Effect Of Preconditioning Research Articles

Exosomes containing miR-451a is involved in the protective effect of cerebral ischemic preconditioning against cerebral ischemia and reperfusion injury.

AimTo study the role of exosomes in the protective effect of cerebral ischemic preconditioning (cerebral‐IPC) against cerebral I/R injury.MethodMouse models of cerebral‐IPC and MCAO/R were established as described previously, and their behavioral, pathological, and proteomic changes were analyzed. Neuro‐2a subjected to OGD/R were treated with exosomes isolated from the plasma of sham‐operated and cerebral‐IPC mice. The differentially expressed miRNAs between exosomes derived from sham‐operated (S‐exosomes) and preconditioned (IPC‐exosomes) mice were identified through miRNA array, and their targets were identified through database search. The control and OGD/R cells were treated with the IPC‐exosomes, miRNA mimic or target protein inhibitor, and their viability, oxidative, stress and apoptosis rates were measured. The activated pathways were identified by analyzing the levels of relevant proteins.ResultsCerebral‐IPC mitigated the cerebral injury following ischemia and reperfusion, and increased the number of plasma exosomes. IPC‐exosomes increased the survival of Neuro‐2a cells after OGD/R. The miR‐451a targeting Rac1 was upregulated in the IPC‐exosomes relative to S‐exosomes. The miR‐451a mimic and the Rac1 inhibitor NSC23766 reversed OGD/R‐mediated activation of Rac1 and its downstream pathways.ConclusionCerebral‐IPC ameliorated cerebral I/R injury by inducing the release of exosomes containing miR‐451a.

Hypoxia preconditioning improves structure and function of astrocytes mitochondria via PGC-1α/HIF signal

The protective effect of astrocytes on nerves was demonstrated by mitochondrial transfer. The neuroprotective effect of hypoxic pretreatment is widely accepted. The aim of this research is to investigate the role of hypoxic preconditioning on astrocytes mitochondria. Rat neuronal cells and astrocytes were isolated and cultured. A hypoxic preconditioned astrocyte and oxygen glucose deprivation (OGD) neuronal cell co-culture experiment was used to detect the effect of hypoxic preconditioning (HP) on nerve damage. The silencing of proliferatoractivated receptor γ coactivator-1α (PGC-1α) with siRNA was used to explore the role of HP in the repair of nerve damage and biogenesis of mitochondria. HP increased astrocyte viability and promoted neuroprotective factor secretion. The expression levels of antioxidant enzymes, PGC-1α and uncoupling protein2 (UCP2) were up-regulated by HP. In addition, HP improved mitochondrial function and reduced oxidative stress induced by OGD. It was found that HP astrocytes had a greater neuroprotective effect than normal astrocytes cells. Neuronal apoptosis and reactive oxygen species levels were down-regulated by cell co-culture. The PGC-1α siRNA experiment showed that hypoxia treatment promotes mitochondrial biogenesis and plays a neuroprotective role. HP significantly enhanced the efficacy of astrocytes in the treatment of neuronal injury.

Modification of ischemia/reperfusion induced infarct size by ischemic preconditioning in hypertrophied hearts.

This study examined the effects of ischemic preconditioning (IP) on the ischemia/reperfusion (I/R) induced injury in normal and hypertrophied hearts. Cardiac hypertrophy in rabbits was induced by L-thyroxine (0.5 mg/kg/day for 16 days). Hearts with or without IP (3 cycles of 5 min ischemia and 10 min reperfusion) were subjected to I/R (60 min ischemia followed by 60 min reperfusion). IP reduced the I/R-induced infarct size from 68% to 24% and 57% to 33% in the normal and hypertrophied hearts, respectively. Leakage of creatine phosphokinase in the perfusate from the hypertrophied hearts due to I/R was markedly less than that form the normal hearts; IP prevented these changes. Although IP augmented the increase in phosphorylated p38-mitogen-activated protein kinase (p38-MAPK) content due to I/R, this effect was less in the hypertrophied than in the normal heart. These results suggest that reduced cardioprotection by IP of the I/R-induced injury in hypertrophied hearts may be due to reduced activation of p38-MAPK in comparison with normal hearts.

