1983
DOI: 10.1016/0049-3848(83)90092-0
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Effects of prostacyclin during cardiopulmonary bypass in men on plasma levels of β-thromboglobulin, platelet factor 4, thromboxane B2, 6-keto-prostaglandin F1α and heparin

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Cited by 18 publications
(4 citation statements)
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“…Studies such as these which measure blood levels rather than directly assessing kinetics and/or production and release of prostaglandins do not provide definitive proof that the vascular endothelium is chronically injured and constantly releasing small quantities of PGI2 into the circulation. (22), and this mechanical process might be expected to elicit PGI2 release (3,15) and ultimately result in intimal proliferation and arterial narrowing and/or occlusion (16).…”
Section: Discussionmentioning
confidence: 99%
“…Studies such as these which measure blood levels rather than directly assessing kinetics and/or production and release of prostaglandins do not provide definitive proof that the vascular endothelium is chronically injured and constantly releasing small quantities of PGI2 into the circulation. (22), and this mechanical process might be expected to elicit PGI2 release (3,15) and ultimately result in intimal proliferation and arterial narrowing and/or occlusion (16).…”
Section: Discussionmentioning
confidence: 99%
“…Nagaoka [16] reported therapeutic interventions in platelet release reaction during CPB, including the use of antiaggregatory vasodilator prostacyclin [17,18], and use of the platelet activation inhibitor aprotinin [19]. The use of PGl 2 -infusion during CPB remains controversial.…”
Section: Discussionmentioning
confidence: 99%
“…The use of PGl 2 -infusion during CPB remains controversial. Some investigators [17,18] have suggested that PGl 2 -treated patients had less platelet loss, b-TG, and PF 4 production than those of untreated patients indicating the protective effects of prostacyclin infusion on platelets in open heart surgery. In contrast, others [19] have not only failed to find any beneficial effect of prostacyclin on platelet count or function, but have also found some adverse results.…”
Section: Discussionmentioning
confidence: 99%
“…On the other hand, vasodilator substances would reduce vasodilatory reserve at normal pressure, thus also limiting the ability of the RC to maintain flow as RCP is reduced. These vasoactive substances have not been completely characterized but include vasoconstrictory thromboxane (7,25) and vasodilatory prostacyclin (8,23,25). Accordingly, some investigators have administered ibuprofen in studies of LC autoregulation (3,5,21).…”
Section: H173mentioning
confidence: 99%