title: Ischemia and reperfusion induced multilamellar vesicles in isolated rabbit hearts: time correlation between morphometric data and metabolic alterations.
abstract: In normoxic hearts a limited number of multilamellar vesicles was found in both endothelial cells and myocytes. The total number of multilamellar vesicles observed in myocytes, particularly those extruded from mitochondria, significantly increased in hearts rendered ischemic for at least 60 mins. The number of multilamellar vesicles extruded from sarcolemma was increased in hearts reperfused after this period of ischemia. The number of multilamellar vesicles in or adjacent to lipid droplets was independent of the duration of ischemia. Multilamellar vesicles were similar in size and periodicity of the lamellae. It is proposed that the number of multilamellar vesicles can be used to quantitate ischemic membrane injury. The formation of multilamellar vesicles was significantly related in time to (a) the accumulation of arachidonic acid and total fatty acids; (b) a decrease in the tissue content of ATP and (c) the release of lactate dehydrogenase (LDH). No significant alterations in the total tissue content of triacylglycerols and phospholipids were detected. The amount of arachidonic acid accumulated in the hearts reflects the degradation of only a minor fraction of the phospholipid pool. Assuming a close relationship between phospholipid degradation, induction of multilamellar vesicles and loss of cellular integrity, the present findings might indicate that the loss of a small part of phospholipids might have serious pathophysiological consequences, as indicated by the morphological changes in cellular membranes and the release of cytoplasmic macromolecules.
authors.affiliation: Department of Physiology, University of Limburg, Maastricht, The Netherlands.
authors.forename: A H
authors.initials: AH
authors.lastname: Schrijvers
authors.forename: M J
authors.initials: MJ
authors.lastname: de Groot
authors.forename: V V
authors.initials: VV
authors.lastname: Heijnen
authors.forename: G J
authors.initials: GJ
authors.lastname: van der Vusse
authors.forename: P M
authors.initials: PM
authors.lastname: Frederik
authors.forename: R S
authors.initials: RS
authors.lastname: Reneman
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D003327:Coronary Disease / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D005227:Fatty Acids / Q000378:metabolism; D007425:Intracellular Membranes / Q000648:ultrastructure*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure*; D010743:Phospholipids / Q000378:metabolism; D011817:Rabbits; D013997:Time Factors; D014280:Triglycerides / Q000378:metabolism
chemical_list: D005227:Fatty Acids; D010743:Phospholipids; D014280:Triglycerides; D000255:Adenosine Triphosphate; D007770:L-Lactate Dehydrogenase