C. Seguin et al., Evidence of functional myocardial ischemia associated with myocardial dysfunction in brain-dead pigs, CIRCULATION, 104(12), 2001, pp. I197-I201
Citations number
25
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Background-Cardiac dysfunction after brain death has been documented, but i
ts mechanisms remain unclear. Myocardial ischemia has been suggested as a p
ossible cause. The aim of the present study was to investigate the existenc
e of an imbalance between myocardial oxygen delivery and demand as a possib
le cause of myocardial dysfunction in brain-dead pigs.
Methods and Results-Interstitial myocardial lactate and adenosine concentra
tions were assessed with cardiac microdialysis in 2 groups of animals: brai
n-dead pigs (n=7) and brain-dead pigs treated with labetalol (10 +/- 3 mg/k
g) (n=7). Heart rate (HR) left ventricular (LV) dP/dt(max), rate-pressure p
roduct (RPP), cardiac output (CO), and left anterior descending coronary ar
tery blood flow (QLAD) were continuously monitored. Brain-dead pigs exhibit
ed a transient significant increase in HR. LV dP/dt(max), RPP, and CO and a
limited increase in QLAD. This resulted in functional myocardial ischemia
attested to by the significantly increased adenosine and lactate microdialy
sate concentrations. In brain-dead pigs treated with labetalol, there was a
moderate increase in HR, QLAD, and adenosine microdialysate concentrations
; LV dP/dt(max), RPP, CO, and myocardial lactate concentrations remained st
able, confirming the preservation of aerobic metabolism.
Conclusions-Brain death was associated with an increase in myocardial inter
stitial adenosine and lactate concentrations, as well as with myocardial dy
sfunction; all were attenuated by labetatol, suggesting an imbalance betwee
n oxygen consumption and oxygen delivery as a possible cause of myocardial
dysfunction after brain death.