BACKGROUND: The present study was designed to evaluate the effect of conventional fluid resuscitation and small volume resuscitation alone and combined with arginine vasopressin (AVP) on cerebral perfusion pressure (CPP) and protein S100B during experimental haemorrhagic shock. MATERIAL AND METHODS: Thirty anaesthetised pigs underwent a penetrating liver trauma. Following haemodynamic decompensation, pigs received either (1) a combination of crystalloid (40 mL kg(-1)) and colloid (20 mL kg(-1)) solutions (fluid, n=10), (2) hypertonic-hyperoncotic solution (HHS; 4 mL kg(-1)) combined with normal saline (HHS+NS; n=10) or (3) HHS combined with AVP (0.2 U kg(-1) followed by an infusion of 2 U kg(-1)h(-1); HHS+AVP; n=10). RESULTS: Compared to baseline, CPP decreased and S100B levels increased significantly at haemodynamic decompensation (S100B: fluid, 0.52+/-0.23 microg L(-1) vs. 0.85+/-0.37 microg L(-1), p<0.05; HHS+NS, 0.47+/-0.18 microg L(-1) vs. 0.90+/-0.33 microg L(-1), p<0.05; HHS+AVP, 0.53+/-0.18 microg L(-1) vs. 0.90+/-0.39 microg L(-1), p<0.01). During the initial 10 min of therapy, CPP of HHS+NS was significantly higher compared to the fluid group, increased more rapidly in the HHS+AVP group, but was not significantly different thereafter. S100B levels decreased close to baseline values (p<0.001), and did not differ between groups. CONCLUSION: HHS+AVP resulted in higher CPP compared to fluid and HHS+NS in the initial phase of therapy, but did not differ thereafter. Haemorrhage-induced hypotension yielded increased S100B levels that were comparable in groups throughout the study period.
BACKGROUND: The present study was designed to evaluate the effect of conventional fluid resuscitation and small volume resuscitation alone and combined with arginine vasopressin (AVP) on cerebral perfusion pressure (CPP) and protein S100B during experimental haemorrhagic shock. MATERIAL AND METHODS: Thirty anaesthetised pigs underwent a penetrating liver trauma. Following haemodynamic decompensation, pigs received either (1) a combination of crystalloid (40 mL kg(-1)) and colloid (20 mL kg(-1)) solutions (fluid, n=10), (2) hypertonic-hyperoncotic solution (HHS; 4 mL kg(-1)) combined with normal saline (HHS+NS; n=10) or (3) HHS combined with AVP (0.2 U kg(-1) followed by an infusion of 2 U kg(-1)h(-1); HHS+AVP; n=10). RESULTS: Compared to baseline, CPP decreased and S100B levels increased significantly at haemodynamic decompensation (S100B: fluid, 0.52+/-0.23 microg L(-1) vs. 0.85+/-0.37 microg L(-1), p<0.05; HHS+NS, 0.47+/-0.18 microg L(-1) vs. 0.90+/-0.33 microg L(-1), p<0.05; HHS+AVP, 0.53+/-0.18 microg L(-1) vs. 0.90+/-0.39 microg L(-1), p<0.01). During the initial 10 min of therapy, CPP of HHS+NS was significantly higher compared to the fluid group, increased more rapidly in the HHS+AVP group, but was not significantly different thereafter. S100B levels decreased close to baseline values (p<0.001), and did not differ between groups. CONCLUSION: HHS+AVP resulted in higher CPP compared to fluid and HHS+NS in the initial phase of therapy, but did not differ thereafter. Haemorrhage-induced hypotension yielded increased S100B levels that were comparable in groups throughout the study period.
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