Protective Effects of Lecithinized
Superoxide Dismutase against Ischemia/Reperfusion Injury in Isolated
Rat Heart |
(Department of Thoracic and Cardiovascular Surgery,
Tohoku University, Sendai, Japan)
Makoto Kamada |
Atushi Iguchi |
Motohisa Tofukuji |
Hitoshi Yokoyama |
Hiroji Akimoto |
Mikio Ohmi |
Koichi Tabayashi |
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Lecithinized superoxide dismutase
(L-SOD) has a higher affinity for cell membranes than recombinant
human superoxide dismutase has. The purpose of this study is
to evaluate the protective effects of L-SOD against ischemia/reperfusion
injury in blood-perfused isolated rat heart subjected to 30-min
global normothermic ischemia. Fifteen isolated hearts were divided
into three groups: group I (n=5), the untreated control
group, group II (n=5) received 3,000 units of L-SOD administered
into the perfusion circuit at the beginning of reperfusion, and
group III (n=5) received 3,000 units of L-SOD administered
into the perfusion circuit 10 min after reperfusion. Left ventricular
developed pressure, maximum positive and negative dp/dt,
coronary vascular resistance and myocardial water content were
assessed in each group. The percent recovery of left ventricular
developed pressure in group II was significantly higher than
that in group I and group III (77.4}11.1% in group II, 38.2}4.4%
in group I, 40.2}4.1% in group III, p<0.01). The percent
recovery of maximum positive dp/dt in group II
was significantly higher than that in group I and group III (70.0}11.2%
in group II, 41.8}7.8% in group I, 38.0}5.7% in group III, p<0.01).
The percent recovery of maximum negative dp/dt
in group II was also significantly higher than that in group
I and group III (74.9}11.0% in group II, 41.3}8.0% in group I,
46.3}5.9% in group III, p<0.01). There was no significant
difference of coronary vascular resistance or myocardial water
content among the three groups. These results suggest that L-SOD
administered at the time of reperfusion has protective effects
against ischemia/reperfusion injury in the isolated rat heart.@Jpn.
J. Cardiovasc. Surg. 29: 315-319 (2000) |
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