Capillary Dysfunction in Striated Muscle Ischemia/Reperfusion

Menger, Michael D.; Rücker, Martin; Vollmar, Brigitte

doi:10.1097/00024382-199707000-00002

Cited by 151 publications

(101 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The question to which extent reduced leakage is just the consequence of decreased leukocyte accumulation and to which extent the reduced perfusion failure is just a consequence of reduced leakage and thus less interstitial tissue pressure 34 or direct results of EPO specific action on the microvasculature (for references, see 7), requires further analysis, which is beyond the scope of the present study. However, it is most reasonable to state for the injured muscle tissue that EPO functions as a pleiotropic factor and exerts protection by interfering with the mechanisms underlying microvascular injury and inflammatory breakdown of endothelial integrity.…”

Section: Microcirculation Of Muscle Tissue After Crush Injury and Epomentioning

confidence: 97%

Erythropoietin improves functional and histological recovery of traumatized skeletal muscle tissue

Rotter

Menshykova

Winkler

et al. 2008

Journal Orthopaedic Research

Self Cite

View full text Add to dashboard Cite

Apart from its hematopoietic effect, erythropoietin (EPO) is known as pleiotropic cytokine with anti-inflammatory and antiapoptotic properties. Here, we evaluated for the first time the EPO-dependent regeneration capacity in an in vivo rat model of skeletal muscle trauma. A myoblast cell line was used to study the effect of EPO on serum deprivation-induced cell apoptosis in vitro. A crush injury was performed to the left soleus muscle in 80 rats treated with either EPO or saline. Muscle recovery was assessed by analysis of contraction capacities. Intravital microscopy, BrdU/laminin double immunohistochemistry and cleaved caspase-3 immunohistochemistry of muscle tissue on days 1, 7, 14, and 42 posttrauma served for assessment of local microcirculation, tissue integrity, and cell proliferation. Serum deprivation-induced myoblast apoptosis of 23.9 AE 1.5% was reduced by EPO to 17.2 AE 0.8%. Contraction force analysis in the EPO-treated animals revealed significantly improved muscle strength with 10-20% higher values of twitch and tetanic forces over the 42-day observation period. EPO-treated muscle tissue displayed improved functional capillary density as well as reduced leukocytic response and consecutively macromolecular leakage over day 14. Concomitantly, muscle histology showed significantly increased numbers of BrdU-positive satellite cells and interstitial cells as well as slightly lower counts of cleaved caspase-3-positive interstitial cells. EPO results in faster and better regeneration of skeletal muscle tissue after severe trauma and goes along with improved microcirculation. Thus, EPO, a compound established as clinically safe, may represent a promising therapeutic option to optimize the posttraumatic course of muscle tissue healing.

show abstract

Section: Microcirculation Of Muscle Tissue After Crush Injury and Epomentioning

confidence: 97%

Erythropoietin improves functional and histological recovery of traumatized skeletal muscle tissue

Rotter

Menshykova

Winkler

et al. 2008

Journal Orthopaedic Research

Self Cite

View full text Add to dashboard Cite

show abstract

“…However, immunolabeling for NOS III protein remained intense in the vasculature of patches of muscle until 8 hours reperfusion. Loss of NOS III activity, caused by either loss or inactivation of NOS III protein, would be expected to result in vasoconstriction, neutrophil extravasation, and edema, which could contribute to cell death by extending the episode of ischemia through the "no-reflow" phenomenon (Ames et al, 1968;Kanwar and Kubes, 1995;Kubes, 1993;Menger et al 1997). Pharmacological treatments that increase NO levels early during reperfusion or ischemic pre-conditioning (which is in part NOS III-mediated), protect skeletal muscle from IRmediated constriction and edema (Akimitsu et al, 1995;Chen et al, 1998;Huk et al, 1997;Pudupakkam et al, 1998).…”

Section: Messina Et Almentioning

confidence: 99%

Localization of Inducible Nitric Oxide Synthase to Mast Cells During Ischemia/Reperfusion Injury of Skeletal Muscle

Messina

Knight

Dowsing

et al. 2000

Laboratory Investigation

View full text Add to dashboard Cite

SUMMARY:Nitric oxide contributes to tissue necrosis after ischemia-reperfusion (IR). A biochemical and immunohistochemical study was made of the amounts and localization of both Ca ϩϩ -independent nitric oxide synthase (NOS) II and Ca ϩϩ -dependent (NOS I and NOS III) in rat skeletal muscle after ischemia and 0.5, 2, 8, 16, and 24 hours reperfusion. NOS II was not detectable in control muscle or during ischemia, was first detected after 2 hours reperfusion, increased further by 8 hours, and remained elevated at 24 hours. Both NOS II and nitrotyrosine, a marker of peroxynitrite formation, were localized exclusively to mast cells except after 24 hours reperfusion when some macrophages and neutrophils also showed positive immunoreactivity. Mast cells underwent extensive degranulation during reperfusion. NOS I was not detected in injured or control muscle. The level of NOS III, which was localized to the endothelium of blood vessels of all sizes in control muscle, decreased progressively during ischemia and reperfusion to reach undetectable levels after 16 hours reperfusion. These findings indicate that most of the nitric oxide formed during IR injury is generated by NOS II located almost exclusively in mast cells. (Lab Invest 2000, 80:423-431).

show abstract

“…Free radicals and cytokines generated by IR injury trigger neutrophil recruitment and adhesion, capillary plugging, endothelial cell swelling, and the eventual collapse of the capillary lumen, leading to a phenomenon called capillary no-reflow. 36,60 Capillary no-reflow results in arterial venous shunting, 42 and a significant reduction of nutritive blood flow within the affected capillary. Importantly, arterial venous shunting and collapsed capillaries have been observed in the limbs of patients with CRPS.…”

Section: Role Of Microvascular Dysfunctionmentioning

confidence: 99%

Complex Regional Pain Syndrome: What's in a Name?

Coderre

2011

The Journal of Pain

View full text Add to dashboard Cite

Within a two year period in the 1940's, two Boston physicians published dramatically opposing views on the underlying nature of a syndrome now known as complex regional pain syndrome (CRPS). Evans suggested, in several papers in [1946][1947], that sympathetic reflexes maintain pain and dystrophy in affected limbs. Foisie, in 1947, suggested arterial vasospasms were key in the etiology of this pain syndrome. Evans' hypothesis established the nomenclature for this syndrome for 60 years, and his term "reflex sympathetic dystrophy" guided clinical treatment and research activities over the same period. Foisie's proposed nomenclature was unrecognized, and had virtually no impact on the field. Recent evidence suggests that Evans' contribution to the field may have in fact lead clinicians and researchers astray all those years. This focus article on CRPS compares recent observations with these 2 earlier theories and asks the question --what if we had adopted Foisie's nomenclature from the beginning?

show abstract

Capillary Dysfunction in Striated Muscle Ischemia/Reperfusion

Cited by 151 publications

References 0 publications

Erythropoietin improves functional and histological recovery of traumatized skeletal muscle tissue

Erythropoietin improves functional and histological recovery of traumatized skeletal muscle tissue

Localization of Inducible Nitric Oxide Synthase to Mast Cells During Ischemia/Reperfusion Injury of Skeletal Muscle

Complex Regional Pain Syndrome: What's in a Name?

Contact Info

Product

Resources

About