title: Angiogenesis in the latissimus dorsi muscle using different regimens of electrical stimulation and pharmaceutical support.
abstract: It is our contention that the prevention of ischemia-reperfusion injuries immediately after latissimus dorsi muscle (LDM) mobilization and enhancement of angiogenesis will be effective in improving cardiomyoplasty results. The investigations were performed on adult sheep. Three hours after LDM mobilization, various stages of leukocyte-endothelium interaction were revealed: leukocytes binding to the endothelium, leukocyte destruction of endothelium, and leukocytes leaving capillaries through gaps in the endothelium. Fifty-six days after mobilization various stages of necrosis were discernible. The area occupied by capillaries was 3.45 +/- 0.26% vs. 3.99 +/- 0.24% in control muscle; most of the endothelial cells exhibited morphologic degeneration. Electrical stimulation with 60 CPM actually decreased the capillary density to 2.15 +/- 0.7%, and most of the endothelial cells were damaged, with disrupted plasma membranes. Muscle subjected to 15 CPM increased the percent of capillaries to 5.01 +/- 0.56%, and endothelial cells appeared normal in ultrastructure. Pharmaceutical support prevented muscle damage and accelerated revascularization. After 56 days of autologous biological glue (ABG) application, the area occupied by capillaries was 5.57 +/- 0.24%. This increased to 8.47 +/- 0.72% when aprotinin (proteinase inhibitor) was added to ABG, and to 9.40 +/- 1.24% with pyrrolostatin (free radical scavenger). Both ABG application with aprotinin and electrical stimulation at 15 CPM prevent the LDM from postmobilization damage, and increase angiogenic potential.
authors.affiliation: Milwaukee Heart Institute, Sinai Samaritan Medical Center, Wisconsin, USA.
authors.forename: V S
authors.initials: VS
authors.lastname: Chekanov
authors.forename: M A
authors.initials: MA
authors.lastname: Maternowski
authors.forename: R
authors.initials: R
authors.lastname: Eisenstein
authors.forename: I
authors.initials: I
authors.lastname: Hernandez
authors.forename: V V
authors.initials: VV
authors.lastname: Nikolaychik
mesh_terms: D000818:Animals; D007611:Aprotinin / Q000494:pharmacology; D001706:Biopsy; D001798:Blood Proteins / Q000494:pharmacology; D002196:Capillaries / Q000737:chemistry / Q000473:pathology / Q000502:physiology; D018421:Cardiomyoplasty / Q000379:methods*; D004558:Electric Stimulation; D004567:Electrodes, Implanted; D004730:Endothelium, Vascular / Q000737:chemistry / Q000473:pathology / Q000502:physiology; D007150:Immunohistochemistry; D007962:Leukocytes / Q000473:pathology; D008854:Microscopy, Electron; D018485:Muscle Fibers, Skeletal / Q000648:ultrastructure; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000473:pathology / Q000601:surgery*; D015428:Myocardial Reperfusion Injury / Q000601:surgery*; D018919:Neovascularization, Physiologic / Q000187:drug effects* / Q000502:physiology*; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis; D015842:Serine Proteinase Inhibitors / Q000494:pharmacology; D012756:Sheep; D013524:Surgical Flaps; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D001798:Blood Proteins; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D015842:Serine Proteinase Inhibitors; D014841:von Willebrand Factor; D007611:Aprotinin