scholarly journals Early Recovery of Regional Performance in Salvaged Ischemic Myocardium following Coronary Artery Occlusion in the Dog

1981 ◽  
Vol 68 (1) ◽  
pp. 225-239 ◽  
Author(s):  
John R. Darsee ◽  
Robert A. Kloner ◽  
Eugene Braunwald
Keyword(s):  
Coronary Artery ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Ischemic Myocardium ◽  
Early Recovery ◽  
Regional Performance

Improved performance of ischemic canine myocardium in response to nifedipine and diltiazem

1980 ◽  
Vol 239 (5) ◽  
pp. H658-H663 ◽  
Author(s):  
J. E. Perez ◽  
B. E. Sobel ◽  
P. D. Henry
Keyword(s):  
Coronary Artery ◽  
Coronary Artery Occlusion ◽  
Aortic Pressure ◽  
Artery Occlusion ◽  
Ischemic Myocardium ◽  
Control Value ◽  
Anesthetized Dogs ◽  
Improved Performance ◽  
Mean Aortic Pressure ◽  
Canine Myocardium

To characterize the effects of Ca2+ antagonists on the performance of the ischemic myocardium, we administered nifedipine and diltiazem to chloralose-anesthetized dogs with coronary artery occlusion and monitored segmental myocardial shortening in ischemic and nonischemic zones with implanted ultrasonic length gauges. Other dogs were treated with nitroglycerin or nitroprusside for comparison. Dosage of all drugs was adjusted to reduce mean aortic pressure by no more than 5 mmHg. Segmental shortening was expressed as percent of control value before occlusion. In control dogs (n = 8), shortening in ischemic zones 20 and 80 min after occlusion averaged -16 +/- 2% and -17 +/- 2%, indicating paradoxical elongation. With nifedipine (1 +/- 0.4 microgram . kg-1 . h-1; n = 8), shortening of ischemic segments before treatment did not differ from controls, but after 60 min of treatment was markedly improved, averaging 31 +/- 4% (P < 0.05). Diltiazem (10 +/- 2 microgram . kg-1 . h-1; n = 8) produced a similar improvement in shortening in ischemic zones. However, nitroglycerin (177 +/- 20 microgram . kg-1 . h-1; n = 8) and nitroprusside (43 +/- 10 microgram . kg-1 . h-1; n = 8) failed to improve shortening in ischemic regions. Thus, Ca2+ antagonists improved performance in ischemic zones, but nitroglycerin and nitroprusside did not.

scholarly journals Effects of Coenzyme Q10 on Ischemic Myocardium during Coronary Artery Occlusion

1986 ◽  
Vol 8 (1) ◽  
pp. 19-25 ◽  
Author(s):  
Yoshiya ISHIKURA ◽  
Shigetoh ODAGIRI ◽  
Masato NAGATA ◽  
Tadashi NAGANO ◽  
Hiroshi YOSHIMATU
Keyword(s):  
Coronary Artery ◽  
Coenzyme Q ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Ischemic Myocardium

scholarly journals Long-Term Preservation of Ischemic Myocardium after Experimental Coronary Artery Occlusion

1978 ◽  
Vol 61 (3) ◽  
pp. 541-551 ◽  
Author(s):  
Derek Maclean ◽  
Michael C. Fishbein ◽  
Eugene Braunwald ◽  
Peter R. Maroko
Keyword(s):  
Coronary Artery ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Ischemic Myocardium ◽  
Long Term Preservation

Ultrastructural Pathology of Ischemic Myocardium as Revealed by the Freeze Fracture Technique

1975 ◽  
Vol 33 ◽  
pp. 426-427
Author(s):  
M. Ashraf ◽  
W. Mayr
Keyword(s):  
Coronary Artery ◽  
Cell Injury ◽  
Freeze Fracture ◽  
Coronary Artery Occlusion ◽  
Myocardial Cell ◽  
Artery Occlusion ◽  
Ischemic Myocardium ◽  
Ultrastructural Changes ◽  
Acute Ischemia ◽  
Thin Sections

Myocardial cells undergo extensive ultrastructural changes during ischemia, easily observed after 30 minutes of coronary artery occlusion. Although various membranous organelles remain intact during acute ischemia, biochemical evidence indicates several metabolic alterations in affected cells. Since cell membranes and membranes of intracellular organelles play an important role in the pathogenesis of myocardial cell injury, changes in their interiors could be informative. However, such changes are not easily detectable in conventional thin sections. This study examined ultrastructural alterations in the membranous organelles of ischemic myocardium using the freeze-fracture technique to improve detection of such changes.After 5 and 24 hours of coronary artery occlusion the hearts from dogs and rats were perfused with buffered glutaraldehyde. Small pieces of the left ventricle were dipped in Freon 22 and immediately frozen in liquid nitrogen before fracturing in a Balzer's freeze-etch apparatus at -100 or -120°C.

Ebselen protects against ischemia-reperfusion injury in a canine model of myocardial infarction

1994 ◽  
Vol 267 (6) ◽  
pp. H2342-H2347 ◽  
Author(s):  
S. Hoshida ◽  
T. Kuzuya ◽  
M. Nishida ◽  
N. Yamashita ◽  
M. Hori ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Infarct Size ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Ischemic Myocardium ◽  
Regional Myocardial Blood Flow

We investigated the infarct-limiting effect of a selenoorganic compound, ebselen [2-phenyl-1,2-benzisoselenazol-3(2H)-one], in a canine coronary artery occlusion-reperfusion model of myocardial infarction. Ebselen, administered 1 h before coronary artery occlusion (50 mg/kg po), significantly reduced infarct size resulting from 90-min coronary artery occlusion followed by 5-h reperfusion (P < 0.05). When we examined the relation between infarct size and plasma ebselen level, infarct size in dogs with plasma ebselen level > 5 microM before reperfusion was significantly smaller (P < 0.05) than that in dogs with plasma ebselen level < or = 5 microM or in the control dogs. This infarct limitation produced by ebselen treatment was associated with an increase in reduced glutathione content and a reduction in myeloperoxidase activity in the ischemic myocardium. No differences between the control and treated groups were found in hemodynamic parameters or regional myocardial blood flow in the course of the experiment. The findings of this study demonstrate that ebselen effectively reduced the myocardial ischemia-reperfusion injury associated with preservation of the glutathione redox state and a reduction in neutrophil infiltration into the ischemic myocardium.

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