Relationships of Adiponectin with Markers of Systemic Inflammation and Insulin Resistance in Infants Undergoing Open Cardiac Surgery

Department of Cardiovascular Surgery, Xijing Hospital, Fourth Military Medical University, No. 15, Changle West Road, Xi'an, Shaanxi 710032, China.
Mediators of Inflammation (Impact Factor: 3.24). 06/2013; 2013(3):187940. DOI: 10.1155/2013/187940
Source: PubMed


Insulin resistance and systemic inflammation frequently occur in infants undergoing cardiac surgery with cardiopulmonary bypass, while adiponectin has been demonstrated to have insulin-sensitizing and anti-inflammatory properties in obesity and type 2 diabetes mellitus. In this prospective study, we aimed to investigate the association of adiponectin with insulin resistance and inflammatory mediators in infants undergoing cardiac surgery with cardiopulmonary bypass.

Methods and results:
From sixty infants undergoing open cardiac surgery, blood samples were taken before anesthesia, at the initiation of cardiopulmonary bypass and at 0, 6, 12, 24, and 48 hours after the termination of cardiopulmonary bypass. Plasma interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF- α ), and adiponectin levels were assessed in blood samples. Insulin resistance was measured by assessment of the insulin requirement to maintain euglycaemia and repeated measurements of an insulin glycaemic index. Insulin glycaemic index, IL-6, and TNF- α increased up to 3-8-fold 6 h after the operation. Adiponectin is negatively correlated with markers of systemic inflammation 6 h after CPB.

Although the level of serum adiponectin decreased significantly, there was a significant inverse association of adiponectin with markers of systemic inflammation and insulin resistance in infants undergoing open cardiac surgery.

