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Mechanisms of myocardial reperfusion injury.
Modulation of the inflammatory response constitutes a potential pharmacological target to protect the heart from reperfusion injury and should aid in development of pharmacological interventions to selectively or collectively attenuate the sequence of events that mediate extension of tissue injury beyond that caused by the ischemic insult.
Canine Myocardial Reperfusion Injury: Its Reduction by the Combined Administration of Superoxide Dismutase and Catalase
The results of this investigation demonstrate that the ‘primary’ myqcardial cellular damage due to ischemia is additive to the cardiac cell damage during the phase of reperfusion, and that the“secondary” effects are mediated by toxic metabolites of oxygen.
Reduction of experimental canine myocardial reperfusion injury by a monoclonal antibody (anti-Mo1, anti-CD11b) that inhibits leukocyte adhesion.
It is demonstrated that administration of anti-Mo1 monoclonal antibody after the induction of regional myocardial ischemia results in reducedMyocardial reperfusion injury as measured by ultimate infarct size.
Activation of estrogen receptor-alpha protects the in vivo rabbit heart from ischemia-reperfusion injury.
Results indicate that activation of ER alpha, but not ER beta, is required for the observed cardioprotective effects of E2, and PPT reduced the release of cardiac-specific troponin-I and reduced the tissue deposition of the membrane attack complex and C-reactive protein similar to that of E1.
Reduction of the Extent of Ischemic Myocardial Injury by Neutrophil Depletion in the Dog
Accumulation of polymorphonuclear neutrophils during the acute inflammatory response may exacerbate tissue injury through the release of activated oxygen products or proteolytic enzymes or both. To
Myocardial protection with preconditioning.
The data indicate that preconditionsing with one brief ischemic interval is as effective as preconditioning with multiple isChemic periods.
Cardiac Actions of Glucagon
  • B. Lucchesi
  • Chemistry, Medicine
    Circulation research
  • 1 June 1968
The results of these studies are discussed in reference to the known metabolic actions of glucagon and the catecholamines and the possibility that they both share a common mechanism of action mediated through an increase in the intracellular concentration of cyclic 3′,5′ AMP.
Sulodexide: a renewed interest in this glycosaminoglycan.
Sulodexide is a highly purified glycosaminoglycan composed of a fast mobility heparin fraction as well as dermatan sulfate that has a longer half-life and a reduced effect on systemic clotting and bleeding.
Coxibs interfere with the action of aspirin by binding tightly to one monomer of cyclooxygenase-1
It is predicted that the cardioprotective effect of low-dose aspirin on COX-1 may be blunted when taken with coxibs, and administration of celecoxib to dogs interferes with the ability of a low dose of aspirin to inhibit AA-induced ex vivo platelet aggregation.