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Cardiac arrest (CA) is a fatal condition with low resuscitation rate and high mortality rate. Most of the survivors have neurological sequelae affecting their quality of life. Targeted temperature management (TTM) has been suggested by a number of studies to increase the survival rate and improve neurological outcome of CA. It is highly recommended by the International Liaison Committee on Resuscitation (ILCOR) for unconscious patients after resuscitation. In this review, we discuss the pathological mechanism of brain injury in CA and applications of TTM in adults with CA, with the aim of providing valuable information for clinical application.
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Objective To research the protective effect of Ento-I against cerebral ischemia-reperfusion injury in rats, and to evaluate its analgesic and anticoagulating effects in mice. Methods The ischemic model was established with line embolism to block the middle cerebral artery of male rats. The 56 rats were randomly assigned into 7 groups of sham-operation, blank-matrix, normal saline, Ento-I plastic of 3 doses (6.67, 3.33, 1.67 mg/kg), and ozagrel sodium (8.3 mg/kg, ip). The effect of Ento-I plastic on anti-cerebral ischemia was measured by nervous function scores and the areas of cerebral infarction were determined by TTC staining for the calculation of cerebral infarction rates. The analgesic effect of Ento-I plastic was determined with acetic acid-induced twisting experiment. Sixty KM mice were randomly allocated into blank-matrix, aspirin, aspirin-plastic, and Ento-I plastic of 3 doses (5, 10 and 20 mg/kg), the number of mouse twisting were recorded right after intraperitoneal injection of 0.7% acetic acid solution at the time of 1 h after the last administration. Moreover, the anticoagulant activity of Ento-I plastic was tested by glass capillary method. Results The results of acetic acid-induced twisting experiment displayed that Ento-I plastic of all 3 dose groups (5, 10 and 20 mg/kg) could significantly reduce the number of body torsion and increase the inhibitory rates of twisting, compared with that of blank matrix group (the inhibitory rates of twisting for 3 dose groups were 21.79%, 48.89%, and 56.15%, respectively), with dose-response manner. According to the results of glass capillary test, the clotting time of mouse blood could be significantly prolonged by mid- (10 mg/ kg) and low-dose (5 mg/kg) of Ento-I plastic with corresponding clotting time of (155.20±54.19) s and (155.80±73.84) s, compared with normal saline group at (92.10±24.61) and blank-matrix group at (80.40±48.09, P<0.05). The experiment results of the isch emia-reperfusion injury by line embolism method in rats exhibited that Ento-I plastic in mid-dose (3.33 mg/kg) could significantly re duce the neurological scores after 24 h of reperfusion injury, from (2.33±0.52) of normal saline group to (1.00±0.00) of mid-dose group (P<0.01). The results from TTC staining revealed that the cerebral infarction rates of normal saline group and blank- matrix group were (24.89±7.24) % and (27.72±7.89)%, respectively, whereas those of 6.67 mg/kg and 3.33 mg/kg group of Ento-I plastic were (14.01±2.65) % and (14.73±4.94)%, respectively. Compared to the 2 negative-control groups, both the high- and mid-dose of Ento-I plastic could significantly reduce the cerebral infarction rates after ischemic reperfusion injury in rats (P<0.01). Conclusion Ento-I plastic demonstrates strong analgesic and anticoagulant effects, and could substantially reduce the neurological scores and reduce cerebral infarction rates for ischemia-reperfusion injured rats. These are likely to be the mechanism of action for Ento-I plastic realizing its anti-cerebral ischemia effect.
