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Hypothermia Protects Against Myocardial Microvascular Damage (No‐Reflow) Even When Initiated After Coronary Artery Reperfusion
Author(s) -
Hale Sharon Lee,
Kloner Robert A
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.857.2
Subject(s) - medicine , ventricle , cardiology , hypothermia , myocardial infarction , ischemia , artery , reperfusion injury , anesthesia
We tested the effects of hypothermia (H) on no‐reflow when H is initiated only at reperfusion; a time point that many studies have shown is too late to reduce myocardial infarct size (IS). Methods Rabbits received 30 m coronary artery occlusion and 3 h reperfusion. Hearts were treated with topical H (~32ºC) at 5 m before (HI, n = 14) or 5 m after (HR, n = 12) reperfusion. Controls remained normothermic (N, ~38ºC, n=14). Ischemic risk zone, no‐reflow zone, and necrosis were measured. Results The ischemic insult was comparable in all groups (26–30% of left ventricle, p = ns). As we and others have observed, H started at this time failed to significantly reduce IS compared with N hearts (27 ± 3% of risk zone, HI; 42± 4%, HR and 34 ± 5%,N p =NS, ANOVA). However, the extent of the no‐reflow defect was significantly reduced in hearts treated with H, even when started after reperfusion (46±9% of the necrotic area, HI; 50±5%, HR; versus 80±8%, N; p <0.05 HI and HR vs. N). There was a significant treatment effect of H on the regression between the extent of the no‐reflow zone and that of the necrotic zone (ANCOVA, p = 0.003). Conclusions This study shows that myocardial temperature reduction dramatically reduces no‐reflow injury even when H is initiated too late to reduce overall IS. These data suggest that the microvasculature is especially receptive to the salvaging properties of hypothermia.