title: Alterations of thrombogenesis, endothelial damage and oxidative stress with reperfusion during femoral artery bypass surgery for peripheral vascular disease.
abstract: Peripheral vascular disease (PVD) is a significant cause of cardiovascular morbidity. We hypothesised that there would be significant alterations of thrombogenesis, platelet activation and endothelial damage, which could be associated with abnormal oxidative stress during femoral artery bypass surgery for PVD, where the femoral artery is cross-clamped (causing acute ischaemia) and reperfused (following revascularisation). To test this hypothesis, we measured sequential changes in von Willebrand factor (vWF, and index of endothelial damage/dysfunction), tissue factor (TF, an index of thrombogenesis) and soluble P-selectin (sP-sel, an index of platelet activation) as well as lipid hydroperoxides (LPO, an index of oxidative stress) in 28 consecutive patients undergoing elective peripheral artery bypass surgery. Mean baseline vWF and sP-sel levels in PVD patients (before clamping) were significantly higher compared with age- and sex-matched controls (unpaired t test, both p < 0.05), but there were no significant differences in TF and LPO levels. There was a correlation between TF and vWF (Spearman's, r = 0.374, p = 0.05), as well as between sP-sel and vWF at the start of surgery (r = 0.467, p = 0.012). The patients undergoing peripheral artery bypass surgery had a mean femoral artery clamp time of 28 min (standard deviation 14 min; range 11-65 min). There were no significant overall changes in sP-sel, vWF, TF and LPO with femoral artery cross-clamping and reperfusion (repeated measures ANOVA, p = NS). In conclusion, we found that during ischaemia-reperfusion during peripheral arterial bypass surgery, thrombogenesis (as measured by plasma TF) and oxidative damage (as measured by LPO) within the affected leg does not increase in the immediate perioperative period. Further studies are required to assess the mechanism(s) of ischaemia-reperfusion injury in PVD, and the contributory role(s) of the endothelium and platelets.
authors.affiliation: Haemostasis Thrombosis and Vascular Biology Unit and Department of Vascular Surgery, City Hospital, Birmingham, UK.
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: Makin
authors.forename: Natali A Y
authors.initials: NA
authors.lastname: Chung
authors.forename: Stanley H
authors.initials: SH
authors.lastname: Silverman
authors.forename: Gregory Y H
authors.initials: GY
authors.lastname: Lip
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology*; D005260:Female; D005263:Femoral Artery / Q000601:surgery; D006801:Humans; D008054:Lipid Peroxides / Q000097:blood; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D019007:P-Selectin / Q000097:blood; D016491:Peripheral Vascular Diseases / Q000150:complications / Q000473:pathology / Q000601:surgery*; D015427:Reperfusion Injury / Q000150:complications*; D013925:Thromboplastin / Q000032:analysis; D013927:Thrombosis / Q000209:etiology*; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D008054:Lipid Peroxides; D019007:P-Selectin; D014841:von Willebrand Factor; D013925:Thromboplastin