The Experts below are selected from a list of 270 Experts worldwide ranked by ideXlab platform
Dominique Erni - One of the best experts on this subject based on the ideXlab platform.
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Hemoglobin vesicles improve wound healing and Tissue Survival in critically ischemic skin in mice.
American journal of physiology. Heart and circulatory physiology, 2009Co-Authors: Jan A. Plock, Andrej Banic, Nassim Rafatmehr, Dubravko Sinovcic, Jonas T. Schnider, Hiromi Sakai, Eishun Tsuchida, Dominique ErniAbstract:Local hypoxia, as due to trauma, surgery, or arterial occlusive disease, may severely jeopardize the Survival of the affected Tissue and its wound-healing capacity. Initially developed to replace b...
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The Choice of Anesthesia Influences Oxidative Energy Metabolism and Tissue Survival in Critically Ischemic Murine Skin
Journal of Surgical Research, 2009Co-Authors: Stefan Schlosser, Timo Spanholtz, Katrin Merz, Cyrill Dennler, Andrej Banic, Dominique Erni, Jan A. PlockAbstract:In surgical animal studies anesthesia is used regularly. Several reports in the literature demonstrate respiratory and cardiovascular side effects of anesthesiologic agents. The aim of this study was to compare two frequently used anesthesia cocktails (ketamine/xylazine [KX] versus medetomidine/climazolam/fentanyl [MCF]) in skin flap mouse models. Systemic blood values, local metabolic parameters, and surgical outcome should be analyzed in critical ischemic skin flap models. Systemic hypoxia was found in the animals undergoing KX anesthesia compared with normoxia in the MCF group (sO(2): 89.2% +/- 2.4% versus 98.5% +/- 1.2%, P < 0.01). Analysis of Tissue metabolism revealed impaired anaerobic oxygen metabolism and increased cellular damage in critical ischemic flap Tissue under KX anesthesia (lactate/pyruvate ratio: KX 349.86 +/- 282.38 versus MCF 64.53 +/- 18.63; P < 0.01 and glycerol: KX 333.50 +/- 83.91 micromol/L versus MCF 195.83 +/- 29.49 micromol/L; P < 0.01). After 6 d, different rates of flap Tissue necrosis could be detected (MCF 57% +/- 6% versus KX 68% +/- 6%, P < 0.01). In summary we want to point out that the type of anesthesia, the animal model and the goal of the study have to be well correlated. Comparing the effects of KX and MCF anesthesia in mice on surgical outcome was a novel aspect of our study.
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Die »falx lunatica« oder die unscharfe Demarkation von kritisch perfundiertem muskulokutanem Gewebe The »falx lunatica« and its demarcation in critically perfused musculocutaneous Tissue
2005Co-Authors: Yves Harder, Andrej Banic, Dominique Erni, M. Amon, Mirko Georgi, Rene Schramm, M. W. Laschke, Michael D. MengerAbstract:With the use of intravital microscopy and a chronic in vivo mouse model, we studied the demarcation of musculocutaneous flaps and evaluated microvascular determinants for Tissue Survival and necrosis. Chronic ischemia resulted in a transition zone, characterized by a red fringe and a distally adjacent white falx, which defined the demarcation by dividing the normal from the necrotic Tissue. Tissue Survival in the red zone was determined by hyperemia, as indicated by recovery of the transiently reduced functional capillary density (FCD), and capillary remodeling, including dilation, hyperperfusion and increased tortuosity. Neovascularisation was not observed over the 10-day observation period. The white rim, appearing as »falx lunatica«, showed a progressive decrease of FCD similar to that of the necrotic distal area, however, without desiccation and thus transparency of the Tissue. The development of the distinct zones of the critically ischemic Tissue could already be predicted by ptO2 analysis at the time of flap elevation. The »falx lunatica« evolved at a ptO2 between 6.2 ± 1.3mmHg and 3.8 ± 0.7 mmHg, while Tissue necrosis developed at < 3.8 ± 0.7 mmHg. Histogical analysis within the red fringe revealed an absence of leukocyte accumulation, whereas the »falx lunatica« demonstrated interstitial edema formation and nuclear rarefaction in muscle fibers, however, absence of necrosis. We thus demonstrate that ischemia-induced necrosis does not demarcate sharply from normal Tissue, but develops beside a fringe of Tissue with capillary remodeling an adjacent »falx lunatica« which survives despite nutritive capillary perfusion failure, probably by oxygen diffusion.
