BACKGROUND: The ideal endpoint of resuscitation after severe hemorrhage should indicate not only that optimal oxygen delivery has been achieved, but also that oxygen utilization has been restored. A modified Foley catheter for simultaneous assessment of microcirculatory blood flow (TBF) and mitochondrial NADH in the urethral wall was used in the female swine. We hypothesized that changes in mitochondrial NADH and TBF are associated with impaired energy metabolism in the urethra and that these changes correlate with impaired tissue perfusion in the bladder during shock and resuscitation. MATERIAL/ METHODS: Female swine n=5 underwent laparotomy. TBF was measured by a laser Doppler flowmeter. Mitochondrial function was evaluated by measuring NADH fluorescence in vivo. Multiparameter sensors (pH, pCO2 and pO2) were placed in the bladder mucosa (BM), and in the skeletal muscle (Sk). Animals underwent hemorrhage and their MAP was maintained at 40 mm Hg by appropriate infusing or withdrawing of blood for 10 min. Animals were resuscitated and observed for 20 min. RESULTS: Urethral NADH increased during shock and recovered during resuscitation, while TBF showed an opposite effect (r(2)=0.74). Skeletal muscle and bladder pO2 decreased during shock (p<0.01) and recovered after resuscitation. NADH increased significantly (p<0.05) during shock and decreased after resuscitation. CONCLUSIONS: Changes in TBF and NADH in the urethral mucosa represent novel markers for the energetic state of the tissue. They could be measured in vivo by a minimally invasive approach and thus could provide important information on the end-points of resuscitation in hemorrhagic shock.
BACKGROUND: The ideal endpoint of resuscitation after severe hemorrhage should indicate not only that optimal oxygen delivery has been achieved, but also that oxygen utilization has been restored. A modified Foley catheter for simultaneous assessment of microcirculatory blood flow (TBF) and mitochondrial NADH in the urethral wall was used in the female swine. We hypothesized that changes in mitochondrial NADH and TBF are associated with impaired energy metabolism in the urethra and that these changes correlate with impaired tissue perfusion in the bladder during shock and resuscitation. MATERIAL/ METHODS: Female swine n=5 underwent laparotomy. TBF was measured by a laser Doppler flowmeter. Mitochondrial function was evaluated by measuring NADH fluorescence in vivo. Multiparameter sensors (pH, pCO2 and pO2) were placed in the bladder mucosa (BM), and in the skeletal muscle (Sk). Animals underwent hemorrhage and their MAP was maintained at 40 mm Hg by appropriate infusing or withdrawing of blood for 10 min. Animals were resuscitated and observed for 20 min. RESULTS: Urethral NADH increased during shock and recovered during resuscitation, while TBF showed an opposite effect (r(2)=0.74). Skeletal muscle and bladder pO2 decreased during shock (p<0.01) and recovered after resuscitation. NADH increased significantly (p<0.05) during shock and decreased after resuscitation. CONCLUSIONS: Changes in TBF and NADH in the urethral mucosa represent novel markers for the energetic state of the tissue. They could be measured in vivo by a minimally invasive approach and thus could provide important information on the end-points of resuscitation in hemorrhagic shock.