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Objective To research the protective effect of Ento-Ⅰagainst cerebral ischemia-reperfusion injury in rats,and to evaluate its analgesic and anticoagulating effects in mice. Methods The ischemic model was established with line embolism to block the middle cerebral artery of male rats. The 56 rats were randomly assigned into 7 groups of sham-operation,blank-matrix,nor? mal saline,Ento-Ⅰplastic of 3 doses(6.67,3.33,1.67 mg/kg),and ozagrel sodium(8.3 mg/kg,ip). The effect of Ento-Ⅰplastic on anti-cerebral ischemia was measured by nervous function scores and the areas of cerebral infarction were determined by TTC staining for the calculation of cerebral infarction rates. The analgesic effect of Ento-Ⅰplastic was determined with acetic acid-induced twisting experiment. Sixty KM mice were randomly allocated into blank-matrix,aspirin,aspirin-plastic,and Ento-Ⅰplastic of 3 doses(5,10 and 20 mg/kg),the number of mouse twisting were recorded right after intraperitoneal injection of 0.7%acetic acid solution at the time of 1 h after the last administration. Moreover,the anticoagulant activity of Ento-Ⅰplastic was tested by glass capillary method. Re?sults The results of acetic acid-induced twisting experiment displayed that Ento-Ⅰplastic of all 3 dose groups(5,10 and 20 mg/kg) could significantly reduce the number of body torsion and increase the inhibitory rates of twisting,compared with that of blank matrix group(the inhibitory rates of twisting for 3 dose groups were 21.79%,48.89%,and 56.15%,respectively),with dose-response man?ner. According to the results of glass capillary test,the clotting time of mouse blood could be significantly prolonged by mid-(10 mg/kg)and low-dose(5 mg/kg)of Ento-Ⅰplastic with corresponding clotting time of(155.20±54.19)s and(155.80±73.84)s,compared with normal saline group at(92.10 ± 24.61)and blank-matrix group at(80.40 ± 48.09,P<0.05). The experiment results of the isch?emia-reperfusion injury by line embolism method in rats exhibited that Ento-Ⅰplastic in mid-dose(3.33 mg/kg)could significantly re?duce the neurological scores after 24 h of reperfusion injury,from(2.33 ± 0.52)of normal saline group to(1.00 ± 0.00)of mid-dose group(P<0.01). The results from TTC staining revealed that the cerebral infarction rates of normal saline group and blank-matrix group were(24.89±7.24)%and(27.72±7.89)%,respectively,whereas those of 6.67 mg/kg and 3.33 mg/kg group of Ento-Ⅰplastic were(14.01±2.65)%and(14.73±4.94)%,respectively. Compared to the 2 negative-control groups,both the high-and mid-dose of Ento-Ⅰplastic could significantly reduce the cerebral infarction rates after ischemic reperfusion injury in rats (P<0.01). Conclu?sion Ento-Ⅰplastic demonstrates strong analgesic and anticoagulant effects,and could substantially reduce the neurological scores and reduce cerebral infarction rates for ischemia-reperfusion injured rats. These are likely to be the mechanism of action for Ento-Ⅰplastic realizing its anti-cerebral ischemia effect.
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Objective To observe the influence of electroacupuncure(EA) at different therapeutic time windows on the effects of inosine on neuronal apoptosis and expression of heat-shock-proteins-70 (HSP70)after focal cerebral ischemic reperfusion injury (CIRI) in rats.Methods The model was established by ligation of the artery for 2 hour.EA was delivered to “baihui” and “dazhui” through acupuncture needles 0.5 hr,2 hr,6 hr and 12 hr respectively following MCAO.The expression level of HSP70 and the number of apoptotic cells were examined by immunohistochemical technique and TUNEL,comparing the average optical density of HSP70 and the number of apoptotic positive cells of cortex penumbra and hippocampus CA1 area in rat brain.Results Compared with the model group,the average optical density of HSP70 in every EA group was increased in apoptotic positive cells of cortex penumbra and hippocampus CA1 area 0.5 h (89.98± 6.55),(128.73 ± 8.03),2 h (90.96±6.38),(132.25±8.78),6 h (93.71±6.12),(132.58±7.04),12 (96.19±7.30),(133.57±6.19)and the number of apoptotic positive cells of cortex penumbra in every EA group was decreased 0.5 h (1.80±0.84),2 h (3.40± 1.14),6 h (5.00± 1.00),12 h (5.00±2.45).The number of apoptotic cells of hippocampus CA1 area was decreased just in the EA group of 0.5 h (1.60± 1.89).Conclusion EA could increase the expression level of HSP70 and at the same time decrease the number of apoptotic cells,EA plays an important part in protecting the neuronal cells of brain after focal cerebral ischemic reperfusion injury.The acupuncture treatment should be taken as far as early.
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0.05).The cerebral infarcted area in SHR were significantly greater than that in SD rats [(42.6?5.6)% vs(29.5?6.7)%,P
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Objective To investigate the effects of pre-ischemic administration of L-NAME on brain protective effects of simvastatin against focal cerebral ischemic/reperfusion injury in rats. Methods ① Animals were subjected to transient 2-hour middle cerebral artery occlusion(MCAO)with the use of the intraluminal filament method previously described by Zea Longa. ② 54 male rats were treated with simvastatin or vehicle by gavage two weeks before MCAO, and L-NAME was injected into laterar ventricle of rats 45 minutes before MCAO. After neurological deficit was assessed at 22 hours of reperfusion, rats were killed, and the brains were rapidly removed. The coronal sections of the brains were prepared and stained with 2% TTC, and the infarct volumes were determined. Another 54 male rats were performed as description above except that the brain tissues were made into homogenate at 22 hours of reperfusion, and the contents of lactic acid(LA) and MDA, and the activities of superoxide dismutase(SOD) in the brain tissues were also measured. Results Administration of simvastatin significantly reduced the size of brain infarct, improved neurological deficits, decreased the contents of LA and MDA and increased the activities of SOD, but L-NAME could abrogate these effects. Conclutions L-NAME could abrogate the protection of simvastatin against ischemic/reperfusion injury,which may be by inhibiting the expression and activity of endothelial NO synthase(eNOS) up-regulated by simvastatin.