Prostacyclin in the circulation of patients with vascular disorders undergoing surgery

1986 ◽  
Vol 71 (6) ◽  
pp. 743-747 ◽  
Author(s):  
J. M. Ritter ◽  
G. Hamilton ◽  
S. E. Barrow ◽  
D. J. Heavey ◽  
N. E. Hickling ◽  
...  

1. The object of this study was to investigate clinical conditions in which increased production of prostacyclin (PGI2) has been reported. 6-Oxo-prostaglandin F1α (6-oxo-PGF1α) is the stable hydrolysis product of PGI2 and was measured in plasma from patients undergoing hepatic or cardiac surgery and in unoperated patients with vascular and hepatic disease, using gas chromatography/mass spectrometry. 2. Blood obtained simultaneously from portal and peripheral veins, during emergency surgery for bleeding oesophageal varices in six patients with cirrhosis of the liver, contained very high concentrations of 6-oxo-PGF1α (range 99–11485 pg/ml of plasma). 6-Oxo-PGF1α was higher in portal than in peripheral blood in five out of six patients. 3. Six unoperated patients with cirrhosis and oesophageal varices which were not bleeding all had normal peripheral plasma concentrations of 6-oxo-PGF1α < 2 pg/ml (normal up to 5 pg/ml). 4. Seventeen patients with severe vascular disease had normal basal plasma 6-oxo-PGF1α concentrations (< 2 pg/ml). 5. Eighteen subjects with atheromatous coronary artery disease underwent aorta–coronary artery grafting, and plasma concentrations of 6-oxo-PGF,α were markedly elevated during surgery (range 55–1207 pg/ml). 6. We conclude that surgery stimulates PGI2 production substantially, and argue that the function of PGI2 may be to limit intravascular extension of thrombus from sites of haemostasis. Inappropriate PGI2 synthesis may contribute to the massive haemorrhage characteristic of oesophageal variceal bleeding.

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
William Hancock-Cerutti ◽  
Marie Lhomme ◽  
Carolane Dauteuille ◽  
Sora Lecocq ◽  
John Chapman ◽  
...  

Plasma concentrations of HDL-C have long been shown to correlate inversely with risk of coronary artery disease (CAD), however the causal nature of this association has not been established. Here we examine the chemical composition and phosphoshingolipidome of HDL in a cohort of subjects with premature CAD, despite having HDL levels ≥90th percentile. We hypothesized that HDL from hyperalphalipoproteinemic subjects with CAD would have distinct compositional changes compared to healthy hyperalphalipoproteinemic subjects, which may relate a reduction in HDL functionality and a pro-atherogenic state. Subjects with HDL ≥90th percentile and CAD (HHDL+CAD, n=25) were compared to healthy subjects with HDL ≥90th percentile (HHDL, n=23). A group of healthy controls with HDL between the 25th and 75th percentile (n=11) was used as reference. HDL subfractions were isolated from EDTA plasma using isopycnic density gradient ultracentrifugation and their chemical composition was assayed using commercial enzymatic assay kits. Quantification of >160 molecular species of total HDL phospho- and sphingolipids was accomplished via a novel method using LC-ESI/MS/MS analysis. The most striking differences were observed in total HDL phospho- and sphingolipid subclasses between groups. When expressed as a percentage of total phosphosphingolipid, phosphatidylcholine (PC) and phosphatidylinositol (PI) were depleted in HHDL+CAD group compared to HHDL, while sphingomyelin (SM) was increased, resulting in a lower PC/SM ratio. The HDL PC/SM ratio has previously been shown to correlate with HDL surface fluidity and antioxidative activity. Additionally, enrichment of PI, a minor, negatively charged phospholipid, has been shown to stimulate cholesterol efflux to reconstituted HDL. Reduction in these two metrics, observed in the HHDL+CAD group, may indicate functionally deficient HDL and may represent pro-atherogenic, HDL-associated biomarkers of CAD in hyperalphalipoproteinemia.


1994 ◽  
Vol 40 (4) ◽  
pp. 552-561 ◽  
Author(s):  
L L Wu ◽  
J Wu ◽  
S C Hunt ◽  
B C James ◽  
G M Vincent ◽  
...  

Abstract We measured plasma homocyst(e)ine [H(e)] and other coronary risk factors in 266 patients with early coronary artery disease from 170 families in which two or more siblings were affected and in 168 unmatched controls. The mean H(e) concentration adjusted for significant correlates (serum creatinine, uric acid, and low-density lipoprotein cholesterol) was 12.0 mumol/L in proband cases compared with 10.1 mumol/L in controls (P = 0.0001). Many (17.6%) of the proband cases had H(e) concentrations exceeding the 95th percentile for the controls (relative odds = 4.9, P &lt; 0.001). H(e) among cases was bimodally distributed even after adjustment for concentrations of plasma vitamins. Concordant high H(e) was seen in at least 10 (12%) of 85 families with two or more affected siblings. We conclude that a substantial proportion of early familial coronary artery disease is probably related to production of high concentrations of H(e) by one or more major genes.


Heart ◽  
2011 ◽  
Vol 97 (12) ◽  
pp. 998-1003 ◽  
Author(s):  
J. R. Ghadri ◽  
A. P. Pazhenkottil ◽  
R. N. Nkoulou ◽  
R. Goetti ◽  
R. R. Buechel ◽  
...  

1993 ◽  
Vol 193 (1) ◽  
pp. 225-230 ◽  
Author(s):  
Rainer M. Arendt ◽  
Ute Wilbert-Lampen ◽  
Lars Heucke ◽  
Michael Schmoeckel ◽  
Klaus Sühler ◽  
...  

2000 ◽  
Vol 36 (3) ◽  
pp. 751-757 ◽  
Author(s):  
Florian Kronenberg ◽  
Markus Stühlinger ◽  
Evi Trenkwalder ◽  
F.S Geethanjali ◽  
Otmar Pachinger ◽  
...  

1997 ◽  
Vol 97 (6) ◽  
pp. 655-657 ◽  
Author(s):  
CAROLINE H MANDEL ◽  
LORI MOSCA ◽  
ELIZABETH MAIMON ◽  
JENNIFER SIEVERS ◽  
ALAN TSAI ◽  
...  

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