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Evolution of a “falx lunatica” in demarcation of critically ischemic myocutaneous Tissue
American journal of physiology. Heart and circulatory physiology, 2004Co-Authors: Yves Harder, Andrej Banic, Dominique Erni, M. Amon, Mirko Georgi, Michael D. MengerAbstract:Using intravital microscopy in a chronic in vivo mouse model, we studied the demarcation of myocutaneous flaps and evaluated microvascular determinants for Tissue Survival and necrosis. Chronic isc...
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Die »falx lunatica« oder die unscharfe Demarkation von kritisch perfundiertem muskulokutanem Gewebe
Chirurgisches Forum 2005, 1Co-Authors: Yves Harder, Andrej Banic, Dominique Erni, M. Amon, Mirko Georgi, Rene Schramm, M. W. Laschke, Michael D. MengerAbstract:With the use of intravital microscopy and a chronic in vivo mouse model, we studied the demarcation of musculocutaneous flaps and evaluated microvascular determinants for Tissue Survival and necrosis. Chronic ischemia resulted in a transition zone, characterized by a red fringe and a distally adjacent white falx, which defined the demarcation by dividing the normal from the necrotic Tissue. Tissue Survival in the red zone was determined by hyperemia, as indicated by recovery of the transiently reduced functional capillary density (FCD), and capillary remodeling, including dilation, hyperperfusion and increased tortuosity. Neovascularisation was not observed over the 10-day observation period. The white rim, appearing as »falx lunatica«, showed a progressive decrease of FCD similar to that of the necrotic distal area, however, without desiccation and thus transparency of the Tissue. The development of the distinct zones of the critically ischemic Tissue could already be predicted by ptO2 analysis at the time of flap elevation. The »falx lunatica« evolved at a ptO2 between 6.2 ± 1.3mmHg and 3.8 ± 0.7 mmHg, while Tissue necrosis developed at < 3.8 ± 0.7 mmHg. Histogical analysis within the red fringe revealed an absence of leukocyte accumulation, whereas the »falx lunatica« demon-strated interstitial edema formation and nuclear rarefaction in muscle fibers, however, absence of necrosis. We thus demonstrate that ischemia-induced necrosis does not demarcate sharply from normal Tissue, but develops beside a fringe of Tissue with capillary remodeling an adjacent »falx lunatica« which survives despite nutritive capillary perfusion failure, probably by oxygen diffusion.
David D. Roberts - One of the best experts on this subject based on the ideXlab platform.
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Thrombospondin-1 and CD47 limit cell and Tissue Survival of radiation injury.
The American journal of pathology, 2008Co-Authors: Jeff S. Isenberg, Fuminori Hyodo, Maria Tsokos, David A. Wink, Justin B. Maxhimer, Michael L. Pendrak, Lisa A. Ridnour, William Degraff, David D. RobertsAbstract:Radiation, a primary mode of cancer therapy, acutely damages cellular macromolecules and DNA and elicits stress responses that lead to cell death. The known cytoprotective activity of nitric oxide (NO) is blocked by thrombospondin-1, a potent antagonist of NO/cGMP signaling in ischemic soft Tissues, suggesting that thrombospondin-1 signaling via its receptor CD47 could correspondingly increase radiosensitivity. We show here that soft Tissues in thrombospondin-1-null mice are remarkably resistant to radiation injury. Twelve hours after 25-Gy hindlimb irradiation, thrombospondin-1-null mice showed significantly less cell death in both muscle and bone marrow. Two months after irradiation, skin and muscle units in null mice showed minimal histological evidence of radiation injury and near full retention of mitochondrial function. Additionally, both Tissue perfusion and acute vascular responses to NO were preserved in irradiated thrombospondin-1-null hindlimbs. The role of thrombospondin-1 in radiosensitization is specific because thrombospondin-2-null mice were not protected. However, mice lacking CD47 showed radioresistance similar to thrombospondin-1-null mice. Both thrombospondin-1- and CD47-dependent radiosensitization is cell autonomous because vascular cells isolated from the respective null mice showed dramatically increased Survival and improved proliferative capacity after irradiation in vitro. Therefore, thrombospondin-1/CD47 antagonists may have selective radioprotective activity for normal Tissues.
