High levels of portal TNF-α during abdominal aortic surgery in man

Cabie, André; Farkas, Jean-Christophe; Fitting, Catherine; Laurian, Claude; Cormier, J M; Carlet, Jean; Cavaillon, Jean‐Marc

doi:10.1016/1043-4666(93)90034-3

Cited by 79 publications

(58 citation statements)

References 29 publications

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“…High levels of endotoxin can be found after intestinal manipulation even before aortic clamping 22 . During aortic surgery, levels of both TNF alpha and endotoxins in the portal vein are higher when compared to systemic blood samples 26 . Our findings support the evidence that ischemia/reperfusion injury of the limbs may affect the gut and the splanchnic region.…”

Section: Discussionmentioning

confidence: 99%

“…In accordance, neutrophil activation, systemic inflammatory response and organ dysfunction are increased in elective AAA repair when transperitoneal is compared with extraperitoneal approach 36 . Although some authors suggest that the intestinal tract would be an important source of inflammation during AAA repair 26,36,37 one clinical study did not find differences in both IL-6 and IL-10 levels when femoral vein samples were compared to systemic blood samples in patients submitted to AAA open repair 21 . In contrast, our experiment showed that IL-6 levels found in the posterior cava vein were similar to those found in portal vein and both were lower than in samples collected at the heart (systemic blood).…”

Section: Discussionmentioning

confidence: 99%

“…We found an increase in IL-6 levels at the portal. Moreover, manipulation of the bowel, mesenteric traction and cooling, direct ischemia caused by vascular clamping, and definitive interruption of the inferior mesenteric and iliac arteries may directly damage the gut [22][23][24][25][26] . In accordance, neutrophil activation, systemic inflammatory response and organ dysfunction are increased in elective AAA repair when transperitoneal is compared with extraperitoneal approach 36 .…”

Section: Discussionmentioning

confidence: 99%

“…During operation, intestinal manipulation, hypothermia, mesenteric traction, and direct intestinal ischaemia might play a role in the production of inflammatory mediators. Moreover, bacterial translocation has been pointed out as a contributing cause of MOF after AAA repair [22][23][24][25][26] . In this context however, various questions remain unanswered.…”

Section: Introductionmentioning

confidence: 99%

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The intestinal tract as the major source of interleukin 6 production during abdominal aortic clamping and hind limb ischaemia-reperfusion injury

et al. 2007

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PURPOSE: The aim of this study was to investigate whether the hind limbs or intestinal tract is the most important initiator of the inflammatory response secondary aortic clamping and hind limb ischemia/reperfusion injury. METHODS: Blood samples of Wistar rats obtained from posterior cava vein, portal vein, and heart cavity during either laparotomy (control group, n=8) or laparotomy + 2 h of aortic clamping and bilateral hind limb ischemia (ischemia group, n=8), or 2 h after ischemia and 2 h of reperfusion (ischemia-reperfusion group, n=8) were assayed for interleukin 6 (IL-6) and C-reactive protein (CRP). RESULTS: Serum IL-6 at the heart (223.6±197.9 [10-832] pg/mL) was higher (p<0.001) than at both portal (133.08±108.52 [4-372] pg/mL) and posterior cava veins (127.58±109.15 [8-388] pg/mL). CRP was not significant different among groups. CONCLUSION: The splanchnic region is also a source of inflammatory response secondary to ischemia and reperfusion of the hind limbs.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The intestinal tract as the major source of interleukin 6 production during abdominal aortic clamping and hind limb ischaemia-reperfusion injury

et al. 2007

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“…Aortic surgery initiates a systemic inflammatory response secondary to bowel manipulation and systemic release of lipopolysaccharide and tumour necrosis factor-a [6]. Cytokines and cellular adhesion molecules are also elevated following both endovascular and open aortic surgery [7][8][9].…”

Section: Peri-operative Evidence Of Cardiovascular Protection By Statinsmentioning

confidence: 99%

A peri‐operative statin update for non‐cardiac surgery. Part II: Statin therapy for vascular surgery and peri‐operative statin trial design

Biccard

2008

Anaesthesia

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SummaryThis is the second of two review articles evaluating peri-operative statin therapy. In surgical patients, the utility of peri-operative statin therapy is strongly suggested by retrospective studies, although it is probably overestimated, as important confounding factors have not been controlled for and hence the literature is considered to be currently inconclusive.This review examines the potential mechanisms and indications for peri-operative statin protection, the efficacy of acute peri-operative beta-blockade in addition to statin therapy, the effect of peri-operative statin therapy withdrawal and the implications of comorbidities associated with peri-operative cardiovascular risk on statin therapy. Recommendations concerning appropriate dosing, duration, therapeutic targets and necessary investigations when prescribing peri-operative statins are made. Peri-operative study design recommendations are suggested, so that future meta-analyses may be more informative. Recommendations are made regarding retrospective reporting of statin studies to minimise the bias inherent in a number of the current retrospective studies on this subject. This is the second of two review articles evaluating perioperative statin therapy. In the first review article, the cellular and metabolic responses to statin therapy were examined. The duration and timing of statin therapy and therapeutic targets in patients with stable and unstable coronary artery disease (CAD) were presented [1]. In this review the evidence regarding the utility and safety of peri-operative statin therapy is examined. The indications for peri-operative statin therapy, the role of acute betablockade, the implications of withdrawal of statin therapy and comorbidities associated with peri-operative cardiac events are discussed. The potential role of intensive therapy in vascular surgical patients is considered. Finally, recommendations for peri-operative statin therapy and clinical trials are made based on the findings reported in these two reviews. Peri-operative evidence of cardiovascular protection by statinsInflammation as a determinant of adverse peri-operative cardiovascular events surgery Approximately half of peri-operative myocardial infarctions occur as a result of vulnerable plaque rupture in coronary arteries which are not critically stenosed [2,3]. Patients who have myocardial infarction or death following vascular surgery have an increased coronary plaque load, as documented by more diseased coronary vessels, more irregular lesions, more coronary segments with irregular lumens and more collaterisation [4].Surgery is associated with a systemic inflammatory response [5]. Aortic surgery initiates a systemic inflammatory response secondary to bowel manipulation and

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