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

Systemic and microcirculatory effects of autologous whole blood resuscitation in severe hemorrhagic shock. Am. J. Physiol. 276 (Heart Circ. Physiol. 45): H2035-H2043, 1999. - 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 Po-2 values were determined by phosphorescence decay. Shock caused a significant increase of arterial Po-2 and decrease of Pco(2), pH, and base excess. In the microcirculation, there was a significant decrease in blood flow ((Q) over dot(B)), functional capillary density (FCD; capillaries with red blood cell flow), and interstitial Po-2 [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 Po-2 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) over dot(B), FCD) and oxygenation at 24 h, SP (23.8% of the animals) showed severe metabolic acidosis and substantial decreases (greater than or equal to 50%) of FCD and interstitial Po-2. FCD, interstitial Po-2, and metabolic state were the main determinants of shock outcome.