Abstract
BackgroundVascular surgery patients have reduced tissues` blood supply, which may lead to mitochondrial dysfunction and accumulation of acylcarnitines (ACs).It has been suggested that remote ischaemic preconditioning (RIPC) has its organ protective effect via promoting mitochondrial function.The aim of this study was to evaluate the effect of RIPC on the profile of ACs in the vascular surgery patients.MethodsThis is a randomised, sham-controlled, double-blinded, single-centre study. Patients undergoing open surgical repair of abdominal aortic aneurysm, surgical lower limb revascularisation surgery or carotid endarterectomy were recruited non-consecutively. The RIPC protocol consisting of 4 cycles of 5 min of ischaemia, followed by 5 min of reperfusion, was applied. A blood pressure cuff was used for RIPC or a sham procedure. Blood was collected preoperatively and approximately 24 h postoperatively. The profile of ACs was analysed using the AbsoluteIDQp180 kit (Biocrates Life Sciences AG, Innsbruck, Austria).ResultsNinety-eight patients were recruited and randomised into the study groups and 45 patients from the RIPC group and 47 patients from the sham group were included in final analysis. There was a statistically significant difference between the groups regarding the changes in C3-OH (p = 0.023)—there was a decrease (− 0.007 µmol/L, ± 0.020 µmol/L, p = 0.0233) in the RIPC group and increase (0.002 µmol/L, ± 0.015 µmol/L, p = 0.481) in the sham group. Additionally, a decrease from baseline to 24 h after surgery (p < 0.05) was detected both in the sham and the RIPC group in the levels of following ACs: C2, C8, C10, C10:1, C12, C12:1, C14:1, C14:2, C16, C16:1, C18, C18:1, C18:2. In the sham group, there was an increase (p < 0.05) in the levels of C0 (carnitine) and a decrease in the level of C18:1-OH. In the RIPC group, a decrease (p < 0.05) was noted in the levels of C3-OH, C3-DC (C4-OH), C6:1, C9, C10:2.ConclusionsIt can be concluded that RIPC may have an effect on the levels of ACs and might therefore have protective effects on mitochondria in the vascular surgery patients. Further larger studies conducted on homogenous populations are needed to make more definite conclusions about the effect of RIPC on the metabolism of ACs.Trial registrationClinicalTrials.gov database, NCT02689414. Registered 24 February 2016—Retrospectively registered, https://clinicaltrials.gov/ct2/show/NCT02689414.
Highlights
Vascular surgery patients have reduced tissuesblood supply, which may lead to mitochondrial dysfunction and accumulation of acylcarnitines (ACs).It has been suggested that remote ischaemic preconditioning (RIPC) has its organ protective effect via promoting mitochondrial function.The aim of this study was to evaluate the effect of RIPC on the profile of ACs in the vascular surgery patients
Ninety-eight patients were recruited and randomised into the study groups and 45 patients from the RIPC group and 47 patients from the sham group were included in final analysis
Changes in the levels of ACs in the RIPC and in the sham group (Table 2) There was a statistically significant difference between the groups regarding the changes in C3-OH (p = 0.023)— there was a significant decrease (− 0.007 μmol/L, ± 0.020 μmol/L, p = 0.0233) in the RIPC group and insignificant increase (0.002 μmol/L, ± 0.015 μmol/L, p = 0.481) in the sham group
Summary
Vascular surgery patients have reduced tissuesblood supply, which may lead to mitochondrial dysfunction and accumulation of acylcarnitines (ACs).It has been suggested that remote ischaemic preconditioning (RIPC) has its organ protective effect via promoting mitochondrial function.The aim of this study was to evaluate the effect of RIPC on the profile of ACs in the vascular surgery patients. We along other investigators have demonstrated that RIPC has protective effects to heart,kidneys, brain and other organs in the case of ischaemia–reperfusion injury [1,2,3,4,5]. Surgery induces acute stress response, which in turn promotes catabolic pathways including fatty-acid catabolism in beta-oxidation hereby increasing the load on mitochondria even more. In the case of mitochondrial dysfunction, fatty acid β-oxidation is diminished, resulting in accumulation of acylcarnitines (ACs) [8, 9]. As more knowledge has been gained about the role of SCACs and MCACs, it is necessary to simultaneously investigate changes of SCACs, MCACs and LCACs
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