RESUMO
Ischemia reperfusion injury [IR injury] is a common problem in clinical conditions. Researches have frequently revealed that ATP- sensitive potassium [K[ATP]] channels and nitric oxide plays a role in protection against ischemic injury in skeletal muscle. The present study aimed at evaluating the possible link between this two pathways. Sixty-eight male wistar rats, were pretreated with saline, diazoxide [K[ATP] opener; 45 mg/Kg, IP], glibenclamide [K[ATP] inhibitor; 5 mg/Kg], or L-NAME [iNOS inhibitor; 20 mg/Kg, IP] before 3 h ischemia and 2 h reperfusion. Activities of antioxidant enzymes superoxide dismutase [SOD] and catalase [CAT], and the level of malondialdehyde [MDA] and expression of iNOS were measured in muscle tissue. Tissue MDA content was significantly increased by IR [p < 0.001]. Diazoxide significantly decreased the IR-induced elevation of tissue MDA level [p < 0.05] and Glibenclamide increased MDA [p < 0.05 vs. IR group]. L-NAME inhibited the effect of diazoxide on decreasing MDA [p < 0.01 vs., diazoxide+IR group] and IR decreased the activity of SOD and CAT [p < 0.01], while pretreatment with diazoxide increased activity of SOD and CAT [p < 0.01]. Glibenclamide decreased SOD and CAT activity after IR [p < 0.05]. L-NAME pretreatment in diazoxide-treated rats abolished the effect of diazoxide on increasing the activity of SOD and CAT [p < 0.05 vs. Diaz+IR]. Expression of iNOS was increased by IR [p < 0.01 vs. Sham group]. Diazoxide significantly decreased iNOS expression after IR [p < 0.05 vs. IR]. L-NAME significantly decreased iNOS expression after IR [p < 0.01] in diazoxide-treated rats [p < 0.01 vs. Diaz+IR]
RESUMO
Patients suffering from Thrornboangiitis Obliterans [TAO] or Buerger's disease have endothelial cell dysfunction and the severity of the disease lies in the need for amputation in more than a quarter of all sufferers. The aim of present study was to determine whether granulocyte colony-stimulating factor mobilized autologous bone-marrow derived mononuclear cells transplantation improves endothelial dysfunction in these patients. Circulating mononuclear cells containing endothelial progenitor cells were obtained from patients following bone-marrow mobilization with granulocyte colony stimulating factor. Mononuclear cells and CD34+ cells were enumerated prior to intramuscular injection into the affected limbs. In this pilot study, autologous bone-marrow derived mononuclear cell therapy collected from peripheral blood following granulocytes colony stimulating factor [G-CSF] mobilization was effective, safe and resulted in sustained clinical results for patients with severe peripheral occlusive arterial diseases