system
Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Animals, Complement Activation, Complement C1 Inactivator Proteins, Complement C3, Eicosanoids, Humans, Intestinal Mucosa, Intestines, Male, Mice, Mice, Inbred BALB C, Mice, Inbred C57BL, Myenteric Plexus, Neutrophils, Nitric Oxide Synthase, Peroxidase, Reperfusion Injury, Splanchnic Circulation.
user
Does human C1 esterase inhibitor attenuate murine mesenteric ischemia/reperfusion induced local organ injury? Context: Complement activation contributes to ischemia and reperfusion (IR)-initiated organ injury. C1 inhibitor (C1 Inh) inhibits the earliest steps of the classical and the mannose binding lectin pathways. To determine whether C1 Inh prevented tissue injury, we performed intestinal IR experiments in BALB/c and C57BL/6 mice. We found that C1 Inh limits mucosal injury in the two strains in a dose dependent manner. Tissue damage was associated with the accumulation of functional polymorphonuclear cells, which was reduced following C1 Inh treatment. Constitutive nitric oxide synthase activity correlated with the development of injury in the C57BL/6 but not in the BALB/c mouse.
assistant
These findings emphasize the importance of complement activation in ischemia/reperfusion and highlight the potential therapeutic use of C1 Inh in limiting or preventing damage caused by IR. Final Decision: yes