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Query: UMLS:C0085631 (agitation)
 12,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coagulation factor activity in platelet concentrates stored under different condtions was investigated. At both 22 C and 4 C, coagulation factors, II, VII, IX, X, XI, and XII and fibrinogen were well maintained up to 72 hours. Factor V activity declined slightly in platelet concentrates stored at 4 C (to 78% at 72 hours), but fell to 47 per cent activity in platelets stored at 22 C. Factor VIII activity declined to approximately 68 per cent of normal activity by 72 hours at both 22 C and 4 C. Agitation did not make a difference in levels of coagulation factors. While the decline in Factor V was clearly more pronounced in platelet concentrates than in platelet-poor plasma from the same units, the decline in Factor VIII was decreased by the presence of platelets. Platelet concentrates are a source of coagulation factor activity which should be considered in a component program.
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PMID:Coagulation factor activity in platelet concentrates. 43 31

Endothelial cells were cultured from various different human vessels, including aortas, pulmonary, ovarian, and umbilical arteries, and pulmonary, ovarian, and umbilical veins. The cultured cells were identified as endothelial cells by the presence of Factor VIII antigen and antiotensin I converting enzyme (kininase II). They retained these markers for at least five passages in culture, and some cells had them for seven passages or more. Endothelial cells from the various vessels were compared with respect to their ability to metabolize angiotensins I and II and bradykinin. Cells from arteries had three to five times the angiotensin I converting enzyme activity as cells from veins. The activity of angiotensinase A (aspartyl aminopeptidase) had a similar distribution, and cells from arteries were consistently more active than cells from veins. Cultures of endothelial cells from pulmonary and umbilical vessels formed prostacyclin in response to mechanical stimulation. Media from cell monolayers that were subjected to a change of medium and gentle agitation inhibited aggregation of human platelets. This inhibitory activity was generated within 2-5 min, and it was not formed by cells that were treated with indomethacin or tranylcypromine. Addition of prostaglandin (PG)H(2) to indomethacin-treated cells restored the ability to form the inhibitor, but cells treated with tranylcypromine were not responsive to PGH(2). In experiments where [(14)C]arachidonic acid was added to the cells before stimulation, the major metabolite identified by thin-layer chromatography was 6-keto PGF(1alpha). Thus, it appears that pulmonary endothelial cells, as well as umbilical cord cells, can form prostacyclin. In experiments comparing the ability of arterial and venous cells to form prostacyclin, arterial cells were more active than venous cells. These studies of cells from various human vessels suggest that the vascular origin of cultured endothelial cells determines how they metabolize vasoactive peptides and form prostacyclin.
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PMID:Human pulmonary endothelial cells in culture. Activities of cells from arteries and cells from veins. 698 68

To delineate the factors involved in the pathogenesis of human retinal vasculopathies, as in vitro model of human retinal vascular cells was developed by using cadaver eyes enucleated four to eight hours after death and stored at +4 C for three to seven days. A pure, viable capillary explant was obtained by microdissection and gentle agitation; the more rapidly occurring postmortem changes in the surrounding nervous tissue of the retina facilitated separation of the vascular explants. Factor VIII indirect immunofluorescent staining revealed that 85% to 90% of the cells harvested from capillaries of 3- to 5-day-old cadaver eyes and all cells cultured from 1-week-old postmortem eyes reacted positively, indicating their endothelial nature. High-glucose medium caused degenerative changes in the cells of the initial explant as well as in the cells of confluent cultures within 24 to 72 hours. The cytotoxic effect of glucose was manifested by accumulation of PAS-positive granules, cytoplasmic vacuolation, and eventual cell degeneration.
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PMID:Human retinal vessels in tissue culture. A preliminary report of the effect of acute glucose poisoning on cultured vascular cells. 712 57