CARDIOVASCULAR ENGINEERING Journal for Extracorporeal Circulation, Assist Devices,Transplantation and Artificial Organs
	Volume 3, 1998, No 2

The Isolated Perfused Rat Heart as Experimental Model to Assessthe Genesis of Myocardial Reoxygenation Injury

M. Samaja, A. F. Corno

Abstract:
Thy myocardial damage induced by the reoxygenation of hypoxic hearts may hinder the surgical repair of cyanotic heart defects. Despite the well known limits of a study performed in vitro on a different species, the isolated perfused rat heart model is useful to assess the role of some factors that determine the reperfusion injury in cyanotic hearts undergoing cardiac surgery. We focus on the acute myocardial responses to oxygen shortage by comparing low-flow ischemia with hypoxemia: the oxygen supply is low with respect to demand in both situations, but the different flows allow to test the role of diffusible substances. Despite important roles of oxygen-derived free radicals and of technical tips such as gradual reoxygenation, the core of the injury observed during reoxygenation or reflow of oxygen-stressed hearts depends on the events that occured during hypoxemia and ischemia. Biochemical regulators as lactate come into play in ischemic hearts to prevent excessive energy waste by downregulating myocardial activity. This mechanism is apparently overriden in hypoxemic hearts. Furthermore, the ATP pool, essentially preserved in ischemic hearts due to preservation of biochemical equilibrium, is critically impaired in hypoxemic hearts. Finally, the distribution of the compounds in the ATP pool appears crucial to determine the myocardial performance upon return to normal oxygen supply conditions. This mechanism may be regarded as an elegant system by which biochemical metabolism eventually regulates myocardial performance and enhances the heart endogenous protective mechanisms.

Keywords:
ischemia, hypoxemia, downregulation, high-energy phosphates, purines, phosphocreatine, lactate, recovery, reoxygenation, cardiac surgery

Address for Correspondence:

Reference:
(CVE. 1998; 3 (2): 120-126)

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