Elsevier

The Annals of Thoracic Surgery

Volume 68, Issue 5, November 1999, Pages 1983-1987
The Annals of Thoracic Surgery

II. Surgical Myocardial Protection
Heart preservation for transplantation: principles and strategies

Presented at the International Symposium on Myocardial Protection From Surgical Ischemic-Reperfusion Injury, Asheville, NC, Sep 21–24, 1997.
https://doi.org/10.1016/S0003-4975(99)01028-0Get rights and content

Abstract

While transplantation is a proven modality for the treatment of end stage organ disease, an important determinant of outcome is the adequacy of organ preservation. Currently, heart preservation is limited to 4 to 6 hours of cold ischemic storage, and the effectiveness depends to a great extent on the solution and its temperature. The formulation of the solution is based on three basic principles: (a) hypothermic arrest of metabolism, (b) provision of a physical and biochemical environment to maintain viability of the structural components of the tissue during hypothermic metabolic slowing, and (c) minimization of reperfusion injury. This review presents the physiologic principles underlying the use of hypothermia and the chemical components of preservation fluids, specifically pertaining to preservation of the heart for transplantation. New approaches designed to protect the heart from surgical ischemic-reperfusion injury are presented as well. The object is to survey current strategies and generate insight into new and promising solutions designed to optimize donor heart preservation.

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

References (23)

  • M.P. Nutt et al.

    Comparison of continuous perfusion and simple cold storage for rabbit heart preservation

    Transplant Proc

    (1991)
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