Oxidative Stress and Nerve Function After Cardiopulmonary Bypass in Patients With Diabetes

Matyal, Robina; Sakamuri, Sruthi; Huang, Ting-Yi; Owais, Khurram; Parikh, Samir M.; Khabbaz, Kamal R.; Wang, Angela Yee-Moon; Sellke, Frank W.; Mahmood, Feroze

doi:10.1016/j.athoracsur.2014.06.041

Cited by 18 publications

(12 citation statements)

References 26 publications

(28 reference statements)

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“…Given that no perfect loading control exists in hypoxic condition, equal loading was confirmed using Ponceau staining. Such normalization was previously realized for AdipoR detection (Mullen et al, 2009; Matyal et al, 2014).…”

Section: Methodsmentioning

confidence: 99%

Sustained Intermittent Hypoxemia Induces Adiponectin Oligomers Redistribution and a Tissue-Specific Modulation of Adiponectin Receptor in Mice

et al. 2019

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Introduction: Hypoxemia is a critical component of several respiratory diseases and is known to be involved in the processes underlying co-morbidities associated to such disorders, notably at the cardiovascular level. Circulating level of Adiponectin (Ad), known as a metabolic regulator and cardio-protective hormone was previously suggested to be reduced by hypoxia but consequences of such variation are unclear. The evaluation of the specific effect of hypoxemia on Ad forms and receptors could improve the understanding of the involvement of Ad axis in hypoxemia-related diseases.Methods: Ad-pathway components were investigated in a murine model of sustained intermittent hypoxemia (FiO2 10%, 8 h/day, 35 days).Results: Sustained intermittent hypoxemia (SIH) induced a redistribution of Ad multimers in favor of HMW forms, without change in total plasmatic level. Mice submitted to hypoxia also exhibited tissue-specific modification of adiporeceptor (AdipoR) protein level without mRNA expression change. A decreased AdipoR2 abundance was observed in skeletal muscle and heart whereas AdipoR1 level was only reduced in muscle. No change was observed in liver regarding AdipoR. Lipid profile was unchanged but glucose tolerance increased in hypoxemic mice.Conclusion: Sustained intermittent hypoxemia, per se, modify Ad oligomerization state as well as AdipoR protein abundance in a tissue-specific way. That suggests alteration in Ad-dependant pathways in pathological conditions associated to SIH. Investigation of Ad-pathway components could therefore constitute useful complementary criteria for the clustering of patients with hypoxemia-related diseases and management of co-morbidities, as well as to develop new therapeutic strategies.

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Section: Methodsmentioning

confidence: 99%

Sustained Intermittent Hypoxemia Induces Adiponectin Oligomers Redistribution and a Tissue-Specific Modulation of Adiponectin Receptor in Mice

et al. 2019

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“…Other evidence strongly supports exaggerated myocardial damage and cell death in DM patients: DM markedly increases morbidity and mortality (up to 90%) following cardioplegic arrest [ 40 – 42 ]; DM promotes pro-apoptotic signaling, apoptosis and contractile dysfunction in reperfused human myocardium [ 43 – 45 ]; and DM exaggerates oxidative damage and anti-oxidant depletion [ 45 , 46 ], transcriptional changes and pro-inflammatory signaling [ 45 , 47 ]. Analysis of I–R injury in ex vivo tissue reveals significantly impaired resistance of myocardium from T1 and T2DM patients, including increased apoptosis (partially caspase- and PARP-dependent) and oncosis [ 48 ].…”

Section: Diabetes Impacts Myocardial Ischemic Tolerance and Cardiopromentioning

confidence: 99%

Myocyte membrane and microdomain modifications in diabetes: determinants of ischemic tolerance and cardioprotection

