title: Purkinje fibers after myocardial ischemia-reperfusion.
abstract: The purpose of this study was to evaluate the effects of ischemia-reperfusion on Purkinje fibers, comparing them with the adjacent cardiomyocytes. In a model of heterotopic heart transplantation in pigs, the donor heart was subjected to 2 hours of ischemia (n=9), preserved in cold saline, and subjected to 24 hours of ischemia with preservation in Wisconsin solution, alone (n=6), or with an additive consisting of calcium (n=4), Nicorandil (n=6) or Trolox (n=7). After 2 hours of reperfusion, we evaluated the recovery of cardiac electrical activity and took samples of ventricular myocardium for morphological study. The prolonged ischemia significantly affected atrial automaticity and A-V conduction in all the groups subjected to 24 hours of ischemia, as compared to 2 hours. There were no significant differences among the groups that underwent prolonged ischemia. Changes in the electrical activity did not correlate with the morphological changes. In the Purkinje fibers, ischemia-reperfusion produced a marked decrease in the glycogen content in all the groups. In the gap junctions the immunolabeling of connexin-43 decreased significantly, adopting a dispersed distribution, and staining the sarcolemma adjacent to the connective tissue. These changes were less marked in the group preserved exclusively with Wisconsin solution, despite the prolonged ischemia. The addition of other substances did not improve the altered morphology. In all the groups, the injury appeared to be more prominent in the Purkinje fibers than in the neighboring cardiomyocytes, indicating the greater susceptibility of the former to ischemia-reperfusion injury.
authors: Center for Tissue Engineering and Regenerative Medicine, Human Histology and Pathology Department, Faculty of Health Sciences, Rey Juan Carlos University, Madrid, Spain. soledad.garcia@urjc.es.
authors: Soledad
authors: S
authors: García Gómez-Heras
authors: Department of Experimental Surgery, Puerta de Hierro. Majadahonda University Hospital, Majadahonda. Madrid, Spain.
authors: Lourdes
authors: L
authors: Álvarez-Ayuso
authors: Department of Hospital Pharmacy, Puerta de Hierro, Majadahonda University Hospital, Majadahonda. Madrid, Spain.
authors: Amalia
authors: A
authors: Torralba Arranz
authors: Center for Tissue Engineering and Regenerative Medicine, Human Histology and Pathology Department, Faculty of Health Sciences, Rey Juan Carlos University, Madrid, Spain.
authors: Héctor
authors: H
authors: Fernández-García
mesh_terms: D000199:Actins / Q000378:metabolism; D000241:Adenosine; D000493:Allopurinol; D000818:Animals; D018031:Connexin 43 / Q000378:metabolism; D003893:Desmin / Q000378:metabolism; D055724:Electrophysiological Phenomena; D005978:Glutathione; D006003:Glycogen / Q000378:metabolism; D016027:Heart Transplantation / Q000009:adverse effects*; D007328:Insulin; D015428:Myocardial Reperfusion Injury / Q000473:pathology* / Q000503:physiopathology*; D032383:Myocytes, Cardiac / Q000473:pathology / Q000502:physiology; D019188:Organ Preservation Solutions; D011690:Purkinje Fibers / Q000293:injuries / Q000473:pathology* / Q000503:physiopathology*; D011887:Raffinose; D034421:Sus scrofa
chemical_list: D000199:Actins; D018031:Connexin 43; D003893:Desmin; D007328:Insulin; D019188:Organ Preservation Solutions; C055206:University of Wisconsin-lactobionate solution; D000493:Allopurinol; D006003:Glycogen; D005978:Glutathione; D000241:Adenosine; D011887:Raffinose