The value of lactate in the early clinical diagnosis of acute mesenteric arterial occlusion was evaluated in an animal model. The superior mesenteric artery of pigs (8-9 weeks old, 20-23 kg) was clamped for 1 h (group 2, n = 9) and 3 h (group 3, n = 6). Reperfusion was recorded for 2 h. Follow-up measurements were done in six animals (group 1). The systolic blood pressure was elevated significantly to about 18-40 mmHg in the initial phase of ischemia (P = 0.02). The intramucosal pHi measured tonometrically was decreased to below a value of 7.08 (P = 0.03), and the flow of superior mesenteric vein was reduced by about 90% ( P = 0.03) in groups 2 and 3. Within 30 min the lactate increased to about 2.05-3.8 mmol/l in the central venous blood sample and 2.8-4.8 mmol/l in the portal vein blood sample in 30 min. After 3 h of ischemia (group 3) the elevated lactate level returned to normal without any significant difference. In the reperfusion period (group 2) the systolic blood pressure stabilized at a depressed level (63-73 mmHg, P = 0.0054), and the flow of the superior mesenteric vein showed a reduction of 41% (P = 0.03). Intramucosal pHi and lactate values returned nearly completely to normal within 2 h. Reperfusion after 3 h of ischemia (group 3) caused marked shock without any sign of recovery at intramucosal pH or mesenteric vein flow. The lactate values increased for above the ischemic level. In conclusion, an elevated lactate level only correlates with the initial phase of acute mesenteric arterial occlusion. A normal lactate concentration cannot exclude the diagnosis of mesenteric ischemia. Reperfusion of the ischemic intestine is characterized by circulatory shock with secondary increased lactate concentration without predictive value for adequate intestinal perfusion.