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Renal ischemic-reperfusion injury following hemorrhagic shock in rats: an experimental study.
OBJECTIVE: To understand the features of renal ischemic-reperfusion injury after hemorrhagic shock in rats.
METHODS: Models of hemorrhagic shock were established in 36 Sprague-Dawley rats that were divided into 6 groups (with 6 rats in each group), 5 groups of which received subsequent resuscitation measures. Another 6 untreated normal rats served as normal control. Renal pathomorphology and the distribution of dendritic cells (DCs) were observed to determine their correlation in the resuscitation groups (at 3, 6, 12, 24 and 48 h respectively after resuscitation), the control and shock groups.
RESULTS: The blood loss of the rats averaged 60.42% of the total blood at the end of hemorrhagic shock. More severe pathological changes were observed in the rats with shock but without receiving resuscitation measures, as compared with the changes in rats with rescuscitation. The rats in shock group had the fewest DC number of all the groups. Among the groups with reperfusion after shock, the most severe renal pathomorphological changes took place 24 h after the resuscitation when the most significant DC activation was noted in positive correlation with renal tissue injury (P<0.01).
CONCLUSIONS: Twenty-four hours after reperfusion, the rats with hemorrhagic shock experience the most severe changes in renal pathomorphology with the most extensive distribution of the DCs, indicating that DCs induce renal tissue injury.
METHODS: Models of hemorrhagic shock were established in 36 Sprague-Dawley rats that were divided into 6 groups (with 6 rats in each group), 5 groups of which received subsequent resuscitation measures. Another 6 untreated normal rats served as normal control. Renal pathomorphology and the distribution of dendritic cells (DCs) were observed to determine their correlation in the resuscitation groups (at 3, 6, 12, 24 and 48 h respectively after resuscitation), the control and shock groups.
RESULTS: The blood loss of the rats averaged 60.42% of the total blood at the end of hemorrhagic shock. More severe pathological changes were observed in the rats with shock but without receiving resuscitation measures, as compared with the changes in rats with rescuscitation. The rats in shock group had the fewest DC number of all the groups. Among the groups with reperfusion after shock, the most severe renal pathomorphological changes took place 24 h after the resuscitation when the most significant DC activation was noted in positive correlation with renal tissue injury (P<0.01).
CONCLUSIONS: Twenty-four hours after reperfusion, the rats with hemorrhagic shock experience the most severe changes in renal pathomorphology with the most extensive distribution of the DCs, indicating that DCs induce renal tissue injury.
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