Do subcutaneous gas tensions closely track ileal mucosal gas tensions in a model of endotoxaemia without anaerobism?
Both subcutaneous tissue gas tensions and intestinal luminal carbon dioxide tensions are rapidly responsive during evolving hypodynamic endotoxic shock. Alterations in tissue gas tensions were not associated with dysoxia.
We demonstrate that MMP-2 activation is an ischemic event that extends into the reperfusion phase, while MLC1 degradation in response to ischemia/reperfusion is strictly a reperfusion event. MLC1 degradation during occlusion is prevented by a compensatory increase in the levels of TIMP-4.