Evidence of functional myocardial ischemia associated with myocardial dysfunction in brain-dead pigs

C. Seguin, Y. Devaux, S. Grosjean, E. M. Siaghy, P. Mairose, N. De Talancé, F. Zannad, D. Ungureanu-Longrois, P. M. Mertes*

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

29 Citations (Scopus)


Background - Cardiac dysfunction after brain death has been documented, but its mechanisms remain unclear. Myocardial ischemia has been suggested as a possible cause. The aim of the present study was to investigate the existence of an imbalance between myocardial oxygen delivery and demand as a possible cause of myocardial dysfunction in brain-dead pigs. Methods and Results - Interstitial myocardial lactate and adenosine concentrations were assessed with cardiac microdialysis in 2 groups of animals: brain-dead pigs (n=7) and brain-dead pigs treated with labetalol (10±3 mg/kg) (n=7). Heart rate (HR), left ventricular (LV) dP/dtmax, rate-pressure product (RPP), cardiac output (CO), and left anterior descending coronary artery blood flow (QLAD) were continuously monitored. Brain-dead pigs exhibited a transient significant increase in HR, LV dP/dtmax, RPP, and CO and a limited increase in QLAD. This resulted in functional myocardial ischemia attested to by the significantly increased adenosine and lactate microdialysate concentrations. In brain-dead pigs treated with labetalol, there was a moderate increase in HR, QLAD, and adenosine microdialysate concentrations; LV dP/dtmax, RPP, CO, and myocardial lactate concentrations remained stable, confirming the preservation of aerobic metabolism. Conclusions - Brain death was associated with an increase in myocardial interstitial adenosine and lactate concentrations, as well as with myocardial dysfunction; all were attenuated by labetalol, suggesting an imbalance between oxygen consumption and oxygen delivery as a possible cause of myocardial dysfunction after brain death.

Original languageEnglish
Pages (from-to)i197-i201
Issue numberSUPPL. 1
Publication statusPublished - 18 Sept 2001
Externally publishedYes


  • Adenosine
  • Ischemia
  • Nervous system, sympathetic
  • Transplantation


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