Possible Protective Effect of Remote Ischemic Preconditioning on Acute Kidney Injury Following Elective Percutaneous Coronary Intervention: Secondary Analysis of a Multicenter, Randomized Study.

Remote ischemic preconditioning (RIPC) is a promising strategy for protecting against ischemic reperfusion injury. This study is a secondary analysis of a randomized study that aimed to evaluate the effect of RIPC on the early increase in serum creatinine (SCr) following percutaneous coronary intervention (PCI), which is associ-ated with contrast-induced acute kidney injury. Patients with stable angina undergoing elective PCI were assigned to control, RIPC, and continuous infusion of nicorandil (nicorandil) groups. The endpoint of this study was the incidence of the early increase in SCr, a predictor of contrast-induced acute kidney injury, which was defined as either a > 20% or absolute increase by 0.3 mg/dl of SCr levels after 24 h of PCI. This study included 220 patients for whom a dataset of SCr values was available. The incidence of the early increase in SCr was significantly lower in the RIPC than in the control (1.3% vs 10.8%, p = 0.03) group, but was not significantly different between the nicorandil and control groups. In multivariate analysis, RIPC remained a significant fac-tor associated with a reduction in the incidence of early increase in SCr. RIPC reduces the incidence of early increase in SCr in patients with stable angina following elective PCI.

Nrf2 mediates the neuroprotective effect of isoflurane preconditioning in cortical neuron injury induced by oxygen-glucose deprivation.

To investigate how nuclear factor-E2-related factor 2 (Nrf2) involved in the protective effect of isoflurane (Iso) preconditioning in oxygen glucose deprivation (OGD)-induced cortical neuron injury. Primary mouse cortical neurons were divided into Control, ML385 (an Nrf2 inhibitor), Iso, Iso + ML385, OGD, ML385 + OGD, Iso + OGD, and Iso + ML385 + OGD groups. Lactate dehydrogenase activity (LDH) release and oxidative stress indexes were quantified. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to detect cell viability, Annexin V-FITC/propidium iodide (PI) staining to measure cell apoptosis, dichloro-dihydro-fluorescein diacetate (DCFH-DA) method to test reactive oxygen species (ROS), and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) and Western blotting to evaluate genes and protein expression. Iso preconditioning reduced LDH release and inhibited cell cytotoxicity in OGD-induced cortical neurons, which was abolished by ML385. Iso preconditioning increased the Nrf2 nuclear translocation in cortical neurons. Meanwhile, Iso decreased the OGD-induced apoptosis with the down-regulations of Bax and Caspase-3 and the up-regulation of Bcl-2, which was reversed by ML385. OGD enhanced the level of ROS and malondialdehyde (MDA) in cortical neurons, but reduced the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), which were aggravated in ML385 + OGD group and mitigated in Iso + OGD group. No observable difference was found between OGD group and Iso + ML385 + OGD group regarding apoptosis-related proteins and oxidative stress-related indexes. Iso preconditioning up-regulated Nrf2 level to play its protective role in OGD-induced mouse cortical neuron injury.

Effects of remote ischemic preconditioning on liver injury following hepatectomy: a systematic review and meta-analysis of randomized control trials.

The protective effect of remote ischemic preconditioning (RIPC) against liver ischemia-reperfusion injury caused by hepatectomy remains controversial. We conducted this meta-analysis to evaluate the effectiveness and safety of RIPC strategies. PubMed, SinoMed, Embase, Cochrane Library, Medline, and Web of Science databases were searched for randomized controlled trials (RCT) that assessed the effectiveness and safety of RIPC strategies. The primary outcomes were operation time, index of liver function on postoperative day (POD) 1, postoperative complications, and postoperative hospital stay. The pooled odds ratios and weighted mean differences at 95% confidence interval (95% CI) were estimated using a fixed-effects or random-effects model. A total of 459 patients were included in seven RCTs. The alanine aminotransferase (ALT) and alanine aminotransferase (AST) values on POD1 were significantly different between the RIPC group and the N-RIPC group (P = 0.009 and P = 0.02, respectively). However, the heterogeneity was significant (I2 = 84% and I2 = 86%), and the results of a sensitivity analysis were unstable. There was no significant difference in the total bilirubin levels (P = 0.25) between the two groups on POD1. Subgroup analysis revealed no significant difference in the AST and ALT levels on POD1 between the RIIPC group and the N-RIPC group, regardless of whether the vascular control technique was used (all P > 0.05). Based on current evidence, RIPC does not alleviate liver injury caused by IRI after hepatectomy.