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Gene silencing of CD47 and antibody ligation of thrombospondin-1 enhance ischemic Tissue Survival in a porcine model: implications for human disease.
Annals of surgery, 2008Co-Authors: Jeff S. Isenberg, Martin J. Romeo, Justin B. Maxhimer, Jeremy Smedley, William A. Frazier, David D. RobertsAbstract:Background:Insufficient Tissue perfusion underlies many acute and chronic diseases. Tissue perfusion in turn requires adequate blood flow, determined in large part by the relative state of relaxation or constriction of arterial vessels. Nitric oxide (NO) produced by vascular cells modulates blood fl
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Thrombospondin-1 limits ischemic Tissue Survival by inhibiting nitric oxide–mediated vascular smooth muscle relaxation
Blood, 2006Co-Authors: Jeff S. Isenberg, Fuminori Hyodo, Ken-ichiro Matsumoto, Martin J. Romeo, Mones Abu-asab, Maria Tsokos, Periannan Kuppusamy, David A. Wink, Murali C. Krishna, David D. RobertsAbstract:The nitric oxide (NO)/cGMP pathway, by relaxing vascular smooth muscle cells, is a major physiologic regulator of Tissue perfusion. We now identify thrombospondin-1 as a potent antagonist of NO for regulating F-actin assembly and myosin light chain phosphorylation in vascular smooth muscle cells. Thrombospondin-1 prevents NO-mediated relaxation of precontracted vascular smooth muscle cells in a collagen matrix. Functional magnetic resonance imaging demonstrated that an NO-mediated increase in skeletal muscle perfusion was enhanced in thrombospondin-1–null relative to wild-type mice, implicating endogenous thrombospondin-1 as a physiologic antagonist of NO-mediated vasodilation. Using a random myocutaneous flap model for ischemic injury, Tissue Survival was significantly enhanced in thrombospondin-1–null mice. Improved flap Survival correlated with increased recovery of oxygen levels in the ischemic Tissue of thrombospondin-1–null mice as measured by electron paramagnetic resonance oximetry. These findings demonstrate an important antag-onistic relation between NO/cGMP signaling and thrombospondin-1 in vascular smooth muscle cells to regulate vascular tone and Tissue perfusion.
Andrej Banic - One of the best experts on this subject based on the ideXlab platform.
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Hemoglobin vesicles improve wound healing and Tissue Survival in critically ischemic skin in mice.
American journal of physiology. Heart and circulatory physiology, 2009Co-Authors: Jan A. Plock, Andrej Banic, Nassim Rafatmehr, Dubravko Sinovcic, Jonas T. Schnider, Hiromi Sakai, Eishun Tsuchida, Dominique ErniAbstract:Local hypoxia, as due to trauma, surgery, or arterial occlusive disease, may severely jeopardize the Survival of the affected Tissue and its wound-healing capacity. Initially developed to replace b...
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The Choice of Anesthesia Influences Oxidative Energy Metabolism and Tissue Survival in Critically Ischemic Murine Skin
Journal of Surgical Research, 2009Co-Authors: Stefan Schlosser, Timo Spanholtz, Katrin Merz, Cyrill Dennler, Andrej Banic, Dominique Erni, Jan A. PlockAbstract:In surgical animal studies anesthesia is used regularly. Several reports in the literature demonstrate respiratory and cardiovascular side effects of anesthesiologic agents. The aim of this study was to compare two frequently used anesthesia cocktails (ketamine/xylazine [KX] versus medetomidine/climazolam/fentanyl [MCF]) in skin flap mouse models. Systemic blood values, local metabolic parameters, and surgical outcome should be analyzed in critical ischemic skin flap models. Systemic hypoxia was found in the animals undergoing KX anesthesia compared with normoxia in the MCF group (sO(2): 89.2% +/- 2.4% versus 98.5% +/- 1.2%, P < 0.01). Analysis of Tissue metabolism revealed impaired anaerobic oxygen metabolism and increased cellular damage in critical ischemic flap Tissue under KX anesthesia (lactate/pyruvate ratio: KX 349.86 +/- 282.38 versus MCF 64.53 +/- 18.63; P < 0.01 and glycerol: KX 333.50 +/- 83.91 micromol/L versus MCF 195.83 +/- 29.49 micromol/L; P < 0.01). After 6 d, different rates of flap Tissue necrosis could be detected (MCF 57% +/- 6% versus KX 68% +/- 6%, P < 0.01). In summary we want to point out that the type of anesthesia, the animal model and the goal of the study have to be well correlated. Comparing the effects of KX and MCF anesthesia in mice on surgical outcome was a novel aspect of our study.
