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- H Kerger, K F Waschke, K V Ackern, A G Tsai, and M Intaglietta.
- Department of Anesthesiology and Operative Critical Care Medicine, Faculty of Clinical Medicine Mannheim, University of Heidelberg, D-68135 Mannheim, Germany.
- Am. J. Physiol. 1999 Jun 1;276(6 Pt 2):H2035-43.
AbstractSystemic 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 (QB), 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 (QB, 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.
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