Heat precondition is a potential strategy to combat hepatic injury triggered by severe heat stress

AimEnvironmental heat stress alters physiological and biochemical functions which leads to multiorgan dysfunction including severe hepatic injury in animals. We hypothesize that heat preconditioning can be potential intervention in combating heat illnesses. Main methodsSprague Dawley rats were exposed to moderate heat stress, severe heat stress and heat preconditioning in heat simulation chamber. Mean arterial pressure, heart rate, skin and core temperature were monitored in pre and post heat exposed animals. After stress exposure, blood for hemodynamic and liver tissue for liver function tests, oxidative stress, inflammatory variables and structural studies were collected from rats. Hepatic mitochondria were isolated to study the key structural alterations and functional changes by transmission electron microscopy. Key findingsThe effect of heat precondition shows improvement in time to attain the core temperature, weight loss, blood pressure and heart rate in rats. Results exhibited decreased levels of liver function tests, elevated levels of free radicals and inflammatory cytokines in heat exposed liver as compared with heat preconditioned animals. Expression levels of mitochondrial heat shock protein 60, superoxide dismutase 1 and uncoupling protein 1 along with activity of electron transport chain complexes I-V were examined and found to be increased in heat preconditioned as compared to heat stressed animals. Morphological studies of liver parenchyma demonstrated reduction in structural deterioration of hepatic lobules and restoration of mitochondrial structural integrity in heat preconditioned rats. SignificancePresent study suggests that heat preconditioning intervention plays a crucial role in protection against heat induced hepatic injury in animals.

Hyperbaric Oxygen Preconditioning Protects Against Cerebral Ischemia/Reperfusion Injury by Inhibiting Mitochondrial Apoptosis and Energy Metabolism Disturbance.

Hyperbaric oxygen (HBO) therapy is considered a safe and feasible method that to provide neuroprotection against ischemic stroke. However, the therapy mechanisms of HBO have not been fully elucidated. We hypothesized that the mechanism underlying the protective effect of HBO preconditioning (HBO-PC) against cerebral ischemia/reperfusion injury was related to inhibition of mitochondrial apoptosis and energy metabolism disorder. To test this hypothesis, an ischemic stroke model was established by middle cerebral artery occlusion (MCAO) in rats. HBO-PC involved five consecutive days of pretreatment before MCAO. In additional experiments, X chromosome-linked inhibitor of apoptosis protein (XIAP) and second mitochondria-derived activator of caspases (SMAC) shRNA and NC plasmids were intraventricularly injected into rat brains after MCAO (2h). After 24h, all rats underwent motor function evaluation, which was assessed by modified Garcia scores. TTC staining for the cerebral infarct and cerebral edema, and TUNEL staining for cell apoptosis, were also analyzed. Reactive oxygen species and antioxidative enzymes in rat brains were detected, as well as mitochondrial complex enzyme activities, ATP levels, and Na+/K+ ATPase activity. Western blot was used to detect apoptotic proteins including Bcl-2, Bax, caspase-3, caspase-9, cyc-c, XIAP, and SMAC. HBO-PC remarkably reduced the infarct volume and improved neurological deficits. Furthermore, HBO-PC alleviated oxidative stress and regulated the expression of apoptosis-related proteins. Moreover, HBO-PC inhibited the decrease in ATP levels, mitochondrial complex enzyme activities, and Na+/K+ ATPase activity to maintain stable energy metabolism. XIAP knockdown weakened the protective effect of HBO, whereas SMAC knockdown strengthened its protective effect. The effects of HBO-PC can be attributed to inhibition of ischemia/hypoxia-induced mitochondrial apoptosis and energy metabolism disturbance. The action of HBO-PC is related to the XIAP and SMAC signaling pathways.