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Die »falx lunatica« oder die unscharfe Demarkation von kritisch perfundiertem muskulokutanem Gewebe The »falx lunatica« and its demarcation in critically perfused musculocutaneous Tissue
2005Co-Authors: Yves Harder, Andrej Banic, Dominique Erni, M. Amon, Mirko Georgi, Rene Schramm, M. W. Laschke, Michael D. MengerAbstract:With the use of intravital microscopy and a chronic in vivo mouse model, we studied the demarcation of musculocutaneous flaps and evaluated microvascular determinants for Tissue Survival and necrosis. Chronic ischemia resulted in a transition zone, characterized by a red fringe and a distally adjacent white falx, which defined the demarcation by dividing the normal from the necrotic Tissue. Tissue Survival in the red zone was determined by hyperemia, as indicated by recovery of the transiently reduced functional capillary density (FCD), and capillary remodeling, including dilation, hyperperfusion and increased tortuosity. Neovascularisation was not observed over the 10-day observation period. The white rim, appearing as »falx lunatica«, showed a progressive decrease of FCD similar to that of the necrotic distal area, however, without desiccation and thus transparency of the Tissue. The development of the distinct zones of the critically ischemic Tissue could already be predicted by ptO2 analysis at the time of flap elevation. The »falx lunatica« evolved at a ptO2 between 6.2 ± 1.3mmHg and 3.8 ± 0.7 mmHg, while Tissue necrosis developed at < 3.8 ± 0.7 mmHg. Histogical analysis within the red fringe revealed an absence of leukocyte accumulation, whereas the »falx lunatica« demonstrated interstitial edema formation and nuclear rarefaction in muscle fibers, however, absence of necrosis. We thus demonstrate that ischemia-induced necrosis does not demarcate sharply from normal Tissue, but develops beside a fringe of Tissue with capillary remodeling an adjacent »falx lunatica« which survives despite nutritive capillary perfusion failure, probably by oxygen diffusion.
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Evolution of a “falx lunatica” in demarcation of critically ischemic myocutaneous Tissue
American journal of physiology. Heart and circulatory physiology, 2004Co-Authors: Yves Harder, Andrej Banic, Dominique Erni, M. Amon, Mirko Georgi, Michael D. MengerAbstract:Using intravital microscopy in a chronic in vivo mouse model, we studied the demarcation of myocutaneous flaps and evaluated microvascular determinants for Tissue Survival and necrosis. Chronic isc...
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Die »falx lunatica« oder die unscharfe Demarkation von kritisch perfundiertem muskulokutanem Gewebe
Chirurgisches Forum 2005, 1Co-Authors: Yves Harder, Andrej Banic, Dominique Erni, M. Amon, Mirko Georgi, Rene Schramm, M. W. Laschke, Michael D. MengerAbstract:With the use of intravital microscopy and a chronic in vivo mouse model, we studied the demarcation of musculocutaneous flaps and evaluated microvascular determinants for Tissue Survival and necrosis. Chronic ischemia resulted in a transition zone, characterized by a red fringe and a distally adjacent white falx, which defined the demarcation by dividing the normal from the necrotic Tissue. Tissue Survival in the red zone was determined by hyperemia, as indicated by recovery of the transiently reduced functional capillary density (FCD), and capillary remodeling, including dilation, hyperperfusion and increased tortuosity. Neovascularisation was not observed over the 10-day observation period. The white rim, appearing as »falx lunatica«, showed a progressive decrease of FCD similar to that of the necrotic distal area, however, without desiccation and thus transparency of the Tissue. The development of the distinct zones of the critically ischemic Tissue could already be predicted by ptO2 analysis at the time of flap elevation. The »falx lunatica« evolved at a ptO2 between 6.2 ± 1.3mmHg and 3.8 ± 0.7 mmHg, while Tissue necrosis developed at < 3.8 ± 0.7 mmHg. Histogical analysis within the red fringe revealed an absence of leukocyte accumulation, whereas the »falx lunatica« demon-strated interstitial edema formation and nuclear rarefaction in muscle fibers, however, absence of necrosis. We thus demonstrate that ischemia-induced necrosis does not demarcate sharply from normal Tissue, but develops beside a fringe of Tissue with capillary remodeling an adjacent »falx lunatica« which survives despite nutritive capillary perfusion failure, probably by oxygen diffusion.
Michael D. Menger - One of the best experts on this subject based on the ideXlab platform.
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Die »falx lunatica« oder die unscharfe Demarkation von kritisch perfundiertem muskulokutanem Gewebe The »falx lunatica« and its demarcation in critically perfused musculocutaneous Tissue
2005Co-Authors: Yves Harder, Andrej Banic, Dominique Erni, M. Amon, Mirko Georgi, Rene Schramm, M. W. Laschke, Michael D. MengerAbstract:With the use of intravital microscopy and a chronic in vivo mouse model, we studied the demarcation of musculocutaneous flaps and evaluated microvascular determinants for Tissue Survival and necrosis. Chronic ischemia resulted in a transition zone, characterized by a red fringe and a distally adjacent white falx, which defined the demarcation by dividing the normal from the necrotic Tissue. Tissue Survival in the red zone was determined by hyperemia, as indicated by recovery of the transiently reduced functional capillary density (FCD), and capillary remodeling, including dilation, hyperperfusion and increased tortuosity. Neovascularisation was not observed over the 10-day observation period. The white rim, appearing as »falx lunatica«, showed a progressive decrease of FCD similar to that of the necrotic distal area, however, without desiccation and thus transparency of the Tissue. The development of the distinct zones of the critically ischemic Tissue could already be predicted by ptO2 analysis at the time of flap elevation. The »falx lunatica« evolved at a ptO2 between 6.2 ± 1.3mmHg and 3.8 ± 0.7 mmHg, while Tissue necrosis developed at < 3.8 ± 0.7 mmHg. Histogical analysis within the red fringe revealed an absence of leukocyte accumulation, whereas the »falx lunatica« demonstrated interstitial edema formation and nuclear rarefaction in muscle fibers, however, absence of necrosis. We thus demonstrate that ischemia-induced necrosis does not demarcate sharply from normal Tissue, but develops beside a fringe of Tissue with capillary remodeling an adjacent »falx lunatica« which survives despite nutritive capillary perfusion failure, probably by oxygen diffusion.
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Evolution of a “falx lunatica” in demarcation of critically ischemic myocutaneous Tissue
American journal of physiology. Heart and circulatory physiology, 2004Co-Authors: Yves Harder, Andrej Banic, Dominique Erni, M. Amon, Mirko Georgi, Michael D. MengerAbstract:Using intravital microscopy in a chronic in vivo mouse model, we studied the demarcation of myocutaneous flaps and evaluated microvascular determinants for Tissue Survival and necrosis. Chronic isc...
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Die »falx lunatica« oder die unscharfe Demarkation von kritisch perfundiertem muskulokutanem Gewebe
Chirurgisches Forum 2005, 1Co-Authors: Yves Harder, Andrej Banic, Dominique Erni, M. Amon, Mirko Georgi, Rene Schramm, M. W. Laschke, Michael D. MengerAbstract:With the use of intravital microscopy and a chronic in vivo mouse model, we studied the demarcation of musculocutaneous flaps and evaluated microvascular determinants for Tissue Survival and necrosis. Chronic ischemia resulted in a transition zone, characterized by a red fringe and a distally adjacent white falx, which defined the demarcation by dividing the normal from the necrotic Tissue. Tissue Survival in the red zone was determined by hyperemia, as indicated by recovery of the transiently reduced functional capillary density (FCD), and capillary remodeling, including dilation, hyperperfusion and increased tortuosity. Neovascularisation was not observed over the 10-day observation period. The white rim, appearing as »falx lunatica«, showed a progressive decrease of FCD similar to that of the necrotic distal area, however, without desiccation and thus transparency of the Tissue. The development of the distinct zones of the critically ischemic Tissue could already be predicted by ptO2 analysis at the time of flap elevation. The »falx lunatica« evolved at a ptO2 between 6.2 ± 1.3mmHg and 3.8 ± 0.7 mmHg, while Tissue necrosis developed at < 3.8 ± 0.7 mmHg. Histogical analysis within the red fringe revealed an absence of leukocyte accumulation, whereas the »falx lunatica« demon-strated interstitial edema formation and nuclear rarefaction in muscle fibers, however, absence of necrosis. We thus demonstrate that ischemia-induced necrosis does not demarcate sharply from normal Tissue, but develops beside a fringe of Tissue with capillary remodeling an adjacent »falx lunatica« which survives despite nutritive capillary perfusion failure, probably by oxygen diffusion.
Jeff S. Isenberg - One of the best experts on this subject based on the ideXlab platform.
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Thrombospondin-1 and CD47 limit cell and Tissue Survival of radiation injury.
The American journal of pathology, 2008Co-Authors: Jeff S. Isenberg, Fuminori Hyodo, Maria Tsokos, David A. Wink, Justin B. Maxhimer, Michael L. Pendrak, Lisa A. Ridnour, William Degraff, David D. RobertsAbstract:Radiation, a primary mode of cancer therapy, acutely damages cellular macromolecules and DNA and elicits stress responses that lead to cell death. The known cytoprotective activity of nitric oxide (NO) is blocked by thrombospondin-1, a potent antagonist of NO/cGMP signaling in ischemic soft Tissues, suggesting that thrombospondin-1 signaling via its receptor CD47 could correspondingly increase radiosensitivity. We show here that soft Tissues in thrombospondin-1-null mice are remarkably resistant to radiation injury. Twelve hours after 25-Gy hindlimb irradiation, thrombospondin-1-null mice showed significantly less cell death in both muscle and bone marrow. Two months after irradiation, skin and muscle units in null mice showed minimal histological evidence of radiation injury and near full retention of mitochondrial function. Additionally, both Tissue perfusion and acute vascular responses to NO were preserved in irradiated thrombospondin-1-null hindlimbs. The role of thrombospondin-1 in radiosensitization is specific because thrombospondin-2-null mice were not protected. However, mice lacking CD47 showed radioresistance similar to thrombospondin-1-null mice. Both thrombospondin-1- and CD47-dependent radiosensitization is cell autonomous because vascular cells isolated from the respective null mice showed dramatically increased Survival and improved proliferative capacity after irradiation in vitro. Therefore, thrombospondin-1/CD47 antagonists may have selective radioprotective activity for normal Tissues.
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Gene silencing of CD47 and antibody ligation of thrombospondin-1 enhance ischemic Tissue Survival in a porcine model: implications for human disease.
Annals of surgery, 2008Co-Authors: Jeff S. Isenberg, Martin J. Romeo, Justin B. Maxhimer, Jeremy Smedley, William A. Frazier, David D. RobertsAbstract:Background:Insufficient Tissue perfusion underlies many acute and chronic diseases. Tissue perfusion in turn requires adequate blood flow, determined in large part by the relative state of relaxation or constriction of arterial vessels. Nitric oxide (NO) produced by vascular cells modulates blood fl
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Thrombospondin-1 limits ischemic Tissue Survival by inhibiting nitric oxide–mediated vascular smooth muscle relaxation
Blood, 2006Co-Authors: Jeff S. Isenberg, Fuminori Hyodo, Ken-ichiro Matsumoto, Martin J. Romeo, Mones Abu-asab, Maria Tsokos, Periannan Kuppusamy, David A. Wink, Murali C. Krishna, David D. RobertsAbstract:The nitric oxide (NO)/cGMP pathway, by relaxing vascular smooth muscle cells, is a major physiologic regulator of Tissue perfusion. We now identify thrombospondin-1 as a potent antagonist of NO for regulating F-actin assembly and myosin light chain phosphorylation in vascular smooth muscle cells. Thrombospondin-1 prevents NO-mediated relaxation of precontracted vascular smooth muscle cells in a collagen matrix. Functional magnetic resonance imaging demonstrated that an NO-mediated increase in skeletal muscle perfusion was enhanced in thrombospondin-1–null relative to wild-type mice, implicating endogenous thrombospondin-1 as a physiologic antagonist of NO-mediated vasodilation. Using a random myocutaneous flap model for ischemic injury, Tissue Survival was significantly enhanced in thrombospondin-1–null mice. Improved flap Survival correlated with increased recovery of oxygen levels in the ischemic Tissue of thrombospondin-1–null mice as measured by electron paramagnetic resonance oximetry. These findings demonstrate an important antag-onistic relation between NO/cGMP signaling and thrombospondin-1 in vascular smooth muscle cells to regulate vascular tone and Tissue perfusion.
