| Traumatic hemorrhagic shock is one of the leading causes of death in civillian accident and military combat. Current treatments of hemorrhagic shock involve rapid and aggressive fluid resuscitation to maintain normal blood pressure and tissue perfusion, but this experiment has been largely based on the Wiggers model of controlled hemorrhagic shock, which did not at all resemble the uncontrolled situation in trauma patients. In the setting of uncontrolled hemorrhage, resuscitation strategies are debatable. Recently, a number of studies have been done for this, but the exact mechanism have not been observed or reported to date. The aim of this study was to investigate the outcome and the mechanism of fluid resuscitation in uncontrolled hemorrhagic shock. The study had three parts: 1) Large volume resuscitation before control of bleeding is helpful? 2) The effect of limited resuscitation (LR) before control of bleeding on the following treatment and its pathophysiology on the aspects of blood flow, energy metabolism and ischemia-reperfusion injury (IR/I). 3) The outcomes of limited resuscitation with hypertonic saline (HS).The main results are as follows:1. Uncontrolled hemorrhagic shock (UHS) was produced in 60 rats by a standardized massive splenic injury with a transected middle branch of splenic artery (MSIA). When the mean arterial pressure (MAP) reached 40mmHg, resuscitation was begun. Ringer,s solution was continued as needed to maintain the following desired endpoints: MAP of 50mmHg, 60mmHg, 80mmHg, 100mmHg(NS50,NS60,NS80,NS100). Animals were observed for 3 hours or untill death. The result shown that all rats in NS80 group and NS100 group died within 3 hours and 6 rats in NS50 survived 3 hours. The survival rate in NSgroup50 was significantly higher than in NS80 and NS100group. Compaired with the NS80 group and NS100 group, the mean survival time in the NS50group was significantly longer. The blood loss and the amount of fluid resuscitation in NS50 group was significantly lower than in NS80 group and NS100group. Hematocrit(Hct) in NS80 group and NS100group rapidly decreased, and were significantly lower than in NS50 group. MAP in NS80 group and NS100 group decreased rapidly after injury, and it was difficult to maintain their MAP goals.2. UHS was produced in 95 rats by MSIA. Experimental design consisted of three phases: a prehospital phase, with uncontrolled bleeding and resuscitation to the MAP of 40mmHg (group1), 50mmHg(group2), 60mmHg(group3), 80mmHg(group4), 100mmHg(group5) with Ringer,s solution for 45 minutes when MAP decreased to 40mmHg; followed by a hospital phase, with controlled of bleeding and continued resuscitation to the MAP of 100mmhg with Ringer,s solution only (NSgroup) or Ringer,s solution and whole blood (NBgroup) for 120 minutes; followed by a 240 minutes observation phase. All animals were observed for 240 minutes or untill death. Mortality rates and blood loss were significantly lower in group1 and group2 compared with group4 and group5. Group4 and group5 required significantly greater fluid volumes than group1 and group2. Mortality rates, blood loss and volume requirments were significantly lower in NBgroup compared with NSgroup. At 165 minutes, Hct in NSgroup rapidly decreased, were significantly lower than in the NBgroup. MAP in NBgroup3, NBgroup4, NBgroup5 were significantly higher than in the NSgroup3, NSgroup4, NSgroup5. MAP and Hct in group1, group2, group3 were significantly higher than in group4 and group5 at 405 minutes. At 165 minutes and 405 minutes, lactate levels in group4 and group5 were significantly worse than group2 and group3; NSgroup were significantly higher than in NBgroup.Blood flow, T-AOC (total antioxidative capacity) level, Na+K+-ATPase and Ca++-ATPase in group1, group2, group3 were significantly higher than in group4 and group5. The content of MDA (malondialdehyde) in group1, group2, group3 were significantly lower than in group4 and group5. Blood flow, T-AOC level, Na+K+-ATPase, Ca++-ATPase in groups resuscitation with Ringer,s solut... |