Effect of storage and preconditioning of healing rat Achilles tendon on structural and mechanical properties

Tendon tissue storage and preconditioning are often used in biomechanical experiments and whether this generates alterations in tissue properties is essential to know. The effect of storage and preconditioning on dense connective tissues, like tendons, is fairly understood. However, healing tendons are unlike and contain a loose connective tissue. Therefore, we investigated if storage of healing tendons in the fridge or freezer changed the mechanical properties compared to fresh tendons, using a pull-to-failure or a creep test. Tissue morphology and cell viability were also evaluated. Additionally, two preconditioning levels were tested. Rats underwent Achilles tendon transection and were euthanized 12 days postoperatively. Statistical analyzes were done with one-way ANOVA or Student’s t-test. Tissue force and stress were unaltered by storage and preconditioning compared to fresh samples, while high preconditioning increased the stiffness and modulus (p ≤ 0.007). Furthermore, both storage conditions did not modify the viscoelastic properties of the healing tendon, but altered transverse area, gap length, and water content. Cell viability was reduced after freezing. In conclusion, preconditioning on healing tissues can introduce mechanical data bias when having extensive tissue strength diversity. Storage can be used before biomechanical testing if structural properties are measured on the day of testing.

Determination of Long-Term Creep Properties for 316H Steel Using Short-Term Tests on Pre-strained Material

Determination of long-term creep rupture properties for 316H steel is both costly and time-consuming and given the level of scatter in the data would need substantial number of tests to be performed. The primary objective of this study is to estimate the long-term creep properties of cross-weld (XW) and as-received (AR) 316H stainless steel by performing accelerated tests on pre-compressed (PC) material. In this work, uniaxial creep rupture tests have been performed on XW specimens and the results have been used to establish a correlation with accelerated test results on the PC material. Moreover, tensile tests have been performed on XW specimens at room temperature and 550 °C to examine the pre-conditioning effects on the mechanical response of the material. Similar power-law creep properties have been found for the creep strain rate and rupture time behaviour of the XW and PC specimens. It also has been found that the creep ductility data points obtained from XW and PC specimens fall upon the estimated trend for the AR material at 550 °C when the data are correlated with the applied stress normalised by 0.2% proof stress. The results show that the long-term creep properties of the XW and AR material can be estimated in much shorter time scales simply by performing tests on the PC material state.

Mechanical Behaviour of Rubber Material with Consideration to Mullins Effect

A stress softening known as the Mullins effect is observed usually in rubberlike material after the first load. This paper describes an experimental test method for defining the nonlinear properties of rubber materials used for finite element analysis. Experimental observations have shown that the Mullins effect induces a permanent set and some anisotropy. To test the Mullins effect the mechanical preconditioning is suggested to stabilize the properties of rubber material. A stress-strain curve will change significantly when the rubber material is strained greater than the previous stabilized level. Therefore, material properties at maximum strain level are obtained to predict behavior of rubber products. To obtain the rubber material constants used for finite element analysis to understand the characteristics of automotive rubber parts, mechanical properties tests such as uniaxial tension, equ-biaxial tension and pure shear tests are required. When the load was repeatedly applied to the rubber specimen, the stress-strain relationship was greatest in the first and second cycles, and the larger the strain range, the more the stress was reduced. The material constants were obtained using the stress-strain data after the rubber specimen was stabilized. The value of stiffness decreased as the maximum strain range increased. The static stiffness of an automotive engine mount is calculated by nonlinear finite element analysis using the experimentally determined material constants and compared with the experimental results considering the mechanical preconditioning effect resulting in a good correlation.

Liraglutide restores late cardioprotective effects of remote preconditioning in diabetic rats via activation of hydrogen sulfide and nuclear factor erythroid 2-related factor 2 signaling pathway.

