Antioxidants, bradykinin antagonists, and subatmospheric wound pressure also improve blood flow and affect the depth

of injury. Local endothelial interactions with neutrophils mediate some of the local inflammatory responses associated with the zone of stasis. Blocking leukocyte adherence with anti !"#$ or anti%intercellular adhesion molecule monoclonal antibodies improves tissue perfusion and tissue survival in animal models, thus indicating that treatment directed at the control of inflammation immediately after injury may spare the zone of stasis. &he last area is termed the zone of hyperemia, which is characterized by vasodilation from inflammation surrounding the burn wound. &his region contains clearly viable tissue from which the healing process begins and is generally not at risk for further necrosis. Antioxidants, bradykinin antagonists, and subatmospheric wound pressure also improve blood flow and affect the depth of injury. Local endothelial interactions with neutrophils mediate some of the local inflammatory responses associated with the zone of stasis. Blocking leukocyte adherence with anti !"#$ or anti%intercellular adhesion molecule monoclonal antibodies improves tissue perfusion and tissue survival in animal models, thus indicating that treatment directed at the control of inflammation immediately after injury may spare the zone of stasis. &he last area is termed the zone of hyperemia, which is characterized by vasodilation from inflammation surrounding the burn wound. &his region contains clearly viable tissue from which the healing process begins and is generally not at risk for further necrosis. Antioxidants, bradykinin antagonists, and subatmospheric wound pressure also improve blood flow and affect the depth of injury. Local endothelial interactions with neutrophils mediate some of the local inflammatory responses associated with the zone of stasis. Blocking leukocyte adherence with anti !"#$ or anti%intercellular adhesion molecule monoclonal antibodies improves tissue perfusion and tissue survival in animal models, thus indicating that treatment directed at the control of inflammation immediately after injury may spare the zone of stasis. &he last area is termed the zone of hyperemia, which is characterized by vasodilation from inflammation surrounding the burn wound. &his region contains clearly viable tissue from which the healing process begins and is generally not at risk for further necrosis. Antioxidants, bradykinin antagonists, and subatmospheric wound pressure also improve blood flow and affect the depth of injury. Local endothelial interactions with neutrophils mediate some of the local inflammatory responses associated with the zone of stasis. Blocking leukocyte adherence with anti !"#$ or anti%intercellular adhesion molecule monoclonal antibodies improves tissue perfusion and tissue survival in animal models, thus indicating that treatment directed at the control of inflammation immediately after injury may spare the zone of stasis. &he last area is termed the zone of hyperemia, which is characterized by vasodilation from inflammation surrounding the burn wound. &his region contains clearly viable tissue from which the healing process begins and is generally not at risk for further necrosis. Antioxidants, bradykinin antagonists, and subatmospheric wound pressure also improve blood flow and affect the depth of injury. Local endothelial interactions with neutrophils mediate some of the local inflammatory responses associated with the zone of stasis. Blocking leukocyte adherence with anti !"#$ or anti%intercellular adhesion molecule monoclonal antibodies improves tissue perfusion and tissue survival in animal models, thus indicating that treatment directed at the control of inflammation immediately after injury may spare the zone of stasis. &he last area is termed the zone of hyperemia, which is characterized by vasodilation from inflammation surrounding the burn wound. &his region contains clearly viable tissue from which the healing process begins and is generally not at risk for further necrosis.

Antioxidants, bradykinin antagonists, and subatmospheric wound pressure also improve blood flow and affect the depth of injury. Local endothelial interactions with neutrophils mediate some of the local inflammatory responses associated with the zone of stasis. Blocking leukocyte adherence with anti !"#$ or anti%intercellular adhesion molecule monoclonal antibodies improves tissue perfusion and tissue survival in animal models, thus indicating that treatment directed at the control of inflammation immediately after injury may spare the zone of stasis. &he last area is termed the zone of hyperemia, which is characterized by vasodilation from inflammation surrounding the burn wound. &his region contains clearly viable tissue from which the healing process begins and is generally not at risk for further necrosis. Antioxidants, bradykinin antagonists, and subatmospheric wound pressure also improve blood flow and affect the depth of injury. Local endothelial interactions with neutrophils mediate some of the local inflammatory responses associated with the zone of stasis. Blocking leukocyte adherence with anti !"#$ or anti%intercellular adhesion molecule monoclonal antibodies improves tissue perfusion and tissue survival in animal models, thus indicating that treatment directed at the control of inflammation immediately after injury may spare the zone of stasis. &he last area is termed the zone of hyperemia, which is characterized by vasodilation from inflammation surrounding the burn wound. &his region contains clearly viable tissue from which the healing process begins and is generally not at risk for further necrosis. Antioxidants, bradykinin antagonists, and subatmospheric wound pressure also improve blood flow and affect the depth of injury. Local endothelial interactions with neutrophils mediate some of the local inflammatory responses associated with the zone of stasis. Blocking leukocyte adherence with anti !"#$ or anti%intercellular adhesion molecule monoclonal antibodies improves tissue perfusion and tissue survival in animal models, thus indicating that treatment directed at the control of inflammation immediately after injury may spare the zone of stasis. &he last area is termed the zone of hyperemia, which is characterized by vasodilation from inflammation surrounding the burn wound. &his region contains clearly viable tissue from which the healing process begins and is generally not at risk for further necrosis. Antioxidants, bradykinin antagonists, and subatmospheric wound pressure also improve blood flow and affect the depth of injury. Local endothelial interactions with neutrophils mediate some of the local inflammatory responses associated with the zone of stasis. Blocking leukocyte adherence with anti !"#$ or anti%intercellular adhesion molecule monoclonal antibodies improves tissue perfusion and tissue survival in animal models, thus indicating that treatment directed at the control of inflammation immediately after injury may spare the zone of stasis. &he last area is termed the zone of hyperemia, which is characterized by vasodilation from inflammation surrounding the burn wound. &his region contains clearly viable tissue from which the healing process begins and is generally not at risk for further necrosis.