained by an increase in systemic vascular resistance. In 10 patients (seven females) (mean age 65 +/- 4 years) undergoing an open heart valve procedure, the effects of a tension-free pericardial closure technique were studied using thermodilution studies and transesophageal echocardiography. The following variables were recorded: mean arterial pressure, mean pulmonary artery pressure, right atrial pressure, cardiac output, stroke volume, systemic vascular resistance, and systolic and diastolic left ventricular dimensions, and left ventricular wall thickness. Observations were made after the heart was decannulated, both while the pericardium was open and after it had been closed by a tension-free technique, and then after closure of the chest. Further observations were made while the chest remained closed, both before and after the pericardium had been reopened by removing the pericardial suture through the chest wall. Closing the pericardium with the tension-free technique while the chest remained open was followed by a fall in cardiac output by 8% and a 15% fall in systemic vascular resistance (both n.s.). These changes caused a 13% reduction in the mean arterial pressure (p = 0.03). Ejection fraction did not change, and systolic and diastolic left ventricular dimensions decreased by 6% and 4% respectively (both n.s.). Opening the pericardium (1.5 to 2 hours after the end of the operation) while the chest remained closed was not followed by significant change in any of the hemodynamic or echocardiographic variables.(ABSTRACT TRUNCATED AT 250 WORDS)
Late occlusion of the saphenous vein graft appears to result in part from wall thickening as an adaptation to increased mean wall stress. Using an established pig model of arteriovenous bypass grafting, the effect of reducing wall stress with an external porous polytetrafluoroethylene stent was investigated. Segments of autologous saphenous vein were implanted by end-to-end anastomoses into both carotid arteries, with one graft supported by a stent 4 mm in diameter. Increases in graft wall dimensions were quantified 4 weeks later by computer-aided planimetry of transverse histological sections. The contribution of hyperplasia (i.e., cell proliferation) to the changes observed was further clarified by measurements of DNA concentration. All grafts showed an increase in external size, but this was restricted by stenting. All grafts also showed an increase in cross-sectional area of the tunica media and tunica intima that was only partly accounted for by an increase in DNA concentration, which indicated that both hyperplasia and hypertrophy had occurred. Stented grafts showed less enlargement of the media but greater enlargement of the intima. Overall wall size was therefore similar in stented and unstented grafts. Stented grafts showed less increase in DNA concentration than unstented grafts. In stented grafts, the residual luminal cross-sectional area was significantly less than in unstented grafts. The data show that external stenting reduces medial enlargement and hyperplasia but increases encroachment of the intima into the lumen. Because final luminal size is thought to be of paramount importance in maintaining long-term patency, external stenting is unlikely to be of benefit.
Occlusion of chest drainage tubes by thrombus is not uncommon after open heart operations. It has been suggested that by coating the tube with phosphatidylcholine (PC), the most prominent phospholipid in the erythrocytes outer membrane, it may be possible to overcome the blood-material interaction responsible for thrombus formation. To test this hypothesis 102 patients (75 males; mean age, 57 +/- 10 years) were randomly allocated to receive either PC-coated or noncoated 32F chest drainage tubes. Preoperative status, type and length of operation, and duration of drainage were similar in the two groups as was postoperative blood loss. Patients receiving PC-coated tubes, however, had less residual blood clot in the tube after removal (0.7 +/- 0.1 versus 3.1 +/- 0.3 g; p < 0.001), a reduced incidence of pericardial effusions (17.6% versus 41.2%; p < 0.01), fewer postoperative supraventricular arrhythmias (2 of 51 versus 10 of 51; p < 0.002), and a shorter hospital stay (8.4 +/- 0.3 versus 9.7 +/- 0.5 days; p < 0.05). Late cardiac tamponade developed in 2 patients in the noncoated group 6 and 10 days postoperatively, which required reexploration. The data show that PC-coated chest drainage tubes are less susceptible to occlusion by thrombus and their use is associated with a significant reduction in postoperative morbidity.