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    • "Myocardial ischemia reperfusion (MI/R) injury is a major perioperative complication that is associated with significant morbidity and mortality in coronary artery bypass graft (CABG) surgery [1] [2] and in patients undergoing heart valve replacement surgery [3] using cardiopulmonary bypass (CPB), especially in patients with comorbidities (e.g., age [4] and diabetes [5]). Volatile anesthetic preconditioning (e.g., isoflurane preconditioning, Iso) provides cardioprotective effects during CABG [6] [7]. "
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    ABSTRACT: Pretreatment with the angiotensin-converting inhibitor captopril or volatile anesthetic isoflurane has, respectively, been shown to attenuate myocardial ischemia reperfusion (MI/R) injury in rodents and in patients. It is unknown whether or not captopril pretreatment and isoflurane preconditioning (Iso) may additively or synergistically attenuate MI/R injury. Methods and Results. Patients selected for heart valve replacement surgery were randomly assigned to five groups: untreated control (Control), captopril pretreatment for 3 days (Cap3d), or single dose captopril (Cap1hr, 1 hour) before surgery with or without Iso (Cap3d+Iso and Cap1hr+Iso). Rabbit MI/R model was induced by occluding coronary artery for 30 min followed by 2-hour reperfusion. Rabbits were randomized to receive sham operation (Sham), MI/R (I/R), captopril (Cap, 24 hours before MI/R), Iso, or the combination of captopril and Iso (Iso+Cap). In patients, Cap3d+Iso but not Cap1hr+Iso additively reduced postischemic myocardial injury and attenuated postischemic myocardial inflammation. In rabbits, Cap or Iso significantly reduced postischemic myocardial infarction. Iso+Cap additively reduced cellular injury that was associated with improved postischemic myocardial functional recovery and reduced myocardial apoptosis and attenuated oxidative stress. Conclusion. A joint use of 3-day captopril treatment and isoflurane preconditioning additively attenuated MI/R by reducing oxidative stress and inflammation.
    Mediators of Inflammation 08/2015; 2015(19, supplement):819232. DOI:10.1155/2015/819232 · 3.24 Impact Factor
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    • "Preliminary data have demonstrated that, during cardiac surgery under CPB, leptin levels inversely correlate to the inflammatory markers with a decrease during the CPB and there after an increase with a peak between the 12 h and 24 h [35] [36] [37] [38]. A similar time course for the perioperative adiponectin levels has been reported [32] [33]. Furthermore Jimenez Rivera et al. have reported significantly lower leptin levels in patients with an excessive postoperative bleeding after cardiac surgery [39]. "
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    ABSTRACT: Background Obesity is suggested to reduce postoperative bleeding in patients undergoing cardiac surgery with cardiopulmonary bypass (CPB) but perioperative hemostasis variations have not been studied. Therefore, we investigated the effects of severe obesity (body mass index [BMI] ≥ 35 kg/m2) on chest tube output (CTO) and hemostasis in patients undergoing cardiac surgery with CPB. Materials and Methods We prospectively investigated 2799 consecutive patients who underwent coronary and/or valve surgery using CPB between 2008 and 2012. 204 patients (7.3%) presented a severe obesity. Results In the severe obesity group, the 6-h and 24-h CTO were significantly reduced by -21.8% and -14.8% respectively (P < 0.0001) compared with the control group. A significant reduction of the mean number of red blood cell units transfused at 24 h was observed in the severe obesity groups (P = 0.01). On admission to the intensive care unit, a significant increase of platelet count (+ 9.2%; P < 0.0001), fibrinogen level (+ 12.2%; P < 0.0001) and prothrombin time (+ 4.1%; P < 0.01) and a significant decrease of the activated partial thromboplastin time (-4.2%; P < 0.01) were observed in the severe obesity group compared with the control group. In multivariate analysis, severe obesity was significantly associated to a decreased risk of excessive bleeding (24-h CTO > 90th percentile; Odds ratio: 0.37, 95% CI: 0.17 to 0.82). No significant differences were observed regarding postoperative thromboembolic events between the two groups. Conclusions Severe obesity is associated with a prothrombotic postoperative state that leads to a reduction of postoperative blood loss in patients undergoing cardiac surgery with CPB.
    Thrombosis Research 08/2014; 134(2):346–353. · 2.45 Impact Factor
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    ABSTRACT: Unlabelled: Diabetes is now one of the most common un-communicable diseases worldwide. Few studies have dealt specifically with the potential therapeutic effect of TNF-α suppressor to decrease oxidative stress markers in patients with diabetes. The aim of this study was to investigate the potential therapeutic and toxic effect of the direct injection of the anti-TNF-α on oxidative stress mediators, proinflammatory cytokines and vascular risk factors associated with diabetes on diabetic rats. Methods: diabetes was induced by streptozotocin, three weeks after the - induction of diabetes, a polyclonal anti-mouse/rat TNF-α rabbit serum was injected in the treated group and sacrificed after 4 weeks. The expression of TNF-α mRNA was measured by RT-PCR. The levels of TNF-α, VEGF, IL-2, IL- 6, HSP-70, troponin-t, 8-OHdG, ICAM-1 and VCAM-1 were evaluated using ELISA. Myeloperoxiase (MPO) and total peroxides (TPs) levels were estimated by biochemical reactions. Results: the treatment of diabetic rats with the anti-TNF-α caused a significant decrease in the TNF-α mRNA expression, which were paralleled with the decreased levels of TNF-α, IL-6, MOP, HSP-70, ICAM-1, VCAM-1, troponin-t and 8-OHdG in the blood serum. On the contrary, all were highly expressed in the diabetic group that may be the leading reasons for the DNA damage and cell loss. Data revealed that TNF-α, HSP-70, IL-6, MPO and adhesion molecules when expressed in diabetic rats, collectively induce dramatic changes. Conclusion: these new findings suggested that targeting TNF-α could effectively reduce expressions of MCP-1, HSP-70, troponin-t, 8-OHdG and VCAM- 1, along with prominent reduction in MPO and IL-6 levels.
    07/2013; 13(3). DOI:10.2174/18715303113139990039
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