BACKGROUND: Tissue oxygen tension can be measured directly in selected organ beds, and these measurements may be more sensitive in assessing the adequacy of resuscitation than global physiologic parameters. We hypothesized that heart tissue oxygen tension would be an important marker for the severity of ischemic insult to the heart during hemorrhagic shock. We further hypothesized that gut oxygen tension measured in the jejunum would prove to be a better measure of splanchnic hypoperfusion than intramucosal pH (pHi). METHODS: Tissue oxygen probes were inserted directly into the myocardium of the left ventricle and into the lumen of the proximal jejunum in 10 anesthetized swine. A pHi catheter was introduced into the stomach. The animals were subjected to a controlled hemorrhage of 50% of estimated blood volume. Gut and cardiac oxygen were monitored continuously during hemorrhage and resuscitation, which was performed with shed blood and crystalloid. RESULTS: While gut O2 and pHi trended together, we were unable to establish a correlation between changes in these two variables during hemorrhage and resuscitation. Heart PO2 decreased significantly during hemorrhage, but surpassed baseline values after resuscitation, a finding not seen in gut PO2. No standard physiologic variables reliably predicted changes in heart PO2 during these experiments. CONCLUSIONS: Tissue oxygen tensions measurements are highly responsive to changes induced during graded hemorrhagic shock and resuscitation. Gut PO2 and pHi appear to be measuring different physiologic processes in the gastrointestinal tract. The compensatory ability of the heart far exceeds that of the gut after ischemic insult. This hemorrhagic shock model appears feasible for the study of various methods of resuscitation.
BACKGROUND: Tissue oxygen tension can be measured directly in selected organ beds, and these measurements may be more sensitive in assessing the adequacy of resuscitation than global physiologic parameters. We hypothesized that heart tissue oxygen tension would be an important marker for the severity of ischemic insult to the heart during hemorrhagic shock. We further hypothesized that gut oxygen tension measured in the jejunum would prove to be a better measure of splanchnic hypoperfusion than intramucosal pH (pHi). METHODS: Tissue oxygen probes were inserted directly into the myocardium of the left ventricle and into the lumen of the proximal jejunum in 10 anesthetized swine. A pHi catheter was introduced into the stomach. The animals were subjected to a controlled hemorrhage of 50% of estimated blood volume. Gut and cardiac oxygen were monitored continuously during hemorrhage and resuscitation, which was performed with shed blood and crystalloid. RESULTS: While gut O2 and pHi trended together, we were unable to establish a correlation between changes in these two variables during hemorrhage and resuscitation. Heart PO2 decreased significantly during hemorrhage, but surpassed baseline values after resuscitation, a finding not seen in gut PO2. No standard physiologic variables reliably predicted changes in heart PO2 during these experiments. CONCLUSIONS: Tissue oxygen tensions measurements are highly responsive to changes induced during graded hemorrhagic shock and resuscitation. Gut PO2 and pHi appear to be measuring different physiologic processes in the gastrointestinal tract. The compensatory ability of the heart far exceeds that of the gut after ischemic insult. This hemorrhagic shock model appears feasible for the study of various methods of resuscitation.