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Mitochondria, as the key passway of neuronal apoptosis after ischemia, is closely related to cerebral ischemia-reperfusion injury. Remote ischemic post-conditioning can alleviate cerebral ischemia-reperfusion injury, and its mechanism is related to alleviating mitochondrial injury and improving its dysfunction. In this paper, cytochrome C/caspase, mitophagy, mitochondrial ATP-sensitive K+ channel and mitochondrial permeability transitionpore were reviewed.
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Objective To investigate the effectiveness of combination treatment of thrombus aspiration and ischemic post-condition on patients with acute ST elevated myocardial infarction(SETMI) undergoing primary percutaneous coronary intervention. Methods A total of 234 patients were randomly divided into two groups: one group received routine treatment (control group, n=111); while another group received the combination treatment of thrombus aspiration and ischemic post-conditioning (treatment group, n=123). The baseline data, coronary lesion, information of percutaneous coronary intervention, data of reperfusion and in-hospital clinical prognosis of the two groups were evaluated. Results The baseline data of the two groups are comparable except TG level was higher in treatment group. Compared with the control group, the peak value of cardiac enzyme was lower while the rate of immediate ST resolution to baseline was higher with less MACE during hospitalization in the treatment group. Other data were all comparable between the two groups. Conclusions The combination of thrombus aspiration and ischemic post-conditioning during primary PCI in patients with acute myocardial infarction can restore cardiac perfusion and reduce MACE during hospitalization.
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Objective To observe the effect of remote post-ischemic conditioning(RPIOC)on the cerebral blood flow,neural function and prognosis of patients with acute cerebral infarction and the risk factors for short-term prognosis.Methods 133 patients with acute cerebral infarction in the Second Hospital of Beijing from January 2016 to December 2017 were selected,and randomly divided into the RIPOC group(66 cases,with RPIOC)and the control group(67 cases,without RIPOC).In the first day after hospital,patients in the RIPOC group were given RIPOC,which was tightening the left aim with a tonometer bandage for 5 minutes per time and 2 times a day at an interval of 5 minutes.All patients were provided routine treatment.All patients' cerebral blood flow,neural function and survival data were recorded.Recovery was assessed by modified Rankin Scale(mRS)180 d after stroke.Logistic regression was used to evaluate the risk factors for prognosis.Results Of the 133 patients enrolled,there were 67 males.The mean age was (73.1 ± 10.1)year.Basic clinical characteristics,neural function and cerebral blood flow were similar between groups(P＞0.05).After 10 d treatment,cerebral blood flow and neural function was significantly increased (P＜0.05)in the RIPOC group.After 180 d follow up,the RIPOC group had significantly higher rate of adverse cerebrovascular events(P＜0.05).Logistic regression analyses demonstrated that advanced age(P =0.003),hypertension(P =0.03)and high NIHSS score(P =0.005)were all risk factors for prognosis.Conclusions RIPOC can enhance the cerebral blood flow,activities of daily living,limb function and prognosis.However,it does not reduce the risk of mortality.Advanced age,hypertension and high NIHSS score are risk factors for short-term prognosis.
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Objective:To explore the effect of remote ischemic post-conditioning (RIPoC) on oxidation/reduction response, energy metabolism and inlfammatory reaction of ischemic myocardial tissue in rats with ischemic reperfusion (IR) injury. Methods:IR model was established by 30 min left anterior descending (LAD) artery occlusion followed by 120 min reperfusion, conditioning was defined as 3 cycles of 30 seconds ischemia followed by 30 seconds reperfusion in adult rats. The rats were divided into 5 groups:①ischemic pre-conditioning (IPC) group, the rats received the conditioning prior to IR treatment,②ischemic post-conditioning (IPoC) group, the rats received 30 min LAD occlusion followed by conditioning at the beginning of 120 min reperfusion, ③ remote ischemic post-conditioning(RIPoC) group, the rats received 30 min LAD occlusion, followed by femoral artery conditioning at the beginning of 120 min reperfusion, ④ IR group, ⑤ Sham group. n=8 in each group.Ischemic myocardial tissue was collected at the end of experiment, superoxide dismutase (SOD) activity was assayed by xanthine oxidase method,malondialdehyde (MDA) content was examined by thiobarbituric acid method, myeloperoxidase (MPO) activity was determined by chemistry colorimetric method, adenosine triphosphate(ATP)amount was measured by bioluminescence method;expressions of myocardial stromal cell derived factor-1 (SDF-1) and vascular endothelial growth factor (VEGF), mitochondrial function related genes Ndufa2, Ndufa4, Cox4il and Cox7a2 were evaluated by real time quantitative PCR. Results:In IPC, IPoC and RIPoC groups, the ischemic myocardial tissue had increased SOD activity and ATP amount, decreased MDA content and MPO activity; induced expressions of SDF-1, VEGF, mitochondrial function related genes Ndufa2, Ndufa4, Cox4il and Cox7a2. Conclusion:RIPoC may increase anti-oxidation/reduction response, protect energy metabolism and reduce inlfammatory reaction in ischemic myocardial tissue, the effect was similar to pre-conditioning and post-conditioningin rats with IR injury.
