BACKGROUND: During hemorrhagic shock blood flow to vital organs is maintained by the diversion of blood from both the splanchnic organs and skeletal muscle. In this swine study, we tested the hypotheses that (1). liver and muscle pH are correlated during both shock and resuscitation and (2). muscle pH during shock is an indicator of potential liver injury after resuscitation. MATERIALS AND METHODS: Hemorrhagic shock was induced over 15 min to lower systolic blood pressure to 40 mm Hg and was maintained for 60 (n = 5) or 90 (n = 5) min. Resuscitation was achieved with shed blood and warm saline to maintain mean pressure >60 mm Hg for 120 min. Liver and muscle pH were measured with microelectrodes throughout the entire shock and resuscitation periods, along with hepatic venous oxygen saturation. Arterial lactate and aspartate aminotransferase were measured at baseline, end of shock, and resuscitation. Correlation between muscle and liver pH was determined. The ability of muscle pH to predict liver injury (40% increase in arterial aspartate aminotransferase) was compared with other predictors: liver pH, arterial lactate, and tonometric-arterial PCO(2) gap. RESULTS: pH values and rates of change were similar in both muscle and liver tissue. Liver pH was well correlated with muscle pH during both shock and resuscitation, R(2) = 0.84. Muscle pH predicts potential liver injury with the same sensitivity as blood lactate in this swine shock model. CONCLUSIONS: Minimally invasive measurement of muscle pH warrants further study as a method to assess splanchnic hypoperfusion and resultant injury.

OBJECTIVES: To determine whether the simultaneous measurement of tissue pH, Pco2, and Po2 with a multiple-parameter fiberoptic sensor can be used to indicate the onset of hepatic dysoxia, to determine critical values, and to assess their use in predicting negative outcomes. DESIGN: Prospective animal study. SETTING: University research laboratory. SUBJECTS: Fourteen Yorkshire swine. INTERVENTIONS: Hemorrhagic shock (n = 11) was induced over 15 mins to lower systolic blood pressure to 40 mm Hg and was maintained for 30, 60, or 90 mins. Resuscitation was achieved with shed blood and warm saline to maintain mean pressure >60 mm Hg for 120 mins. Sham animals (n = 3) were subjected to 90 mins of sham shock, followed by a 120-min recovery period. MEASUREMENTS AND MAIN RESULTS: The multiple-parameter sensor continuously measured tissue pH, Pco2, and Po2. pH and Pco2, indicators of anaerobic metabolism, were plotted against tissue Po2. All shocked animals, but no sham animals, showed a biphasic relationship between Po2 and both pH and Pco2. Curves were fit to both an exponential and a dual-line linear function to determine critical values for Po2, pH, and Pco2. The length of time the animal was dysoxic was evaluated as a predictor of negative outcome. Critical values determined from the exponential models were more sensitive indicators of negative outcome than values determined from the linear model and more sensitive than arterial lactate and tonometric intramucosal pH and Pco2. CONCLUSIONS: The multiple-parameter sensor offers the unique opportunity to study solid as well as hollow organ dysoxia through the simultaneous measurement of interstitial pH, Pco2, and Po2 in a small tissue region. The gradual transition from sufficient oxygen availability to dysoxia as a result of hemorrhage was better described by an exponential equation. The length of time that pH was below or Pco2 was above the critical value determined from the exponential model was predictive of a negative outcome.

The purpose of this study was to investigate the feasibility of using near infrared (NIR) spectroscopy of the liver to simultaneously assess oxygen content in combination with tissue pH, an indicator of anaerobic metabolism. Six anesthetized swine were subjected to 45 min of hemorrhagic shock followed by resuscitation with blood and crystalloid. Calibration models between NIR spectra and reference measurements of tissue pH, hepatic venous oxygen saturation (S(V)O2), and blood hemoglobin concentration (Hb) were developed using partial least-squares regression. Model accuracy was assessed using cross validation. The average correlation (R2) between NIR and reference measurements was 0.87, 0.68, and 0.93, respectively for pH, Hb, and S(V)O2. Estimated accuracy, the root mean squared deviation between spectral, and reference measurements was 0.03 pH units, 0.3 g/dL, and 6%. NIR determination of hepatic oxygen content and tissue pH during shock and resuscitation demonstrated that there can be a variance between hepatic venous oxygenation and regional tissue acidosis. NIR spectroscopy provides a technique to explore the implications of post-shock depression of tissue pH and evaluate new methods of resuscitation.

We used a load-insensitive index of systolic left ventricular (LV) function and an analysis of diastolic pressure-dimension relationships to test the hypothesis that recombinant human (rh) tumor necrosis factor-alpha (TNF alpha) impairs LV function in dogs. Animals were studied 7-10 d after aseptic implantation of instrumentation to monitor cardiac output, external anterior-posterior LV diameter, and LV and pleural pressures. Data were analyzed from seven dogs that received active rhTNF alpha (100 micrograms/kg over 60 min) and from five dogs that received heat-inactivated rhTNF alpha. At 24 h after infusion of active rhTNF alpha, the slope of the LV end-diastolic dimension-stroke work relationship decreased significantly, indicating a decrement in LV systolic contractility. Simultaneously, LV unstressed dimension increased significantly, suggesting diastolic myocardial creep. The end-diastolic relationship between LV transmural pressure and normalized LV dimension (strain) was markedly displaced to the left, suggesting increased diastolic elastic stiffness. Despite these changes in LV performance, cardiac index was maintained by tachycardia. The abnormalities in LV function were resolved by 72 h. We conclude that rhTNF alpha reversibly impairs LV systolic and diastolic function in unanesthetized dogs. Because dysfunction occurs greater than 6 h after the infusion of rhTNF alpha and persists for 24-48 h, the mechanism underlying this phenomenon may involve secondary mediators or a change in myocardial gene expression.