Cardiac arrest (CA) is a leading cause of mortality worldwide. Most of post-resuscitation related deaths are due to post-cardiac arrest syndrome (PCAS). After cardiopulmonary resuscitation (CPR), return of spontaneous circulation (ROSC) leads to renal ischemia-reperfusion injury, also known as PCAS. Many studies have focused on brain and heart injuries after ROSC, but renal failure has largely been ignored. Therefore, we investigated the protective effects of therapeutic hypothermia (TH) on asphyxial CA-induced renal injury in rats.Thirty rats were randomly divided into five groups: 1) the control group (sham); 2) the normothermic CA (nor.); 3) a normothermic CA group that received TH immediately within 2 h after CPR (Hypo. 2 hrs); 4) a normothermic CA group that received TH within 4 h after CPR (Hypo. 4 hrs); and 5) a normothermia CA group that received TH within 6 h after CPR (Hypo. 6 h). One day after CPR, all rats were sacrificed. Compared with the normothermic CA group, the TH groups demonstrated significantly increased survival rate (P < 0.05); decreased serum blood urea nitrogen, creatinine, and lactate dehydrogenase levels; and lower histological damage degree and malondialdehyde concentration in their renal tissue. Terminal deoxynucleotidyl transferase dUTP nick end labeling stain revealed that the number of apoptotic cells significantly decreased after 4 h and 6 h of TH compared to the results seen in the normothermic CA group. Moreover, TH downregulated the expression of cyclooxygenase-2 in the renal cortex compared to the normothermic CA group one day after CPR. These results suggest that TH exerts anti-apoptotic, anti-inflammatory, and anti-oxidative effects immediately after ROSC that protect against renal injury. 相似文献
It has been suggested that propofol can modulate microglial activity and hence may have potential roles against neuroinflammation following brain ischemic insult. However, whether and how propofol can inhibit post‐cardiac arrest brain injury via inhibition of microglia activation remains unclear. A rat model of asphyxia cardiac arrest (CA) was created followed by cardiopulmonary resuscitation. CA induced marked microglial activation in the hippocampal CA1 region, revealed by increased OX42 and P2 class of purinoceptor 7 (P2X7R) expression, as well as p38 MAPK phosphorylation. Morris water maze showed that learning and memory deficits following CA could be inhibited or alleviated by pre‐treatment with the microglial inhibitor minocycline or propofol. Microglial activation was significantly suppressed likely via the P2X7R/p‐p38 pathway by propofol. Moreover, hippocampal neuronal injuries after CA were remarkably attenuated by propofol. In vitro experiment showed that propofol pre‐treatment inhibited ATP‐induced microglial activation and release of tumor necrosis factor‐α and interleukin‐1β. In addition, propofol protected neurons from injury when co‐culturing with ATP‐treated microglia. Our data suggest that propofol pre‐treatment inhibits CA‐induced microglial activation and neuronal injury in the hippocampus and ultimately improves cognitive function.
ObjectiveTo evaluate whether a text message (TM) alert system for trained volunteers contributed to early cardiopulmonary resuscitation, the use of automated external defibrillators (AEDs), return of spontaneous circulation (ROSC) and survival in out-of-hospital cardiac arrest (OHCA) patients in a region with above-average survival rates.DesignData on all OHCA patients in 2012 (non-TM group) were compared with those of all OHCA patients in 2018 (TM group). The association of the presence of a TM alert system with ROSC and survival was assessed with multivariate regression analyses.ResultsTM responders reached 42 OHCA patients (15.9%) earlier than the first responders or ambulance. They connected 31 of these 42 OHCA patients (73.8%) to an AED before the ambulance arrived, leading to a higher percentage of AEDs being attached in 2018 compared to the 2012 non-TM group (55% vs 46%, p = 0.03). ROSC was achieved more often in the TM group (61.0% vs 29.4%, p < 0.01). Three-month and 1‑year survival did not differ significantly between the two groups (29.3% vs 24.3%, p = 0.19, and 25.9% vs 23.5%, p = 0.51). Multivariate regression analyses confirmed the positive association of ROSC with the TM alert system (odds ratio 1.49, 95% confidence interval 1.02‑2.19, p = 0.04).ConclusionA TM alert system seems to improve the chain of survival; because TM responders reached patients early, AEDs were attached more often and more OHCA patients achieved ROSC. However, the introduction of a TM alert system was not associated with improved 3‑month or 1‑year survival in a region with above-average survival rates. 相似文献
