Bl. Bufkin et al., PRECONDITIONING DURING SIMULATED MIDCABG ATTENUATES BLOOD-FLOW DEFECTS AND NEUTROPHIL ACCUMULATION, The Annals of thoracic surgery, 66(3), 1998, pp. 726-731
Citations number
24
Categorie Soggetti
Surgery,"Cardiac & Cardiovascular System","Respiratory System
Background. Ischemic preconditioning (IP) may be cardioprotective in m
inimally invasive direct coronary artery bypass where cardioplegia is
not used. This study tested the hypothesis that IP of the area at risk
(AAR) would attenuate postischemic injury from transient coronary art
ery occlusion. Methods. In 19 anesthetized dogs, the left anterior des
cending coronary artery was occluded for 30 minutes (simulating corona
ry occlusion during anastomosis) followed by 3 hours of reperfusion. I
n 10 dogs, occlusion was preceded by 5 minutes of occlusion and 5 minu
tes of reperfusion (IP), whereas 9 other dogs had no IP (control, C).
Results. Thirty minutes of left anterior descending occlusion caused c
omparable dyskinesis (systolic shortening, sonomicrometry) in the AAR
in C (baseline, 29% +/- 3% to 3% +/- 2%) and in IP (baseline, 29% +/-
2% to -0.3% +/- 2%). After 3 hours of reperfusion, systolic shortening
was significantly depressed in C (20% +/-. 4%), and was not significa
ntly improved by IP (24% +/- 3%, p = 0.8 versus C). Postischemic diast
olic stiffness in the AAR was not altered by IP versus C (0.60 +/- 0.1
2 versus 0.41 +/- 0.13). plasma creatine kinase activity was similar b
etween C and IF at the end of reperfusion (20 +/- 11 versus 16 +/- 5 U
/g). Postischemic AAR blood now tin milliliters per minute per gram of
tissue) at 180 minutes of reperfusion decreased by 56% versus baselin
e in C (from 1.04 +/- 0.4 to 0.46 +/- 0.12; p < 0.05) compared with no
change in IF (from 0.74 +/- 0.23 to 0.60 +/- 0.10), but there was no
significant group difference at this time. Myeloperoxidase activity as
an index of neutrophil accumulation in AAR was decreased in IF versus
C (0.4 +/- 0.09 versus 0.7 +/- 0.04 U/mu g tissue). Conclusions. Isch
emic preconditioning does not decrease postischemic wall motion and on
ly modestly increases postischemic blood flow abnormalities in the AAR
, but does significantly inhibit neutrophil accumulation. (Ann Thorac
Surg 1995;66:72632) (C) 1998 by The Society of Thoracic Surgeons.