RESUMO
Arterial blood lactate increases as a result of poor tissue perfusion. In splanchnic hypoperfusion, increased hepatic lactate uptake may delay increases in arterial blood lactate. We hypothesized that during isolated reduction of mesenteric blood flow, maintaining systemic blood volume and flow by fluid resuscitation may prevent systemic hyperlactatemia and therefore mask splanchnic ischemia. In a randomized study, 7 pigs were subjected to 4 h of splanchnic hypoperfusion by reducing the superior mesenteric artery blood flow to 4 +/- 0.8 mL/kg min [mean +/- standard deviation (SD)]. Seven pigs served as controls. Fluid was administered in order to keep the pulmonary artery occlusion pressure at 5 to 8 mm Hg. Cardiac output, portal vein, superior mesenteric, and hepatic arterial blood flow were measured every 30 min. Arterial, mixed venous, hepatic, portal, and mesenteric venous blood lactate, and jejunal mucosal pCO2 were measured at baseline and thereafter at 30-min intervals. The initial decrease in portal venous blood flow in the ischemic animals was subsequently counterbalanced by increasing hepatic arterial blood flow from 2 +/- 1 mL x kg(-1) x min(-1) at baseline to 11 +/- 4 mL x kg(-1) x min(-1) [after 4 h of ischemia; mean +/- standard deviation (SD), P = 0.02]. Jejunal mucosal- and mesenteric vein-arterial pCO2 gradients increased in the ischemic group from 11 +/- 8 mm Hg to 73 +/- 5 mm Hg (P = 0.02), and from 10 +/- 4 mm Hg to 44 +/- 8 mm Hg, respectively (P = 0.02). Mesenteric and portal venous lactate increased in the ischemic animals from 1.1 +/- 0.3 mmol/L to 4.2 +/- 1.0 mmol/L (P = 0.02), and from 1.0 +/- 0.2 mmol/L to 1.6 +/- 0.3 mmol/L, respectively (P = 0,03). While mesenteric lactate production and hepatic lactate uptake increased in parallel in the ischemic animals from 5 +/- 6 micromol x kg(-1) x min(-1) to 14 +/- 5 micromol x kg(-1) x min(-1) (P = 0.04), and from 14 +/- 7 micromol x kg(-1) x min(-1) to 24 +/- 6 micromol x kg(-1) x min(-1), respectively (P = 0.02), hepatic venous and arterial lactate, and apparent splanchnic lactate uptake and extraction did not change. We conclude that the hepatic lactate uptake increases in response to hepatic lactate influx. Systemic hyperlactatemia and increased hepatic venous lactate concentrations are late consequences of mesenteric hypoperfusion if hypovolemia is prevented. The net exchange of lactate across the splanchnic region does not reflect hepato-portal lactate kinetics in this animal model of intestinal hypoperfusion.
