Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0729233 (Thoracic)
 6,478 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human arterial endothelial cells were cultured in vitro for up to 40 cumulative population doublings. Culture conditions similar to those required for long-term propagation of human umbilical vein endothelial cells were employed. These included fibronectin-coated culture vessels, 5 to 20% fetal bovine serum, endothelial cell growth factor, and heparin. Thoracic aorta endothelial cells were larger than iliac artery endothelial cells. Both cell types stained positively for Factor VIII antigen by immunofluorescence. A decrease in confluent density as a function of population doubling level was correlated with the appearance of large, senescent cells in the cultures. Serum growth factors to which the arterial endothelial cells responded included insulin, transferrin, epidermal growth factor, thrombin, and somatomedins. The effect of thrombin did not require the availability of the active site of the protease. The effect of the somatomedins was only seen in the presence of heparin. Neither platelet-derived growth factor nor hydrocortisone induced arterial endothelial cell proliferation. These growth factor responses were also observed on the part of human umbilical vein endothelial cells.
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PMID:Growth factor responses of human arterial endothelial cells in vitro. 375 96

The degree of mixing in fluid layers immediately adjacent to the endothelial surface is a major variable in assessment of prostacyclin (PGI2) production by cultured endothelial cells or intact vessel endothelium in vitro. Lack of adequate mixing should lead to underestimation of true production because PGI2 immediately adjacent to endothelium would be only poorly sampled upon buffer collection. Thoracic aortas from 38 New Zealand white rabbits were therefore excised, opened longitudinally, and mounted endothelial side uppermost in a buffer-filled chamber which excluded cut tissue edges from study. Production of PGI2 under unstirred and magnetically stirred conditions was measured by radioimmunoassay (RIA) for 6-keto-PGF1 alpha. For animals pretreated with the combination of papaverine and heparin (see below), unstimulated and arachidonate-stimulated 6-keto-PGF1 alpha increased with stirring rate toward limits of 2.9 and 28.5 ng/cm2/min, respectively. Unstimulated and stimulated 6-keto PGF1 alpha measured at 650 rpm, for example, were greater than their values at 0 rpm by factors of 3.5 (2P less than .01) and 3.7 (2P less than .001), respectively. The process of vessel excision, however, produces another variable: degree of injury to endothelium caused by such factors as secondary vessel contraction and thrombin generation. Vessel contraction and thrombin generation can be minimized, respectively, by the use of a smooth muscle relaxant and heparin administered prior to killing of the animals. The rabbits were, therefore, grouped according to intravenous (IV) treatment, prior to killing, with saline, papaverine (4 mg/kg), heparin (200 U/kg) or the combination of papaverine and heparin (same doses). As compared with pretreatment with saline, papaverine alone, or heparin alone, pretreatment with the combination of papaverine and saline led to increases in stimulated 6-keto-PGF1 alpha of 1.6- to 2.8-fold. By transmission electron microscopy, endothelium from animals pretreated with saline showed ultrastructural changes, including disruption of cytoplasm, separation without detachment of most endothelial cells from subendothelium, and focal areas of denudation. In contrast, ultrastructural integrity of endothelium was preserved in aortas of animals pretreated with combined papaverine and heparin. These results support the hypothesis that unstirred diffusional layers lead, in vitro, to underestimation of PGI2 production, especially when vessels are protected from excisional injury.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Prostacyclin production in vitro by rabbit aortic endothelium: correction for unstirred diffusional layers. 390 18

The use of plasmapheresis in cardiac surgery has failed to show an unequivocal benefit. However, the further processing of plasmapheresed blood to obtain a platelet-rich concentrate, termed platelet gel, may reduce patient susceptibility to infection through poorly understood mechanisms related to a combination of platelets, white blood cell content, and expedited wound healing. The purpose of the study was to retrospectively evaluate the incidence wound infections in patients undergoing cardiac surgery. Platelet gel (PG) patients (n = 382) received topical administration of a mixture of platelet concentrated plasma, 10% calcium chloride (5 mL), and bovine thrombin (5000 units). A control group (NoPG, n = 948) operated on concurrently with the treatment group did not receive PG, but otherwise received similar wound care. A historical control (HC, n = 929) included patients operated on before the availability of PG. After Institutional Review Board approval, 20 factors reported in the literature to predispose individuals for increased infection were recorded along with infections classified either as superficial or deep sternal according to the Society of Thoracic Surgeon criteria. All data were obtained from our institutional contribution to the Society of Thoracic Surgeon database. All adult (>19 years of age) patients undergoing cardiac surgery at our institution between October 2002 and June 2005 were included in this study (n = 2259). The incidence of superficial infection was significantly lower in the PG group (0.3%) compared both with the NoPG (1.8%) and HC (1.5%) groups (p < .05). There was a similar relationship found when comparing deep sternal wound infections (PG, 0.0% vs. NoPG, 1.5%; p < .029 and PG vs. HC, 1.7%;p < .01). In conclusion, the application of PG in patients undergoing cardiac surgery seems to confer a level of protection against infection, although the mechanisms of action remain to be elucidated.
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PMID:Use of platelet gel and its effects on infection in cardiac surgery. 1652 57

We considered that a moderate reduction of the central blood volume (CBV) may activate the coagulation system. Lower body negative pressure (LBNP) is a non-invasive means of reducing CBV and, thereby, simulates haemorrhage. We tested the hypothesis that coagulation markers would increase following moderate hypovolemia by exposing 10 healthy male volunteers to 10 min of 30 mmHg LBNP. Thoracic electrical impedance increased during LBNP (by 2.6 +/- 0.7 Omega, mean +/- SD; P < 0.001), signifying a reduced CBV. Heart rate was unchanged during LBNP, while mean arterial pressure decreased (84 +/- 5 to 80 +/- 6 mmHg; P < 0.001) along with stroke volume (114 +/- 22 to 96 +/- 19 ml min(-1); P < 0.001) and cardiac output (6.4 +/- 2.0 to 5.5 +/- 1.7 l min(-1); P < 0.01). Plasma thrombin-antithrombin III complexes increased (TAT, 5 +/- 6 to 19 +/- 20 microg l(-1); P < 0.05), indicating that LBNP activated the thrombin generating part of the coagulation system, while plasma D-dimer was unchanged, signifying that the increased thrombin generation did not cause further intravascular clot formation. The plasma pancreatic polypeptide level decreased (13 +/- 11 to 6 +/- 8 pmol l(-1); P < 0.05), reflecting reduced vagal activity. In conclusion, thrombin generation was activated by a modest decrease in CBV by LBNP in healthy humans independent of the vagal activity.
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PMID:Early activation of the coagulation system during lower body negative pressure. 1965 65