Preparing the spinal cord - priming or preconditioning? : A systematic review of experimental studies

Objectives. Paraplegia is devastating complication associated with thoracic and thoracoabdominal aortic aneurysm repair. Vast evidence has been gathered on pre-, peri- and postoperative protective adjuncts aiming to minimize spinal cord ischemia. This review focuses on the pretreatment phase of open surgical or endovascular aortic procedures and gathers the experimental data on the interventional preconditioning and priming methods that increase the spinal cord ischemic tolerance. Design. By the start of March 2021, a systematic review was performed in PubMed, Scopus and Web of Science core collection to identify the articles that reported (i) either an ischemic preconditioning, remote ischemic preconditioning or priming method prior to (ii) experimental spinal cord ischemia performed in endovascular or open surgical fashion mimicking either thoracic, abdominal or thoracoabdominal aortic aneurysm procedures. (iii) The outcomes were reported via neurological, motor-evoked potential, somatosensory-evoked potential, histopathological, immunohistochemical, physiological analysis, or in different combinations of these measurements. Results. The search yielded 7802 articles, and 57 articles were included in the systematic review. The articles were assessed by the evaluated species, the utilized pretreatment, the measured protective effects, and the suggested underlying mechanisms. Conclusions. The reviewed articles showed several possible mechanisms in ischemic and remote ischemic preconditioning for prevention of spinal cord ischemia. The main suggested method for priming was arteriogenetic stimulus. Future studies should confirm these hints of arteriogenetic stimulus with more precise quantification of the protective recruitment process.Peer reviewe

Pharmacological Preconditioning with Diazoxide in the Experimental Hypothermic Circulatory Arrest Model

Background: Hypothermic circulatory arrest includes a remarkable risk for neurological injury. Diazoxide, a mitochondrial adenosine triphosphate-dependent potassium ion (K+ATP) channel opener, is known to have cardioprotective effects. We assessed its efficacy in preventing ischemic injury in a clinically relevant animal model. Methods: Eighteen piglets were randomized into a diazoxide group (n = 9) and a control group (n = 9). Animals underwent 60 minutes of hypothermic circulatory arrest at 18 degrees C. Diazoxide (5 mg/kg + 10 mL NaOH + 40 mL NaCl) was infused during the cooling phase. Metabolic and hemodynamic data were collected throughout the experiment. After 24-hour follow-up, whole brain, heart, and kidney biopsy specimens were collected for analysis. Results: Cerebellar Cytochrome-C and caspase-3 activation was higher in the control group (P = .02 and P = .016, respectively). Antioxidant activity tended to be higher in the diazoxide group (P = .099). Throughout the experiment, the oxygen consumption ratio was higher in the control animals (P-g = .04), as were the lactate levels (P-g = .02). Cardiac function tended to be better in diazoxide-treated animals. Conclusion: Diazoxide might confer neuroprotective effect as implied by the immunohistochemical analysis of the brain. Additionally, the circulatory effects of diazoxide were beneficial, supporting its neuroprotective effect.Peer reviewe

Exploring effects of remote ischemic preconditioning in a pig model of hypothermic circulatory arrest

Objectives. During aortic and cardiac surgery, risks for mortality and morbidity are inevitable. Surgical setups involving deep hypothermic circulatory arrest (DHCA) are effective to achieve organ protection against ischemic injury. The aim of this study was to identify humoural factors mediating additive protective effects of remote ischemic preconditioning (RIPC) in a porcine model of DHCA. Design. Twenty-two pigs were randomized into the RIPC group (n=11) and the control group (n=11). The RIPC group underwent four 5-minute hind limb ischemia-reperfusion cycles prior to cardiopulmonary bypass and DHCA. All animals underwent identical surgical procedures including 60min DHCA at 18 degrees C. Blood samples were collected from vena cava and sagittal sinus at several time points. After the 8-hour follow-up period, the brain, heart, and kidney tissue samples were collected for tissue analyses. Results. Serum levels of brain damage marker S100B recovered faster in the RIPC group, after 4hours of the arrest, (pPeer reviewe

Diazoxide Attenuates Ischemic Myocardial Injury in a Porcine Model

Background: We hypothesized that diazoxide, a mitochondrial ATP-sensitive potassium channel opener, has cardioprotective effects during acute myocardial ischemia. Diazoxide is suggested to act through protein kinase Ce (PKC epsilon) activation. Methods: Twelve piglets were randomly assigned to receive intravenous infusion of diazoxide (3.5 mg/kg) with solvent or only solvent (6 animals per group) before cardiac ischemia. Myocardial ischemia was induced by occluding the left circumflex artery (LCX) for 40 minutes. The reperfusion and follow-up period lasted for three hours. Throughout the experiment hemodynamic measurements and blood samples were collected, and after the follow-up period the hearts were harvested for transmission electron microscopy (TEM) as well as histopathological and immunohistochemical analyses. Results: TEM showed less ischemic damage on a cellular level in the diazoxide group (P = .004) than in the control group. Creatinine kinase MB levels (Pt*g = .030) were lower, and oxygen consumption (Pt*g = .037) and delivery (Pg = .038) were higher in the diazoxide group compared to the controls. Conclusion: Diazoxide preserves myocardial cellular structure and cellular function, and thus it may have benefits in treating ischemic myocardial injury.Peer reviewe

Ultrasound-guided closure of the femoral artery during venoarterial decannulation using a large-bore closure device

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Exploring Spinal Cord Protection by Remote Ischemic Preconditioning : An Experimental Study

Background. Paraplegia is one of the most severe complications occurring after the repair of thoracic and thoracoabdominal aortic aneurysms. Remote ischemic preconditioning (RIPC) has been shown to mitigate neurologic damage, and this study assessed its efficacy in preventing spinal cord ischemia. Methods. The study randomized 16 female pigs into an RIPC group (n = 8) and a control group (n = 8). The RIPC group underwent four cycles of 5-minute ischemia-reperfusion episodes by intermittent occlusion of the left iliac artery. All animals underwent systematic closure of the left subclavian artery and segmental arteries of the descending thoracic aorta to the level of diaphragm. Motor-evoked potential monitoring was performed in both hind limbs. Continuous electrocardiogram and hemodynamics were monitored, and pulmonary artery blood samples were collected. A neurologic assessment was performed 6 hours after the procedure. The thoracic and lumbar portions of the spinal cord were collected for histologic and immunohistochemical analysis. Results. The bilateralmotor-evoked potential amplitude responses were higher in the RIPC group (p <0.05) than in the control group; the difference was detected already before spinal cord ischemia. Paraplegia occurred in 1 control animal. Immunohistochemical total scores of antioxidant response regulator nuclear factor erythroid 2-related factor 2 were better in the RIPC group (11.0; range, 8.5 to 14.0) than in the control group (5.2; range, 1.0 to 9.0; p = 0.023). Conclusions. RIPC induces electrophysiologic changes in the central nervous system that may confer spinal cord protection extending the resistance to ischemia. The significantly higher nuclear factor erythroid 2-related factor 2 scores suggest better neuronal cell protection against oxidative stress in the RIPC group. (C) 2017 by The Society of Thoracic SurgeonsPeer reviewe