ABSTRACTPurposeThe present study explored the influence of liraglutide on remote preconditioning-mediated cardioprotection in diabetes mellitus along with the role of nuclear factor erythroid 2-related factor 2 (Nrf2), hypoxia inducible factor (HIF-1α) and hydrogen sulfide (H2S).MethodsStreptozotocin was given to rats to induce diabetes mellitus and rats were kept for eight weeks. Four cycles of ischemia and reperfusion were given to hind limb to induce remote preconditioning. After 24 h, hearts were isolated and subjected to 30 min of ischemia and 120 min of reperfusion on Langendorff system. Liraglutide was administered along with remote preconditioning. Cardiac injury was assessed by measuring the release of creatine kinase (CK-MB), cardiac troponin (cTnT) and development of left ventricular developed pressure. After ischemia-reperfusion, hearts were homogenized to measure the nuclear cytoplasmic ratio of Nrf2, H2S and HIF-1α levels.ResultsIn diabetic rats, there was more pronounced injury and the cardioprotective effects of remote preconditioning were not observed. Administration of liraglutide restored the cardioprotective effects of remote preconditioning in a dose-dependent manner. Moreover, liraglutide increased the Nrf2, H2S and HIF-1α levels in remote preconditioning-subjected diabetic rats.ConclusionsLiraglutide restores the lost cardioprotective effects of remote preconditioning in diabetes by increasing the expression of Nrf2, H2S and HIF-1α.

The Effects of Ozone Oxidative Preconditioning on Subarachnoid Hemorrhage via Rat Cerebral Vasospasm Model

Objective: Cerebral vasospasm after subarachnoid hemorrhage (SAH) is a major cause of morbidity and mortality. Inflammation is the major molecular mechanism observed in vasospastic SAH. Ozone (O3) has been used as a therapeutic agent in the treatment of various conditions and diseases for years. The aim of this study was to evaluate the anti-inflammatory effect of ozone oxidative preconditioning (OOP) in a rat model of SAH in order to assess the therapeutic potential of O3 in SAH therapy. Materials and Methods: In the presented study, an experimental in vivo SAH rat model that provided constriction of large cerebral arteries was used. The inflammatory response of cerebral vasospasm after SAH and the effects of OOP were evaluated by comparing the mRNA levels of inflammatory molecules (tumor necrosis factor-α, interleukin-1β, and intercellular adhesion molecule-1) in the serum samples of rats. Results: The level of inflammatory molecules increased in vasospasm at 12 h, 24 h, and 48 h in the posttreatment groups. However, intraperitoneal OOP decreased the level of inflammatory molecules dramatically. Conclusions: Our study indicated that O3 treatment has potential in the management of inflammation created in a rat SAH model. These findings may inform further studies investigating possible uses of O3 in the treatment of vasospasm.

Total Intravenous Anesthesia for Myocardial Protection and Preconditioning

AbstractPerioperative myocardial injury is common after any major surgical procedure even with best possible anesthesia and surgical management. Organ preservation during surgical procedure prevents morbidity and mortality. The effect of ischemic preconditioning on myocardial as well as other organ protection is well known. A variety of other agents also shown to have preconditioning thus protective effect on myocardium during anesthesia and surgery. The beneficial effect of volatile anesthetic preconditioning is well studied. However, the effect of intravenous anesthetic agents on this context is still way to go. This review is an attempt to look into the latest available research regarding the preconditioning and myocardial protective effect of intravenous anesthetic agents.

Study on the time-effectiveness of exercise preconditioning on heart protection in exhausted rats.

To investigate the persistence time and the effectiveness of exercise preconditioning (EP) on myocardial protection in exhausted rats from myocardial enzymes, electrocardiogram (ECG), cardiac function, and mitochondrial respiratory function after cessation of exercise training. One hundred and twelve healthy male Sprague-Dawley rats were randomly divided into seven groups (n = 16): control group (CON), exhaustive exercise (EE) group, EP group, and EE after EP (EP + EE); furthermore, EP + EE group was randomly divided into 1D, 3D, 9D, and 18D groups (1D, 3D, 9D, and 18D) and performed exhaustive treadmill exercise at a speed of 30 m/min on the 1st, 3rd, 9th, and 18th days separately after EP exercise stopped. We detected the serum contents of N-terminal pro B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) by the enzyme-linked immunosorbent assays method, recorded ECG, detected heart function by pressure volume catheter, measured the respiratory rates of rat myocardial mitochondria state 3 and 4 of complex I, complex II, and IV by high-resolution breathing apparatus. EP could decrease the serum content of NT-proBNP and cTnI, improved the electrical derangement and the left ventricular function in exhausted rats. Moreover, the protective effect was more obvious in the 9th day after EP stopped, whereas it would disappear when EP stopped for more than 18 days. Compared with EE group, the respiratory rate value of myocardial mitochondrial complex increased in 1D, 3D, and 9D groups. Therefore, the protective effect of EP on the heart of exhausted rats decreased with the prolongation of stopping training time, and the effect was significant within 3 days of discontinuing training, then decreased gradually, and completely disappeared in the 18th day. EP enhanced the cardiac function in exhausted rats through raising the nicotinamide adenine diphosphate hydride (NADH) electron transport chain and increased the respiration rates of mitochondrial respiratory complex I and IV state 3, thereby improved myocardial mitochondrial respiratory function and energy metabolism.