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Objective To investigate the effects of limb ischemic post-conditioning (LIpostC) alone or its combination with therapeutic hypothermia (TH) on systemic inflammatory response and lung injury after cardiac arrest (CA) and resuscitation. Methods Twenty-one healthy male pigs weighing (37±2) kg were randomly divided into 3 groups (n = 7 each): control group, LIpostC group, and LIpostC+TH group. The animal model was established by 10 minutes of untreated CA and then 5 minutes of cardiopulmonary resuscitation (CPR).Coincident with the start of CPR, LIpostC was induced by four cycles of 5 minutes of limb ischemia followed by 5 minutes of reperfusion in the LIpostC and LIpostC+TH groups. After successful resuscitation, TH was implemented by surface cooling to reach a temperature of 32-34℃ until 4 hours post-resuscitation, followed by a re-warming rate of 1 ℃/h for 4 hours in the LIpostC+TH group. Normal temperature was maintained in the control and LIpostC groups. The resuscitation outcomes in each group were recorded during CPR. At 15 minutes prior to CA (baseline) and during 4 hours post-resuscitation, the level of arterial lactate was measured and PaO2/FiO2 was calculated, and extra-vascular lung water index (EVLWI) and pulmonary vascular permeability index (PVPI) were measured meanwhile by a PiCCO monitor. At 15 minutes prior to CA (baseline) and during 24 hours post-resuscitation, the levels of serum tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were measured by enzyme linked immunosorbent assay (ELISA). Results Six animals in each group were successfully resuscitated. Coronary perfusion pressure (CPP), duration of resuscitation, number of shocks and epinephrine dosage during CPR were not statistically significant among the three groups. The baseline of arterial lactate, PaO2/FiO2, EVLWI, PVPI and cytokines prior to CA were also not statistically significant among the three groups. The levels of serum TNF-α and IL-6 after resuscitation were gradually increased in all the three groups; however, the values of TNF-αand IL-6 were significantly lower in the LIpostC and LIpostC+TH groups than that in the control group, and they were further decreased in the LIpostC+TH group when compared to the LIpostC group [TNF-α (ng/L): 305±22 vs. 343±26 at 4 hours, 350±29 vs. 389±18 at 24 hours; IL-6 (ng/L): 239±14 vs. 263±19 at 24 hours, all P < 0.05]. The levels of lactate reached the peak at 2 hours post-resuscitation and then gradually decreased in all the three groups; it finally returned to the baseline in the LIpostC and LIpostC+TH groups, which was markedly lower than that in the control group (mmol/L: 1.4±0.7, 1.2±0.3 vs. 3.1±1.7, both P < 0.05). During 4 hours post-resuscitation, PaO2/FiO2 was significantly higher and EVLWI and PVPI were markedly lower in the LIpostC and LIpostC+TH groups than that in the control group; additionally, PaO2/FiO2 and EVLWI were further improved in the LIpostC+TH group than the LIpostC group [4-hour PaO2/FiO2 (mmHg, 1 mmHg = 0.133 kPa): 391±26 vs. 361±20; 4-hour EVLWI (mL/kg): 10.1±1.5 vs. 12.1±1.2, both P < 0.05]. Conclusion LIpostC can be used to alleviate systemic inflammatory response and lung injury after porcine CA and CPR, and its combination with TH further enhanced its protective effects.
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Objective: To investigate the effect of adiponectin levels with its related mechanism in diabetic myocardial ischemia-reperfusion injury and ischemia post-conditioning in experimental rats. Methods: A total of 80 male SD rats were randomly divided into 6 groups: Normal sham (NS) group,n=8, Normal ischemia-reperfusion injury (NIRI) group,n=16, Normal ischemia post-conditioning (NIPO) group,n=16 and Diabetic mellitus sham (DMS) group,n=8, Diabetic mellitus ischemia-reperfusion injury (DMIRI) group,n=16, Diabetic mellitus ischemic post-conditioning (DMIPO) group,n=16. DM rats model was established by intraperitoneal injection of streptozotocin; IR model was established by occlusion of left anterior descending (LAD) coronary artery for 30 min followed by reperfusion for 120min; IPO model was established by 3 cycles of ischemia for 10s and reperfusion for10s; the rats in Sham group received silk line wrapping of LAD without occlusion. The myocardial infarction (MI) area was measured by TTC staining, plasma adiponectin level was examined by ELISA, the protein expressions of p-Akt and total-Akt were detected by Western blot analysis. Results: Compared with NIRI group, NIPO group had decreased MI area,P<0.05, while DMIRI group and DMIPO group had increased MI area,P<0.01; compared with NS group, NIRI group and NIPO group showed up-regulated expression of adiponectin and p-Akt,P<0.05 and DMS group showed down-regulated p-Akt,P<0.05. Compared with NIPO group, three DM groups presented down-regulated adiponectin and p-Akt,P<0.05. Linear correlation analysis indicated that plasma adiponectin expression level was negatively related to MI area and positively related to myocardial tissue p-Akt expression with the correlation coefifcient at 0.63 and 0.65 respectively, P<0.01. Conclusion: Down-regulated plasma adiponectin expression may cause the inactivation of PI3K/Akt signal pathway and therefore aggravate DM ischemia-reperfusion injury which cannot be protected by ischemic post-conditioning in experimental rats.