Severe body stress induced by hypoxemia and hypotension may lead to total body energy state deterioration. The perfusion of the most vital organs is maintained at the expense of “less vital” organs. In this study, we used a multisite-multiparametric (MSMP) monitoring system for real-time evaluation of Tissue Blood Flow (TBF) and mitochondrial NADH fluorescence of the brain and the small intestine following hemorrhage. In Group 1 of rats, after hemorrhage, Mean Arterial Pressure (MAP) was decreased to 40 mmHg with no further perturbations for 30 min and after 2 h of resuscitation. In Group 2, MAP was maintained at 40 mmHg for 30 min. During hemorrhage, in both groups, the intestinal TBF and NADH deteriorated, while the brain remained relatively well protected. In Group 1, all parameters partly recovered within the hemorrhage phase, while in Group 2 complete recovery occurred only after resuscitation. At the end of the experiment, both models showed a decrease in intestinal viability (TBF decreased, NADH increased), while the brain metabolic state in Group 2 slightly declined. Our unique multiparametric monitoring device demonstrated that, under hemorrhage, the small intestine responded entirely differently from the brain. This may suggest the potential usefulness of the monitoring of less vital organs, as proxy organs, in critical conditions such as massive hemorrhage. This study also highlights the importance of mitochondrial function monitoring in similar conditions in the clinical environment. The main conclusions of this study are as follows:

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Effects of Hemorrhage and Resuscitation

  • Avraham Mayevsky,
  • Efrat Barbiro-Michaely,
  • Michael Tolmasov,
  • Mira M. Mandelbaum-Livnat

摘要

Severe body stress induced by hypoxemia and hypotension may lead to total body energy state deterioration. The perfusion of the most vital organs is maintained at the expense of “less vital” organs. In this study, we used a multisite-multiparametric (MSMP) monitoring system for real-time evaluation of Tissue Blood Flow (TBF) and mitochondrial NADH fluorescence of the brain and the small intestine following hemorrhage. In Group 1 of rats, after hemorrhage, Mean Arterial Pressure (MAP) was decreased to 40 mmHg with no further perturbations for 30 min and after 2 h of resuscitation. In Group 2, MAP was maintained at 40 mmHg for 30 min. During hemorrhage, in both groups, the intestinal TBF and NADH deteriorated, while the brain remained relatively well protected. In Group 1, all parameters partly recovered within the hemorrhage phase, while in Group 2 complete recovery occurred only after resuscitation. At the end of the experiment, both models showed a decrease in intestinal viability (TBF decreased, NADH increased), while the brain metabolic state in Group 2 slightly declined. Our unique multiparametric monitoring device demonstrated that, under hemorrhage, the small intestine responded entirely differently from the brain. This may suggest the potential usefulness of the monitoring of less vital organs, as proxy organs, in critical conditions such as massive hemorrhage. This study also highlights the importance of mitochondrial function monitoring in similar conditions in the clinical environment. The main conclusions of this study are as follows: