Modulation of hemorrhagic shock by intestinal mucosal N-G-nitro-L-arginineand L-arginine in the anesthetized rat

Maintaining intestinal function protects against shock of various origins. Nitric oxide (NO) can protect tissues. The present research examined whethe r the presence of 50 CIM NG-nitro-L-arginine (NOLARG), a nitric oxide synth ase (NOS) inhibitor, or L-arginine (LARG), the substrate of NOS, in the jej unal lumen of the anesthetized rat could affect the progress of hemorrhagic shock. The jejunal lumen was perfused with saline containing C-14-inulin a nd (H2O)-H-3 to measure net H2O absorption and absorptive site blood flow ( ASBF), Luminal NOx (NO3- +NO2-) secretion into the gut effluent and blood p ressure (BP) were also measured, The animals were bled to and maintained at 40 mmHg for 60 min and then reinfused. Survival time was significantly dec reased in luminally-perfused NOLARG animals, but was significantly increase d in LARG perfused animals. Most deaths occurred during the hemorrhage peri ods. Animals perfused with LARG through the ileal lumen required significan tly less blood to be reinfused to maintain blood pressure during the hemorr hage periods. There were not significant differences in BP among surviving animals. Net H2O absorption and ASBF were significantly decreased only in N OLARG-perfused animals in the period just before and after reinfusion. Ther e were no significant differences in luminal NOx secretion among the groups . Thus, intestinal mucosal NOS substrates or antagonists modulate the progr ess of hemorrhagic shock, but the mechanism was not defined in these experi ments.