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Repeated, transient lactate exposure does not "precondition" rat myocardium
F Aresta1, G Gerstenblith, R G Weiss
1Peter Belfer Laboratory, Department of Medicine, Johns Hopkins Hospital, Baltimore, MD 21287-6568, USA.
Canadian Journal of Physiology and Pharmacology
|February 12, 1998
Summary
Ischemic preconditioning (IPC) protects the heart, but its mechanism is unclear. Researchers found that lactate exposure, mimicking IPC, did not improve heart recovery after prolonged ischemia, challenging its role in cardioprotection.
Area of Science:
- Cardiovascular Physiology
- Metabolic Biochemistry
Background:
- The cardioprotective mechanisms of ischemic preconditioning (IPC) remain incompletely understood.
- While adenosine, protein kinase C, and heat shock proteins are implicated, lactate's role as a preconditioning trigger is increasingly suggested.
- Lactate accumulation during ischemia may activate key preconditioning pathways.
Purpose of the Study:
- To investigate whether repeated lactate exposure, mimicking tissue lactate levels during brief ischemia, confers cardioprotective benefits similar to IPC.
- To determine if lactate itself can act as a preconditioning agent.
Main Methods:
- Isolated rat hearts were divided into three groups: IPC, control, and lactate-preconditioning.
- IPC hearts underwent two 5-min ischemia-reperfusion cycles.
- Lactate-preconditioned hearts received two 5-min exposures to 15 mM lactate with intervening reflow periods.
- All hearts were subsequently subjected to 30 minutes of total normothermic ischemia followed by 30 minutes of reflow.
Main Results:
- Lactate exposure achieved tissue lactate concentrations comparable to those during IPC.
- Ischemic preconditioning significantly improved left ventricular developed pressure recovery (56.8%) compared to control (14.2%) and lactate-preconditioned (9.5%) hearts.
- No significant difference in contractile recovery was observed between lactate-preconditioned and control hearts.
- End-diastolic pressure during reperfusion was significantly lower in IPC hearts than in the other two groups.
Conclusions:
- Repeated, transient lactate exposure, even at levels mimicking IPC, did not enhance cardiac recovery after prolonged ischemia in this rat heart model.
- The findings suggest that lactate, at the tested concentrations and exposure patterns, may not be a primary mediator of IPC-induced cardioprotection.
- Further research is needed to elucidate the precise role of lactate in cardiac protection during ischemic events.