HYPERTONIC SALINE DEXTRAN DOES NOT INCREASE CARDIAC CONTRACTILE FUNCTION DURING SMALL-VOLUME RESUSCITATION FROM HEMORRHAGIC-SHOCK IN ANESTHETIZED PIGS

Small volumes of hypertonic saline dextran (10% of shed blood volume [ SBV]) restore cardiac output (GO) and increase arterial pressure in he morrhagic shock. Besides rapid expansion of plasma volume, a positive inotropic effect has been proposed as an additional mechanism for the immediate onset of the cardiovascular response. This study compares th e effects of 7.2% saline/10% dextran 60 (HSDex, n = 8) and normal sali ne (NS; n = 6) on central hemodynamics and cardiac contractility asses sed by end-systolic elastance (Ees; conductance technique) and segment al preload recruitable stroke work (sPRSW; sonomicrometry). In anesthe tized open chest pigs (28 +/- 1 kg, mean +/- SEM) shock was induced by blood withdrawal (40% of blood volume) to maintain mean arterial pres sure (MAP) at 45 mm Hg for 75 min. Resuscitation was started by bolus infusion (2 min) of either HSDex (10% of SBV) or the identical sodium load of NS (80% of SBV); 30 min later both groups received 6% dextran (10% of SBV). Hemorrhagic shock reduced CO (-45%) and left ventricular end-diastolic volume (Ved; -70%) while Ees increased (NS: 2.2 +/- 0.4 to 7.5 +/- 1.8 mm Hg/mL, P < 0.05; HSDex: 1.9 +/- 0.2 to 9.1 +/- 2.6 mm Hg/mL, P = 0.085). Within 5 min after infusion of either solution C O returned to baseline values and MAP (NS +55%, HSDex +64%) and Ved (100%) increased. Neither HSDex nor NS increased Ees above shock levels (NS, 8.7 +/- 4.9 mm Hg/mL; HSDex, 7.3 +/- 2.6 mm Hg/mL) and no group differences occurred in other measurements of contractility (dP/dt(40) , sPRSW). Plasma osmolality increased to 328 +/- 3 mOsmol/kg with HSDe x. Throughout the postresuscitation period CO and MAP remained higher with HSDex (analysis of variance, P ( 0.05). After hemorrhagic-traumat ic shock and resuscitation using either HSDex or NS, no differences in cardiac contractility could be measured. We conclude that the instant aneous restoration of central hemodynamics after small volume resuscit ation with HSDex largely depends on rapid augmentation of ventricular preload due to plasma volume expansion.