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Profile of Sandy Clanachan, PhD

Sandy Clanachan
Department of Pharmacology
970 Medical Sciences
Edmonton AB  T6G 2H7

Tel: 780.492.0511
Fax: 780.492.1217


Most of the current research activities in the Clanachan Laboratory are concerned with the pharmacological actions of drugs in the mammalian cardiovascular system. Of particular interest is study of the mechanisms that are responsible for the ability of adenosine, adenosine receptor agonists, estrogen and nitric oxide to protect the heart from the deleterious consequences of ischemia and to enhance the recovery of cardiac function during reperfusion.

Metabolic mechanisms of cardioprotection in response to ischemic preconditioning, estrogen and other cardioprotective interventions are also being studied in models of global and low-flow normothermic ischemia and reperfusion as well as in hearts subjected to reperfusion after cardioplegic arrest and prolonged hypothermic storage. In addition to factors affecting the source of protons during myocardial ischemia and reperfusion, related studies are investigating the fate of protons by examining the role of the various membrane-located ion transport mechanisms that influence the flux of protons and other ions across the plasma membrane. Previous work has examined the hemodynamic actions of adenosine receptor agonists in vivo in normal animals and in animals with ischemia-induced left ventricular dysfunction.

Ongoing studies:

  1. examination of drug-induced alterations in myocardial glucose and glycogen metabolism in isolated working hearts perfused under conditions of appropriate energy supply and demand, particularly an assessment of the therapeutic potential of optimization of rates of glycolysis and glucose oxidation,
  2. elucidation of the mechanisms of mechanical dysfunction and their correction in hearts subjected to cardioplegia and prolonged hypothermic storage, particularly the consequences of ischemia- and drug-induced alterations in the nitric oxide guanylyl cyclase pathway,
  3. clarification of the metabolic mechanisms involved in the classical and late phases of cardioprotection in response to ischemia- and drug-induced preconditioning using models where hearts are subjected to global or low-flow normothermic ischaemia and reperfusion as well as to normothermic reperfusion after cardioplegic arrest and prolonged hypothermic stora
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