Systemic and microcirculatory effects of autologous whole blood resuscitation in severe hemorrhagic shock

Abstract

Systemic and microcirculatory effects of autologous whole blood resuscitation after 4-h hemorrhagic shock with a mean arterial pressure (MAP) level of 40 mmHg were investigated in 63 conscious Syrian golden hamsters. Microcirculation of skeletal skin muscle and subcutaneous connective tissue was visualized in a dorsal skinfold. Shed blood was retransfused within 30 min after 4 h. Animals were grouped into survivors in good (SG) and poor condition (SP) and nonsurvivors (NS) according to 24-h outcome after resuscitation and studied before shock, during shock (60, 120, and 240 min), and 30 min and 24 h after resuscitation. Microvascular and interstitial[Formula: see text] values were determined by phosphorescence decay. Shock caused a significant increase of arterial[Formula: see text] and decrease of[Formula: see text], pH, and base excess. In the microcirculation, there was a significant decrease in blood flow (Q˙B), functional capillary density (FCD; capillaries with red blood cell flow), and interstitial [Formula: see text][1.8 ± 0.8 mmHg (SG), 1.3 ± 1.3 mmHg (SP), and 0.9 ± 1.1 mmHg (NS) vs. 23.0 ± 6.1 mmHg at control]. Blood resuscitation caused immediate MAP recompensation in all animals, whereas metabolic acidosis, hyperventilation, and a significant interstitial [Formula: see text] decrease (40–60% of control) persisted. In NS (44.4% of the animals), systemic and microcirculatory alterations were significantly more severe both in shock and after resuscitation than in survivors. Whereas in SG (31.8% of the animals) there was only a slight (15–30%) but still significant impairment of microscopic tissue perfusion (Q˙B, FCD) and oxygenation at 24 h, SP (23.8% of the animals) showed severe metabolic acidosis and substantial decreases (≥50%) of FCD and interstitial[Formula: see text]. FCD, interstitial[Formula: see text], and metabolic state were the main determinants of shock outcome.