Effects of intense remote ischemic preconditioning in patients undergoing elective off-pump coronary artery bypass graft surgery: a pilot study

Effects of intense remote ischemic preconditioning in patients undergoing elective off-pump coronary artery bypass graft surgery: a pilot study

Organoprotective Effect of Remote Ischemic Preconditioning during Living Donor Liver Transplantation, A Prospective Randomized Double-Blinded Study

Background: Ischemia reperfusion injury (IRI) during liver transplantation carries a substantial risk for graft damage, and other major organ injury. Strategies to minimize IRI in the grafted liver are of paramount importance. Remote ischemic preconditioning (RIP) is a recently described technique that can offer a liver protective effect against IRI. Patients and Methods: In this prospective randomized study, consent was obtained from 80 couples (donor– recipient) prepared for liver transplantation (LT). Patients were divided randomly (using closed envelope technique) into two groups: RIP group (n=35) as RIP procedure was run in the donor non-dominant hand just at the start of parenchymal transection and control group (n= 35). In all the study cases, the pressure cuff was wrapped around the recipient arm. In RIP group, four sets of 5 minutes manual pressure cuff elevation to 200 mmHg, separated by 5 minutes of release (Using the non-dominant hand). Results: No statistically significant difference was found between the biochemical profile (SGPT, CRP, and bilirubin) of the recipients in both of the study groups. Similarly, post-operative kidney function (Serum creatinine) was comparable findings in the two studied groups. Conclusion: RIP in living donor liver transplantation failed to show a protective effect neither on the graft response to reperfusion injury, nor the on the postoperative kidney functions. Future studies are recommended taking into consideration histopathological, tissue damage scores.

Effect of 3-Day and 21-Day Hypoxic Preconditioning on Recovery Following Cerebral Ischemia in Rats.

We have previously reported that in a rat model of chronic hypoxia, HIF-1α and its target genes have significantly accumulated by 3days of exposure, whereas no significant increase in capillary density has occurred; there is a significant increase in capillary density at 21days of chronic hypoxic exposure. In this study we hypothesize that by utilizing 3days and 21days of hypoxic preconditioning, we would distinguish between the relative neuroprotective contributions of the accumulation of HIF-1α and its target genes and angiogenic adaptation in a rat middle cerebral artery occlusion (MCAO) model. Rats were randomly assigned to either hypoxic precondition groups (3-day and 21-day hypoxia) or normoxic control group. Hypoxic animals were kept in a hypobaric chamber at a constant pressure of 0.5 atmosphere (380mmHg, equivalent to 10% normobaric oxygen at sea level) for either 3 or 21days. Normoxic controls were housed in the same room next to the hypobaric chamber. Erythropoietin (EPO) was measured at 3 and 21days of hypoxia using Western blotting analysis. Infarct volumes were measured following 24hours of permanent MCAO. We found that EPO is upregulated at 3days of hypoxia and returns to baseline by 21days of hypoxia. The infarct volumes following 24-hour MCAO were significantly reduced with 3-day hypoxic preconditioning when compared to normoxic controls (%, 31.8±5, n=9 vs. 50.1±10.9, n=7). No significant differences in infarct volume were seen between the normoxic controls and 21-day hypoxic preconditioned rats. We have shown that a 3-day hypoxic preconditioning, but not 21-day hypoxic preconditioning, provides significant neuroprotection against focal ischemia in rats, supporting a larger role for the accumulations of HIF-1α and upregulation of its target genes in the neuroprotection against focal ischemia.