The effects of a new calcium channel blocker, 1-[bis(4-fluorophenyl)methyl]-4-(2,3,4-trimethoxybenzyl)-piperazine dihydrochloride (KB-2796), on delayed neuronal death (DND) in the hippocampus were examined in gerbils in comparison with those of pentobarbital and flunarizine. The neuronal density in the hippocampal CA1 subfield was counted on the seventh day of recirculation following 5 min of bilateral carotid occlusion, and protein biosynthesis in the brain was also determined at 1, 2, 4, 24, and 72 h following occlusion. The drugs were intraperitoneally administered after recirculation. KB-2796 (10 mg/kg) significantly prevented DND in the CA1 subfield. Pentobarbital (40 mg/kg), but not flunarizine (3 and 10 mg/kg), inhibited DND. Protein synthetic activity in the CA1 subfield was reduced by ischemia and the reduction was not restored even at 72 h after recirculation. KB-2796 did not ameliorate the reduction of protein synthesis in the CA1 subfield by 24 h after recirculation, but in one of three animals restoration of protein synthesis was observed at 72 h of recirculation. Pentobarbital also restored the reduced protein synthesis in two of three animals at 72 h. These results suggest that calcium influx into neurons participates in the pathogenesis of DND, and also that KB-2796 might prevent both morphological and functional cell damage in CA1 neurons induced by transient ischemia. 相似文献
For the first time the involvement of C-Reactive protein (CRP) in early (acute) and delayed ischemic (IPC) and pharmacological (chemical) preconditioning (CPC) in an in vivo model of rat myocardial infarction was presented. Acute IPC was produced by three 5 minute occlusion (ischemia) periods interspersed with 5 minute reperfusion, followed by 30 minute occlusion of the left coronary artery and 2 hour reperfusion injury. Acute CPC was produced by a k-opioid receptor agonist U50488H (5 mg/kg) applied i.v. 15 minutes before 30 minute ischemia/ 2 hour reperfusion. Delayed preconditioning was produced by 30 minute ischemia/ 2 hour reperfusion, induced 24 hour after either ischemic or pharmacological preconditioning. The myocardial ischemia/reperfusion injury was evaluated on the basis of total and cardiac creatine kinase isoenzyme activity, functional recovery of the heart (ECG), infarct size (% IS/RA) and mortality at the end of the experiments. The results obtained showed that: k-opioid receptor agonist U50488H mimics both the acute and delayed IPC in the above experimental protocol; Both acute IPC and most probably CPC act by opening of K(ATP) channels (the effects were blocked by nonspecific ATP-sensitive K channel blocker glybenclamide), and via activation of protein kinase C (a selective protein kinase C inhibitor chelerythrine blocked the efects); C-reactive protein (CRP) was significantly elevated by 54% in non-preconditioned acute ischemia/reperfusion injury. The elevation was more pronounced (82% increase) 24 hour after non-preconditioned ischemia/reperfusion injury. It reflected very well the increase in cardiac isoenzymes, infarct size and mortality of the rats, and can be used as a marker of the severity of myocardial injury in this model; The increase of CRP was prevented by both IPC and CPC in early, and especially in late preconditioning. This confirms the involvement of CRP as a marker in cardiac ischemic/reperfusion injury. It was concluded that in addition to the established involvement of adenosine, bradykinin, opioid and other receptors, a suppression of myocardial CRP/complement production might be involved in the biological mechanism of preconditioning. This could be a promising perspective in clinical interventions against ischemia/reperfusion injuries of the heart. 相似文献
