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1 Department of Anesthesiology and Operative Critical Care Medicine, Faculty of Clinical Medicine Mannheim, University of Heidelberg, D-68135 Mannheim, Germany; and 2 Department of Bioengineering, University of California San Diego, La Jolla, California 92093
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 PO2 values were determined by
phosphorescence decay. Shock caused a significant increase of arterial
PO2 and decrease of
PCO2, pH, and base excess. In the
microcirculation, there was a significant decrease in blood flow
(
B),
functional capillary density (FCD; capillaries with red blood cell
flow), and interstitial PO2
[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 PO2 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
(
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
PO2. FCD, interstitial
PO2, and metabolic state were the
main determinants of shock outcome.
microcirculation; autologous blood; partial pressure of oxygen; functional capillary density; base excess; phosphorescence decay
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