Russell

Toit

Peart

et al. 2017

Cardiovasc Diabetol

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Cardiovascular disease, predominantly ischemic heart disease (IHD), is the leading cause of death in diabetes mellitus (DM). In addition to eliciting cardiomyopathy, DM induces a ‘wicked triumvirate’: (i) increasing the risk and incidence of IHD and myocardial ischemia; (ii) decreasing myocardial tolerance to ischemia–reperfusion (I–R) injury; and (iii) inhibiting or eliminating responses to cardioprotective stimuli. Changes in ischemic tolerance and cardioprotective signaling may contribute to substantially higher mortality and morbidity following ischemic insult in DM patients. Among the diverse mechanisms implicated in diabetic impairment of ischemic tolerance and cardioprotection, changes in sarcolemmal makeup may play an overarching role and are considered in detail in the current review. Observations predominantly in animal models reveal DM-dependent changes in membrane lipid composition (cholesterol and triglyceride accumulation, fatty acid saturation vs. reduced desaturation, phospholipid remodeling) that contribute to modulation of caveolar domains, gap junctions and T-tubules. These modifications influence sarcolemmal biophysical properties, receptor and phospholipid signaling, ion channel and transporter functions, contributing to contractile and electrophysiological dysfunction, cardiomyopathy, ischemic intolerance and suppression of protective signaling. A better understanding of these sarcolemmal abnormalities in types I and II DM (T1DM, T2DM) can inform approaches to limiting cardiomyopathy, associated IHD and their consequences. Key knowledge gaps include details of sarcolemmal changes in models of T2DM, temporal patterns of lipid, microdomain and T-tubule changes during disease development, and the precise impacts of these diverse sarcolemmal modifications. Importantly, exercise, dietary, pharmacological and gene approaches have potential for improving sarcolemmal makeup, and thus myocyte function and stress-resistance in this ubiquitous metabolic disorder.

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“…In 2014, Brassard et al reported lower cerebral oxygenation in patients with diabetes who received cardiopulmonary bypass support, whereas differences in mean arterial blood pressure were not significant (23). Maytal et al showed higher oxidative stress reflected by increased protein oxidation levels and decreased levels of antioxidative enzymes in patients with uncontrolled diabetes and cardiopulmonary bypass support; however, blood pressure and other parameters of perfusion were not analyzed in their study (24). In our patient cohort, neither increased serum creatinine nor the presence of diabetes corresponded to perfusion differences between cardiopulmonary bypass systems.…”

Section: Discussionmentioning

confidence: 88%

Conventional or minimized cardiopulmonary bypass support during coronary artery bypass grafting? – An analysis by means of perfusion and body mass index

et al. 2018

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The use of minimized cardiopulmonary bypass support to reduce the side effects of extracorporeal circulation is still contradictorily discussed. This study compares perfusion operated by conventional (CCPB) and minimized (MCPB) cardiopulmonary bypass support during coronary artery bypass grafting (CABG). This study includes the data of 5164 patients treated at our department between 2004 and 2014. Tissue perfusion during cardiopulmonary bypass support and cardiac arrest was assessed by means of body mass index, hemodilution, blood pressure with corresponding pump flow and venous oxygen saturation, serum lactate, and serum pH. Hemodilution was more pronounced after CCPB: hemoglobin had dropped to 4.47 ± 0.142 g/dL after CCPB and to 2.77 ± 0.148 g/dL after MCPB (P = 0.0022). Despite the higher pump flow in conventional circuits (4.86–4.95 L/min vs. 4.1–4.18 L/min), mean blood pressure was higher during minimized bypass support (53 ± 10 vs. 56 ± 13 mm Hg [aortic clamping], 57 ± 9 vs. 61 ± 12 mm Hg [34°C], 55 ± 9 vs.59 ± 11 mm Hg [aortic clamp removal], P < 0.0001) at all time points. Venous oxygen saturation remained on comparable levels of >70% during both conventional and minimized cardiopulmonary bypass support. The increase in serum lactate was more pronounced after CCPB (8.98 ± 1.28 vs. 3.66 ± 1.25 mg/dL, P = 0.0079), corresponding to a decrease in serum pH to acidotic levels (7.33 ± 0.06 vs. 7.35 ± 0.06, P < 0.0001). These effects were evident in all BMI ranges. Minimized cardiopulmonary bypass support provides efficient perfusion in all BMI ranges and is thus equivalent to conventional circuits.

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Oxidative Stress and Nerve Function After Cardiopulmonary Bypass in Patients With Diabetes

Cited by 18 publications

References 26 publications

Sustained Intermittent Hypoxemia Induces Adiponectin Oligomers Redistribution and a Tissue-Specific Modulation of Adiponectin Receptor in Mice

Sustained Intermittent Hypoxemia Induces Adiponectin Oligomers Redistribution and a Tissue-Specific Modulation of Adiponectin Receptor in Mice

Myocyte membrane and microdomain modifications in diabetes: determinants of ischemic tolerance and cardioprotection

Conventional or minimized cardiopulmonary bypass support during coronary artery bypass grafting? – An analysis by means of perfusion and body mass index

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