B. Heindl et al., VOLATILE ANESTHETICS REDUCE ADHESION OF BLOOD-PLATELETS UNDER LOW-FLOW CONDITIONS IN THE CORONARY SYSTEM OF ISOLATED GUINEA-PIG HEARTS, Acta anaesthesiologica Scandinavica, 42(8), 1998, pp. 995-1003
Background: inhibitory effects of volatile anaesthetics on platelet ag
gregation have been demonstrated in several studies. However, the infl
uence of volatile anaesthetics on intracoronary platelet adhesion has
not been elucidated so far. Methods: Isolated hearts of guinea pigs we
re perfused with buffer in the absence or presence of volatile anaesth
etics (0.5 and 1 MAC) at constant coronary flow rates of 5 ml/min for
25 min, then 1 ml/min for 30 min and again 5 ml/min for 10 min. Before
, during and after low-flow perfusion, a bolus of human platelets was
applied into the coronary system. To simulate thrombogenic conditions,
0.3 U/ml human thrombin was infused during low-flow perfusion and rep
erfusion. The number of platelets sequestered to the endothelium was c
alculated from the difference between coronary in- and output of plate
lets. The myocardial production of lactate and consumption of pyruvate
and coronary perfusion pressure were also determined. Results: At a f
low rate of 5 ml/min only about 3% of the applied platelets did not em
erge from the coronary system, in any group. In contrast, 13.1+/-1.2%
(mean+/-SEM) of infused platelets became adherent in low-flow perfusio
n in the control group without anaesthetic. The adherence was reduced
with each 1 MAC isoflurane (to 6.2+/-1.2%), sevoflurane (to 4.4+/-0.9%
) or halothane (to 3.2+/-1.5%) (each P<0.05 vs, control). Volatile ana
esthetic, 0.5 MAC, did not inhibit platelet adhesion to a statisticall
y significant extent in any case. Perfusion pressure and metabolic par
ameters were not statistically different between the control and the h
earts exposed to anaesthetics. Conclusion: Volatile anaesthetics in a
concentration of 1 MAC can reduce the adhesion of platelets in the cor
onary system under reduced flow conditions. This action does not arise
from vasodilation or inhibition of ischaemic stress.