Remote ischemic preconditioning (rIPC), induced by cycles of transient limb ischemia and reperfusion (IR), is cardioprotective. The optimal rIPC-algorithm is not established. We investigated the effect of cycle numbers and ischemia duration within each rIPC-cycle and the influence of effector organ mass on the efficacy of cardioprotection. Furthermore, the duration of the early phase of protection by rIPC was investigated. Using a tourniquet tightened at the inguinal level, we subjected C57Bl/6NTac mice to intermittent hind-limb ischemia and reperfusion. The rIPC-protocols consisted of (I) two, four, six or eight cycles, (II) 2, 5 or 10 min of ischemia in each cycle, (III) single or two hind-limb occlusions and (IV) 0.5, 1.5, 2.0 or 2.5 h intervals from rIPC to index cardiac ischemia. All rIPC algorithms were followed by 5 min of reperfusion. The hearts were subsequently exposed to 25 min of global ischemia and 60 min of reperfusion in an ex vivo Langendorff model. Cardioprotection was evaluated by infarct size and post-ischemic hemodynamic recovery. Four to six rIPC cycles yielded significant cardioprotection with no further protection by eight cycles. Ischemic cycles lasting 2 min offered the same protection as cycles of 5 min ischemia, whereas prolonged cycles lasting 10 min abrogated protection. One and two hind-limb preconditioning were equally protective. In our mouse model, the duration of protection by rIPC was 1.5 h. These findings indicate that the number and duration of cycles rather than the tissue mass exposed to rIPC determines the efficacy of rIPC.
Coronavirus disease 2019 (COVID-19) is one of the respiratory system diseases with unknown etiology and clinical characteristics. Defects in the liver and kidneys appear to be common in Covid-19 patients. Aspartate transaminase (AST) enzyme, Urea, creatinine, and Alanine Aminotransferase (ALT) enzyme levels are frequently exalted at the start or within the infection. This pretext suggests that Covid-19 interferes with the functions of the liver and kidneys. The current study was aimed to estimate the biochemical biomarkers changes that related to liver and kidney functions, such as ALT, AST, urea, and creatinine, in infected patients. 50 patients were diagnosed with infected between May 1 and 1 August 2020, in Dayala Hospital. 100 samples included 50 control and 50 infected were carried out to evalute the level of biochemical biomarkers (the plasma urea, creatinine, ALT and AST).The results showed increased of ALT, AST, BUN and creatinine levels in the infected samples compare with the control samples. The mean serum kidney parameter (Urea, creatinine ) levels were 57.84±10.46, 1.61±0.18respectively, while the mean value of serum liver enzyme (AST, ALT) levels were 41.94±4.59 and 42.54±4.45, respectively, with high significant different (P<0.001) with control healthy group.
Background: Remote Ischemic Preconditioning (rIPC) and the antiarrhythmic peptide analogue, Rotigaptide (ZP123), protects against myocardial ischemia-reperfusion injury through potentially similar mechanisms. We aimed to study whether the cardioprotective effects of Rotigaptide and rIPC interacts. Methods:We used male New Zealand White rabbit hearts mounted in a Langendorff system and exposed to 30 min of global no-flow ischemia and 120 min of reperfusion. A total of 48 rabbits were randomized into 6 groups: control (n=6), Rotigaptide (1 µM) before (n=9) or after (n=9) ischemia, rIPC (n=7), rIPC+Rotigaptide before (n=9) or after (n=8) ischemia. rIPC was induced by four cycles of 5-min ischemia and reperfusion on the left hind limb achieved by intermittent tourniquet occlusion. Primary endpoint was infarct size measured by tetrazolium staining.Results: rIPC reduced infarct size compared to controls. Rotigaptide alone did not affect infarct size irrespective of administration before ischemia or during reperfusion. The combination of rIPC and Rotigaptide before ischemia reduced infarct size, whereas the effect of rIPC was abrogated by Rotigaptide when administered during reperfusion. No significant changes in hemodynamic recovery were observed when compared to control group. Conclusion:In contrast to in vivo rIPC, in vitro Rotigaptide did not yield cardioprotection in our rabbit model, but Rotigaptide attenuated the effect of rIPC. These findings indicate that modification of myocardial gap junction is involved in cardioprotection by rIPC.
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