HEPATIC, RENAL, AND CEREBRAL TISSUE HYPERCARBIA DURING SEPSIS AND SHOCK IN RATS

Earlier observations had indicated profound increases in the carbon di oxide tension of the myocardium, gastric wall, liver parenchyma, and r enal cortex in the setting of extreme low-flow states of cardiac arres t and resuscitation, hemorrhagic shock, and anaphylactic shock. In ven ous blood draining the intestines, kidneys, and pelvic viscera, signif icant increases in PCO2 have also been observed during septic shock. I n the present study, we investigated hepatic, renal, and cerebral cort ical tissue carbon dioxide tension during intra-abdominal sepsis and s hock in Sprague-Dawley rats. Peritonitis was induced by cecal ligation and fecal spillage. Over an interval of 320 +/- 60 minutes, we measur ed progressive reduction in mean aortic pressure from 152 +/- 11 mm Hg to 25 +/- 8 mm Hg and a decline in cardiac index from 492 +/- 75 ml/k g/min to 169 +/- 57 ml/kg/min. These hemodynamic deficits were accompa nied by increases in liver tissue PCO2, from 58 +/- 4 mm Hg to 110 +/- 27 mm Hg (p = 0.006), in renal tissue PCO2, from 38 +/- 7 mm Hg to 11 5 +/- 24 mm Hg (p < 0.001), and in cerebral cortical tissue CO2, from 59 +/- 6 mm Hg to 108 +/- 16 mm Hg (p = 0.001). Arterial blood lactate content increased from 0.8 to 5.26 +/- 0.2 mmol/L (p = 0.001). Increa ses in blood lactate content preceded the changes in tissue PCO2 in ea ch of these organs. These studies demonstrate that tissue hypercarbia is a more general phenomenon of low flow states, including that of cir culatory shock associated with septic peritonitis.