II. Surgical Myocardial ProtectionHeart preservation for transplantation: principles and strategies
Section snippets
Continuous cold perfusion
Perfusion storage involves the continuous infusion of a cold preservation fluid through the vasculature of the harvested organ [3]. Modifications of the cold ischemic storage fluids, in view of the unique physiologic environment of the continuous perfusion circuit permit the adaptation of the fluids for this use. Experimental studies have demonstrated the superiority of this method over cold ischemic storage 4, 5. One study with isolated rabbit hearts documented return of greater than or equal
Cold ischemic storage
The cornerstone of cold ischemic storage is hypothermia at 4° to 8°C and the chemical constituents of the fluid. Hypothermia decelerates metabolism and the ionic constituents facilitate rapid cessation of electrical activity. The formulation of the preservation solution is based on three principles: (a) hypothermic arrest of metabolism, (b) provision of a physical and biochemical environment that maintains viability of the structural components of the tissue during hypothermic metabolic arrest,
Harmful effects of cold ischemic storage
While hypothermia and cold ischemic storage delay cell death, certain processes are activated that ultimately can be deleterious to the preserved organ. These include: (a) cellular swelling, (b) extracellular edema, (c) cellular acidosis, (d) depletion of metabolic substrate, (e) reperfusion injury, (f) calcium overload, and (g) endothelial injury. Cooling also reduces glucose utilization, adversely alters intracellular hydrogen regulation and slows tissue oxygen uptake. It induces shift to the
Opioid agonists and hibernation induction trigger
Several studies have demonstrated that opioid-like agents can impact significantly on the ability of cardiac tissue to tolerate periods of ischemia and hypoxia [18]. Activation of the delta subtype opioid receptors can result in improved functional recovery following ischemia-reperfusion [19]. Delta opioid peptides have also been shown to inhibit beta-adrenergic signaling pathways via Gi/o proteins involved in adenylate cyclase production [20]. This mechanism of action is not unlike that of
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