Autologous saphenous vein grafts, unlike internal mammary artery grafts, suffer many late occlusions as a result of excessive proliferation of vascular smooth muscle cells and the superimposition of atheroma on the resulting thickened intima. We investigated the possible basis of this difference using organ cultures. Internal mammary artery segments and freshly isolated and surgically prepared saphenous vein segments were obtained from patients undergoing coronary artery bypass grafting. Internal mammary artery and freshly isolated vein segments showed a high degree of endothelial coverage and medial cell viability that were maintained during culture. Surgically prepared veins showed partial endothelial denudation and medial cell injury, both of which tended to be reversed during culture. Neointimal thickening was greater in surgically prepared vein (72 +/- 13 microns; n = 11) than in freshly isolated vein (44 +/- 8 microns; n = 10) or internal mammary artery (34 +/- 4 microns; n = 13) segments. The occurrence of proliferating cells in the medial layer was also significantly greater in surgically prepared vein (2.8 +/- 1.0/mm; n = 11) than in freshly isolated vein (0.8 +/- 0.3/mm; n = 9) or internal mammary artery (0.6 +/- 0.3/mm; n = 10) segments. The data show that although the smooth muscle proliferation was similar in undamaged saphenous vein and internal mammary artery, it was significantly greater in damaged vein. This implies that the greater intimal proliferation seen in saphenous vein grafts may arise not from intrinsic differences in arterial and venous smooth muscle cells but from a greater susceptibility to injury.
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.
A modified battery-powered toothbrush for performing coronary artery endarterectomy is described. The device facilitates the dissection of the atheromatous core, is safe and inexpensive.
The short-term hemodynamic effects of pericardial closure on cardiac function were studied during steady-state anesthesia and ventilation in 10 patients (6 men) (mean age, 59 +/- 9 years) who underwent an open-heart valve operation. Observations were made after the heart was decannulated, both while the pericardium was open and after it had been closed, and then after closure of the chest after the pericardium had been reopened by removing the pericardial suture through the chest wall. The effect of closing the pericardium before closing the chest was an immediate reduction in cardiac output (thermodilution) of 1.39 +/- 0.24 L/min from 5.09 +/- 0.40 L/min (p less than 0.001). The heart rate remained stable, but there was a decrease in stroke volume of 29% and an increase in systemic vascular resistance of 34% (both, p less than 0.01). The mean arterial pressure increased slightly by 2% (not significant). Opening the pericardium (1.5 to 2 hours after the end of the operation) while the chest remained closed was followed by an increase in cardiac output of 1.33 +/- 0.15 L/min from 4.12 +/- 0.62 L/min (p less than 0.001). As the heart rate and the mean blood pressure changed insignificantly, there was an increase in stroke volume of 15 +/- 3 mL from 53 +/- 5 mL and a reduction in systemic vascular resistance of 473 +/- 83 dyne . s . cm-5 from 1,721 +/- 181 dyne.s.cm-5 (both, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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.
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A 74-year-old female presented in cardiogenic shock four weeks following a severe episode of ischaemic chest pain. Physical examination was suggestive of a ventricular septal defect, and this was confirmed by cross-sectional echocardiography and right heart catheterisation. As the resting electrocardiogram was consistent with an extensive anterior myocardial infarct of indeterminate age, a diagnosis of ventricular septal defect subsequent to infarction was made and the patient taken to the operating theatre for urgent repair. At operation, however, the defect was found to be congenital in origin.
OBJECTIVE: Intimal smooth muscle cell proliferation is an early feature of atherosclerosis. Its progression is difficult to monitor in humans and previous studies have mostly relied on necropsy material. The aim of this study was therefore to establish whether intimal proliferation occurred in an organ culture of human internal mammary artery. METHODS: Segments of freshly isolated internal mammary artery were maintained din standard tissue culture medium containing 30% calf serum for 14 d. Tissue viability (measured by ATP concentration) was maintained during processing and throughout the culture period [211(SEM 28) nmol ATP.g-1 wet weight on d 1 v 208(27) on d 14]. RESULTS: Histological transverse sections of cultured internal mammary artery showed the development of a neointima containing smooth muscle cells identified by immunocytochemistry for alpha actin. Pulse labelling of cultures with [3H]-thymidine showed proliferating cells predominantly in a neointimal layer with few dividing cells in the media. Cultured de-endothelialized vessels showed less neointimal thickening than cultured freshly isolated vessels [16(3) v 36(5) microns, p < 0.0025] as well as a reduced number of dividing cells per mm of neointimal length [3.1(0.6) v 5.5(1.1), p < 0.05]. CONCLUSIONS: Intimal proliferation occurred in organ culture of internal mammary artery. There is evidence for a factor derived from the endothelium, which may be important in the development of intimal proliferation.
Occlusion of saphenous vein coronary artery bypass grafts remains a significant clinical problem. Early occlusion can be minimized by optimizing surgical techniques and by antithrombotic treatments. Unfortunately, no modification of surgical technique or drug therapy has been shown to reduce late vein graft occlusion. This results from excessive proliferation of vascular smooth muscle cells and the superimposition of atheroma on the resulting thickened intima. Understanding the basic mechanisms underlying this response may be helpful in developing strategies to reduce vein graft occlusion.
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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.
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