Summary: The changes of tumor necrosis factor-α (TNF-α) and brain ultrastructure during cardiopulmonary resuscitation and the effects of ulinastation injection were observed, and the mechanism was investigated. Twen...Summary: The changes of tumor necrosis factor-α (TNF-α) and brain ultrastructure during cardiopulmonary resuscitation and the effects of ulinastation injection were observed, and the mechanism was investigated. Twenty-four adult healthy Sprague-Dawley rats were randomly divided into control group (8 rats), resuscitation group (8 rats) and ulinastatin (UTI) group (8 rats). Rats in control group underwent tracheotomy without clipping the trachea to induce circulatory and respiratory standstill. Rats in resuscitation and ulinastatin group were subjected to the procedure of establishing the model of cardiopulmonary cerebral resuscitation (CPCR). Rats in ulinastatin group were given with UTI 104 U/kg once after CPCR. In the control group, the plasma was collected immediate, 30 min, 2 h, 4 h, and 6 h after tracheotomy. In resuscitation group and UTI group, plasma was collected immediate after tracheotomy, 30 min, 2 h, 4 h and 6 h after successful resuscitation. The plasma levels of TNF-α were determined by radioimmunoassay (RIA). At the end of the experiment, 2 rats were randomly selected from each group and were decapitated. The cortex of the brain was taken out immediately to observe the ultrastructure changes. In control group, there were no significant differences in the level of TNF-α among different time points (P>0.05). In resuscitation group, the level of TNF-α was increased obviously after resuscitation (P<0.01) and reached its peak 2 h later after resuscitation. An increasing trend of TNF-α showed in UTI group. There were no differences in TNF-α among each sample taken after successful resuscitation and that after tracheotomy. The utrastructure of brains showed the injury in UTI group was ameliorated as compared with that in resuscitation group. In early period of CPCR, TNF-α was expressed rapidly and kept increasing. It indicated that TNF-α might take part in the tissue injury after CPCR. The administration of UTI during CACR could depress TNF-α and ameliorate brain injury. By regulating the expression of damaging mediator, UTI might provide a protective effect on the tissue injury after CPCR.展开更多
Objectives To evaluate retrospectively the potential benefits of combined utilization of various assisted circulation devices in cardiac arrest patients who did not respond to conventional cardiopulmonary cerebral res...Objectives To evaluate retrospectively the potential benefits of combined utilization of various assisted circulation devices in cardiac arrest patients who did not respond to conventional cardiopulmonary cerebral resuscitation (CPCR). Methods Assisted circulation devices, including emergency cardiopulmonary bypass (ECPB), intra-aortic balloon pump (IABP), and left ventricular assist device (LVAD), were applied to 16 adult patients who had cardiac arrest 82 rain-56 h after open heart surgery and did not respond to 20 rain or longer conventional CPCR. ECPB was applied to 2 patients, ECPB plus IABP to 8 patients, ECPB plus IABP and LVAD to 6 patients. Results One patient recovered fully and one patient died. Of the other 14 patients, 13 resumed spontaneous cardiac rhythm and one did not; none of them could be weaned from ECPB. Further treatment of the 14 patients with combinations of assisted circulation devices enabled 6 patients to recover. One of the 7 recovered patients died of reoccurring cardiac arrest after 11 days; the other 6 were discharged in good condition and were followed up for 3-49 months (mean =22 months). Of the 6 discharged patients one suffered cerebral embolism during LVAD treatment, resulting in mild limitation of mobility of the right limbs ; the other 5 never manifested any central nervous system complications. There was no late deaths giving a 37.5% (6/16) long-term survival rate. Conclusions ECPB could effectively reestablish blood circulation and oxygen supply, rectify acidosis, and improve internal milieu. The combined utilization of ECPB, IABP, and LVAD reduces the duration of ECPB, improves the incidence of recovery, and offers beneficial alternatives to refractory cardiac arrest patients.展开更多
文摘Summary: The changes of tumor necrosis factor-α (TNF-α) and brain ultrastructure during cardiopulmonary resuscitation and the effects of ulinastation injection were observed, and the mechanism was investigated. Twenty-four adult healthy Sprague-Dawley rats were randomly divided into control group (8 rats), resuscitation group (8 rats) and ulinastatin (UTI) group (8 rats). Rats in control group underwent tracheotomy without clipping the trachea to induce circulatory and respiratory standstill. Rats in resuscitation and ulinastatin group were subjected to the procedure of establishing the model of cardiopulmonary cerebral resuscitation (CPCR). Rats in ulinastatin group were given with UTI 104 U/kg once after CPCR. In the control group, the plasma was collected immediate, 30 min, 2 h, 4 h, and 6 h after tracheotomy. In resuscitation group and UTI group, plasma was collected immediate after tracheotomy, 30 min, 2 h, 4 h and 6 h after successful resuscitation. The plasma levels of TNF-α were determined by radioimmunoassay (RIA). At the end of the experiment, 2 rats were randomly selected from each group and were decapitated. The cortex of the brain was taken out immediately to observe the ultrastructure changes. In control group, there were no significant differences in the level of TNF-α among different time points (P>0.05). In resuscitation group, the level of TNF-α was increased obviously after resuscitation (P<0.01) and reached its peak 2 h later after resuscitation. An increasing trend of TNF-α showed in UTI group. There were no differences in TNF-α among each sample taken after successful resuscitation and that after tracheotomy. The utrastructure of brains showed the injury in UTI group was ameliorated as compared with that in resuscitation group. In early period of CPCR, TNF-α was expressed rapidly and kept increasing. It indicated that TNF-α might take part in the tissue injury after CPCR. The administration of UTI during CACR could depress TNF-α and ameliorate brain injury. By regulating the expression of damaging mediator, UTI might provide a protective effect on the tissue injury after CPCR.
文摘Objectives To evaluate retrospectively the potential benefits of combined utilization of various assisted circulation devices in cardiac arrest patients who did not respond to conventional cardiopulmonary cerebral resuscitation (CPCR). Methods Assisted circulation devices, including emergency cardiopulmonary bypass (ECPB), intra-aortic balloon pump (IABP), and left ventricular assist device (LVAD), were applied to 16 adult patients who had cardiac arrest 82 rain-56 h after open heart surgery and did not respond to 20 rain or longer conventional CPCR. ECPB was applied to 2 patients, ECPB plus IABP to 8 patients, ECPB plus IABP and LVAD to 6 patients. Results One patient recovered fully and one patient died. Of the other 14 patients, 13 resumed spontaneous cardiac rhythm and one did not; none of them could be weaned from ECPB. Further treatment of the 14 patients with combinations of assisted circulation devices enabled 6 patients to recover. One of the 7 recovered patients died of reoccurring cardiac arrest after 11 days; the other 6 were discharged in good condition and were followed up for 3-49 months (mean =22 months). Of the 6 discharged patients one suffered cerebral embolism during LVAD treatment, resulting in mild limitation of mobility of the right limbs ; the other 5 never manifested any central nervous system complications. There was no late deaths giving a 37.5% (6/16) long-term survival rate. Conclusions ECPB could effectively reestablish blood circulation and oxygen supply, rectify acidosis, and improve internal milieu. The combined utilization of ECPB, IABP, and LVAD reduces the duration of ECPB, improves the incidence of recovery, and offers beneficial alternatives to refractory cardiac arrest patients.