Abstract. According to biophysical principles, colour and size are important phenotypic factors that may influence body temperature and activity in ectothermic insects. In taxa showing female-limited polymorphism, males and female morphs differ in body colour, size and activity pattern. However, no previous study has evaluated whether such phenotypic and behavioural variation relates to differences between males and female morphs in thermal properties. In the present study, the relationships between body colour, size, activity and body temperature are examined under laboratory and field conditions, for the polymorphic damselfly Enallagma cyathigerum (Charpentier, 1840) (Odonata: Zygoptera). Contrary to expectation, males and female colour morphs of this species do not differ in thermal properties (i.e. heating characteristics or field body temperatures). When questioning phenotype and activity, temperature does not appear to be relevant for understanding the maintenance of female-limited polymorphism. 相似文献
Matrigel promotes angiogenesis in the myocardium from ischemic injury and prevents remodelling of the left ventricle. We assessed the therapeutic efficacy of intracardiac matrigel injection and matrigel‐mediated stem cell homing in a rat myocardial infarction (MI) model. Following MI, matrigel (250 μl) or phosphate‐buffered solution (PBS) was delivered by intracardiac injection. Compared to the MI control group (MI‐PBS), matrigel significantly improved left ventricular function (n= 11, P < 0.05) assessed by pressure–volume loops after 4 weeks. There is no significant difference in infarct size between MI‐matrigel (MI‐M; 21.48 ± 1.49%, n= 10) and MI‐PBS hearts (20.98 ± 1.25%, n= 10). The infarct wall thickness of left ventricle is significantly higher (P < 0.01) in MI‐M (0.72 ± 0.02 mm, n= 10) compared with MI‐PBS (0.62 ± 0.02 mm, n= 10). MI‐M hearts exhibited higher capillary density (border 130.8 ± 4.7 versus 115.4 ± 6.0, P < 0.05; vessels per high‐power field [HPF; 400×], n= 6) than MI‐PBS hearts. c‐Kit+ stem cells (38.3 ± 5.3 versus 25.7 ± 1.5 c‐Kit+ cells per HPF [630×], n= 5, P < 0.05) and CD34+ cells (13.0 ± 1.51 versus 5.6 ± 0.68 CD34+ cells per HPF [630×], n= 5, P < 0.01) were significantly more numerous in MI‐M than in MI‐PBS in the infarcted hearts (n= 5, P < 0.05). Intracardiac matrigel injection restores myocardial functions following MI, which may attribute to the improved recruitment of CD34+ and c‐Kit+ stem cells. 相似文献
Erythropoietin (EPO) protects the myocardium from ischaemic injury and promotes beneficial remodelling. We assessed the therapeutic efficacy of intracardiac EPO injection and EPO-mediated stem cell homing in a rat myocardial infarction (MI) model. Following MI, EPO (3000 U/kg) or saline was delivered by intracardiac injection. Compared to myocardial infarction control group (MIC), EPO significantly improved left ventricular function ( n = 11–14, P < 0.05) and decreased right ventricular wall stress ( n = 8, P < 0.05) assessed by pressure-volume loops after 6 weeks. MI-EPO hearts exhibited smaller infarction size (20.1 ± 1.1% versus 27.8 ± 1.2%; n = 6–8, P < 0.001) and greater capillary density (338.5 ± 14.7 versus 259.8 ± 9.2 vessels per mm; n = 6–8, P < 0.001) than MIC hearts. Direct EPO injection reduced post-MI myocardial apoptosis by approximately 41% (0.27 ± 0.03% versus 0.42 ± 0.03%; n = 6, P = 0.005). The chemoattractant SDF-1 was up-regulated significantly assessed by quantitative realtime PCR and immunohistology. c-Kit+ and CD34+ stem cells were significantly more numerous in MI-EPO than in MIC at 24 hrs in peripheral blood ( n = 7, P < 0.05) and 48 hrs in the infarcted hearts ( n = 6, P < 0.001). Further, the mRNAs of Akt, eNOS and EPO receptor were significantly enhanced in MI-EPO hearts ( n = 7, P < 0.05). Intracardiac EPO injection restores myocardial functions following MI, which may attribute to the improved early recruitment of c-Kit+ and CD34+ stem cells via the enhanced expression of chemoattractant SDF-1. 相似文献
Periodogram techniques on detrended data were used to determine the incidence of Trypanosoma brucei brucei infection on the distribution of the core temperature of rats and the expression of temperature rhythms. In such an animal model, sudden episodic hypothermic bouts were described. These episodes of hypothermia are used here as temporal marks for the purpose of performing punctual comparisons on temperature organization. The experiment was conducted on 10 infected and 3 control Sprague-Dawley rats reared under a 24 h light-dark cycle. Core temperature was recorded continuously throughout the experiment, until the animals' death. Temperature distributions, analyzed longitudinally across the full duration of the experiment, exhibited a progressive