CO2 in static mesenteric venous blood during intestinal ischemia and ischemic preconditioning in rats

During intestinal ischemia, CO2 accumulates in tissue as a result of bicarb onate buffering of anaerobic acid generation. Previous studies have shown t hat nitric oxide (NO) generated during ischemic preconditioning acts as a g lycolytic modulator, thus decreasing tissue lactate production. We studied If ischemic preconditioning induces NO-dependent changes in static mesenter ic venous blood Pco(2) values and CO2 accumulation during intestinal Ischem ia. Superior mesenteric venous (smv) acid base variables were studied in 4 groups of rats: a control group (C), an ischemic (90-min period of flow arr est) group (I), an ischemic group subjected to previous ischemic preconditi oning (P), and an ischemic group subjected to previous ischemic preconditio ning in which nitric oxide synthase (NOS) was inhibited by N-nitro-L-argini ne methyl ester (L-NAME) administration (P+N). Preconditioning Induced acid osis in smv blood during reperfusion before ischemia, but this effect was c ounteracted by L-NAME. Group P showed the lowest values of end-ischemic tis sue lactate, smv blood CO2 accumulation, and LDH In perfusate, whereas grou p P+N showed the highest level of LDH In perfusate but the lowest end-ische mic smv blood Pco(2) and acidity. We conclude that lower ischemic CO2 accum ulation in static smv blood, but not lower end-ischemic Pco(2), was related with the protective effect of Ischemic preconditioning in our rat model. T hus, the use of stagnant smv blood Pco(2) as an indicative of intestinal dy soxia can lead to misinterpretations if a broader acid-base picture is not considered.