KATP channel opening is an endogenous mechanism of protection against the no-reflow phenomenon but its function is compromised by hypercholesterolemia
Satoshi Genda, MD*,
Tetsuji Miura, MD, PhD, FACC*,*,
Takayuki Miki, MD, PhD*,
Yoshihiko Ichikawa, MD* and
Kazuaki Shimamoto, MD, PhD*
* Second Department of Internal Medicine, Sapporo Medical University, Sapporo, Japan
View larger version (58K):
[in a new window]
|
Figure 1 A representative example of a heart after 30-min coronary occlusion and 90-min reperfusion. (A) Triphenyltetrazolium chloride stained the noninfarcted region red, and the infarcted region remained unstained. The nonischemic region was stained by Evans blue dye. (B) Under ultraviolet light, the no-reflow zone was identified as a region deficient in fluorescence of thioflavin-S.
|
|
View larger version (141K):
[in a new window]
|
Figure 2 An example of the histology slide in a rabbit heart that received 60-min coronary occlusion and five days of reperfusion. The infarcted region consisted of central core of coagulation necrosis (C) and an organized zone (i.e., granulation tissue [G]) surrounding the core of necrosis (hematoxylin-eosin staining). The organized zone (G) and total infarct area (i.e., G plus C) were measured by NIH image, and the volume of the organized zone expressed as a percentage of total infarct size was calculated for each heart as an index of the extent of infarct healing. N = noninfarcted myocardium.
|
|
View larger version (26K):
[in a new window]
|
Figure 3 Relationship between infarct size and organized infarct volume expressed as a percentage of the entire infarct (%OZ/IS) five days after infarction. Control = untreated controls; Glibenclamide = normal rabbits treated with glibenclamide; Hyperchol = hypercholesterolemic rabbits; Hyperchol/nicorandil = hypercholesterolemic rabbits treated with nicorandil. The %OZ/IS was inversely correlated with infarct size in all study groups. However, the slope of the regression line in the hypercholesterolemic group (open circles; y = –27.8x + 100.8, r = 0.96) was significantly more negative than that in the untreated control group (open squares; y = –9.5x + 96.3, r = 0.73). The slope of the regression line in the glibenclamide-treated group (open triangles; y = –18.3x + 101.2, r = 0.96) was also more negative than that in the untreated controls, but the difference did not reach statistical significance. The regression line in the nicorandil-treated hypercholesterolemic group (closed circles; y = –26.7x + 109.4, r = 0.64) was significantly shifted upward compared with that in the hypercholesterolemic group.
|
|
|
