The effects of exogenous lactate and pyruvate on the recovery of coronary flow in the rat heart after ischaemia

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Abstract
Objective: The effect of exogenous lactate and pyruvate on the recovery of coronary flow (total, regional) after ischaemia as a function of the duration of ischaemia was evaluated. Methods: Isolated, ejecting rat hearts were subjected to ischaemia for 15, 30, or 45 minutes. Glucose (11 mM) was present as the basal substrate in the perfusion medium and lactate (5 mM) or pyruvate (5 mM) was added as the cosubstrate. Flow variables were measured by the timed collection of coronary effluents and by the radioactive microsphere technique. Results: In the lactate perfused hearts, reactive hyperaemia was present after 15 minutes but absent after 30 and 45 minutes of ischaemia. Total coronary flow was significantly reduced after 45 minutes of ischaemia. Transmural flow was impaired after 15, 30, and 45 minutes of ischaemia in the lactate perfused hearts, – that is, flow in the inner layers of the left ventricle was transiently reduced after 15 minutes and remained continuously depressed after 30 and 45 minutes of ischaemia. The pyruvate perfused hearts showed reactive hyperaemia after 15 and 30 minutes of ischaemia. After 45 minutes total coronary flow was reduced below the value before ischaemia, and in particular, the inner layers of the left ventricle were severely deprived of flow as in lactate perfused hearts. When neither lactate nor pyruvate was added to the perfusion medium (containing glucose), impairment of coronary flow in the inner layers of the left ventricle was only transiently obvious after 30 and 45 minutes of ischaemia. Impaired perfusion of the inner layers during reperfusion resulted in delayed washout of lactate dehydrogenase. Conclusions: Exogenous substrates modify the recovery of flow after ischaemia. In the presence of exogenous lactate, severe disturbances of flow are already obvious after 30 minutes of ischaemia in the inner layers of the left ventricle. Exogenous pyruvate delays impairment of flow in the inner layers compared with exogenous lactate. Cardiovascular Research 1993;27:1088-1093

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