shift from a bimodal to unimodal pattern, suggesting a weakening of the day/night core temperature differences. After hypothermic events, the robustness of the circadian rhythm substantially weakened, also affecting the ultradian components. The ultradian periods were reduced, suggesting fragmentation of temperature generation. Moreover, differences between daytime and nighttime ultradian patterns decreased during illness, confirming the weakening of the circadian component. The results of the experiments show that both core temperature distribution and temperature rhythm were disrupted during the infection. These disruptions worsened after each episode of hypothermia, suggesting an alteration of the temperature regulatory system. 相似文献
The effects of acute and repeat administration of the serotonin (5-HT)(1) agonists TFMPP [N -(3-trifluoromethyl)phenylpiperazine hydrochloride] and CGS12066B [7-trifluoromethyl-4- (4-methyl-1-piperazinyl)pyrrolo[1,2-a ]-quinoxaline dimaleate] were evaluated on 5-HT synthesis rates using the alpha-[(14) C]methyl-l-tryptophan (alpha-MTrp) autoradiographic method. In the acute treatment study, TFMPP (10 mg/kg) and CGS12066B (5 mg/kg) were injected intraperitoneally 30 min before an alpha-MTrp injection. In an acute study TFMPP reduced overall brain 5-HT synthesis, in the dorsal and median raphe, and in almost all of their projection areas, with the exception of the parietal, sensory-motor, and frontal cortices, the accumbens nucleus, and the caudate. Acute CGS12066B treatment did not have overall significant effect, but the rates did decrease in the cell body areas of 5-HT neurons. In a 7-day treatment with TFMPP (10 mg/kg/day) or CGS12066B (5 mg/kg/day), the 5-HT synthesis rates (24 h after last dose) decrease, with both compounds, in almost all of the nerve terminal structures. TFMPP reduced the synthesis in the dorsal and median raphe, while CGS12066B reduced it only in the dorsal raphe. This data suggests that after a 7-day treatment with TFMPP and CGS12066B, the rate of 5-HT synthesis in the dorsal raphe is restored and is reduced in many projection areas. The observed effects in the 7-day treatment could also be related to actions through the postsynaptic 5-HT(1B) sites and/or other 5-HT receptors since this compounds have limited selectivity. 相似文献
Stroke is the second leading cause of death and disability in the world, with a heavy burden on patients, their families, and society. At present, a major focus of cerebrovascular disease research is to find a safe and effective new method to promote early functional recovery in the acute phase of cerebral infarction. Major ozonated autohemotherapy (MOAH) can maintain ATP and energy metabolism in cerebral ischemia and hypoxia, and reduce cell apoptosis. In the current study, the model of middle cerebral artery occlusion in the Sprague Dawley rat was established and evaluated by the clinical functional score, Hoechst staining, immunohistochemistry, Western blot analysis, and biochemical detection. Then, the effects of MOAH on neurological function, apoptosis, and oxygen free radical damage after acute ischemia in middle cerebral artery were evaluated. Moreover, the potential two mechanisms have been illustrated for MOAH effects. This study would lay a theoretical foundation for the application of MOAH and find an effective and early treatment method for the cerebral infarction. 相似文献
In this paper, effects of a brain tumor located in a dispersive human head model on specific absorption rate (SAR) and temperature rise distributions due to different types of RF sources at 4G and 5G cellular frequencies are investigated with the use of a multiphysics model. This multiphysics model analyzes the dispersive human head with the brain tumor and provides the SAR and temperature rise distributions in the head due to the RF source operated at 4G and 5G cellular frequencies in a single finite-difference time-domain simulation. An adjacent antenna operated at 4G and 5G cellular frequencies to the human head is considered as the RF source for near-field exposure, while a plane wave field radiated by base stations operated at 4G and 5G cellular frequencies is considered as the RF source for far-field exposure. Numerical results show that the brain tumor in the head slightly affects the SAR and temperature rise distributions due to different RF sources at 4G and 5G cellular frequencies. 相似文献