S. Lindal et al., MYOCARDIAL AND MICROVASCULAR INJURY FOLLOWING CORONARY SURGERY AND ITS ATTENUATION BY MODE OF REPERFUSION, European journal of cardio-thoracic surgery, 9(2), 1995, pp. 83-89
In 14 patients undergoing coronary surgery, repeated atrial biopsies w
ere obtained before and at the end of ischemia, and at 20 and 60 min o
f reperfusion. In half of the patients reperfusion was initiated with
an abrupt rise in blood temperature and pressure, in the other half wi
th a gradual rise. The biopsies were prepared for transmission electro
n microscopy and analyzed by stereological technique. In all biopsies,
myocytic injury, as revealed by mitochondrial changes and intracellul
ar edema, occurred following ischemia (P=0.0003 and 0.007, respectivel
y). The intracellular edema regressed following 20 min of reperfusion
(P=0.008). The myocytic mitochondrial changes persisted during reperfu
sion towards the end of the observation period (P=0.0001). Interstitia
l edema increased following ischemia (P=0.007) and persisted following
60 min of reperfusion (P=0.009). The capillary part was significantly
reduced after 20 min of reperfusion (P=0.003), probably reflecting in
terstitial edema. Most changes were reversible in nature, although foc
i of irreversible changes were shown. In patients with a gradual start
of reperfusion there was a significant regression of interstitial ede
ma (P=0.005) at 60 min reperfusion compared to the patients with an ab
rupt start, where the same changes seemed to persist or even increase.
The study demonstrates that ''reperfusion injury'' occurs in human my
ocardium. It can be discerned from ''ischemic'' injury, and it may be
reduced by a gentle mode of reperfusion.