Renal protective effect of remote ischemic preconditioning: a meta-analysis of randomized controlled trials

Background The incidence of acute kidney injury (AKI) is ∼21.6% in hospitalized patients with an increased incidence of mortality. Although many trials have been done to prevent or treat AKI, most of these efforts have yielded limited success.Objectives This study aimed to detect the effects of remote ischemic preconditioning (RIPC) on the incidence and outcomes of AKI.Study design A meta-analysis was used to address this concern.Settings A meta-analysis-based study following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines was conducted.Methods The databases such as MEDLINE, EMBASE, PubMed, and Cochrane were systemically searched to identify all published prospective, randomized, and controlled clinical trials in the last 5 years comparing RIPC with control in different procedures.Results A total of 26 studies were identified for inclusion in this study, involving 3978 patients. The risk of bias was low. Meta-analysis showed that the rate of AKI was significantly lower in the RIPC group, there was no statistically significant difference in the overall mortality, and there was no significant change in serum creatinine value. Regarding serum neutrophil gelatinase-associated lipocalin and estimated glomerular filtration rate, the study favors the RIPC group than the control group. There was no significant difference in the period of hospital stays, whereas the length of ICU stay was remarkably reduced in the RIPC group.Limitations The definitions of AKI adopted in respective trials were different. Comorbidities among the studies that may raise protective threshold were different. In our analysis, preoperative kidney function of the studies was different, and the use of different anesthetic protocols might confound the effect of RIPC.Conclusion RIPC offers a novel, noninvasive, and inexpensive treatment strategy for decreasing AKI incidence and improving the outcome in high-risk patients.

Effect of preshipment preconditioning and injectable antioxidant trace elements (Cu, Mn, Se, Zn) and vitamins (A, E) on plasma metabolite and hormone concentrations and growth in weaned beef cattle.

Weaning and transport represent a high stress time for calves. Preconditioning (PC) by weaning before the transport separate these stressors. The stressors generate oxidative stress, which can be reduced by mineral and vitamin supplementation (MVS) with an antioxidant capacity. Our objective was to evaluate the effect of PC and MVS on performance of steers. The experiment used a 2 × 2 factorial arrangement design, considering a 26-d PC treatment from weaning to transport to the feedlot (day 0), and injectable MVS on days −45, −26, and 0. The MVS consisted of Cu, Zn, Mn, Se, vitamin E (0.2, 0.8, 0.2, 0.1, and 1 mg/kg body weight [BW], respectively), and vitamin A (1,190 IU/kg). Sixty Angus-crossbred steers (186.4 ± 27.6 kg) were randomly assigned to the four treatments (MVS+PC; N+PC; MVS+N; N+N; n = 15 per treatment). BW was recorded on days −45, −26, 0, 8, 15, and 29. On day 0, an additional BW was taken 30 min after the 5-h transportation (day 0.5). Between days 0 and 29, dry matter intake (DMI) and average daily gain (ADG) to DMI ratio (G:F) were measured. Between days −26 and 29 plasma concentrations of glucose, nonesterified fatty acids (NEFA), cortisol, insulin, total antioxidant status (TAS), and thiobarbituric acid-reactive substances were evaluated. Data were analyzed using the MIXED procedure of SAS with repeated measures, using treatment, time, and treatment × time as fixed effects and steer as a random effect. Between days −26 and 0, there was an interaction of MVS × PC (P ˂ 0.01) for ADG. From days −26 to 0, N+N and N+PC had the greatest and lesser ADG, respectively. On day 0.5, no-PC steers tended to lose BW, whereas the PC steers tended to gain BW (P = 0.09). In the period days 0 to 8, there were no differences (P ≥ 0.27) in DMI, but the PC steers had greater G:F and ADG (P < 0.01) compared with no-PC steers. Plasma NEFA concentration on day 0 was affected by MVS × PC (P < 0.01) because MVS decreased plasma NEFA concentration in no-PC steers, but it increased in the PC steers. Plasma concentrations of glucose, insulin, and cortisol did not differ among treatments (P ≥ 0.23). There was an MVS × PC interaction (P = 0.09) for TAS on day 0; N+N had the greatest TAS concentrations and MVS+N had the lowest TAS concentrations. In conclusion, a 26-d PC decreased steers BW compared with no-PC steers. The BW loss during PC was not recovered 29 d after feedlot entry. Despite this BW loss, MVS treatment decreased BW loss in the steers allocated to PC treatment on the day of transport.