The endothelin-1 receptor antagonist BQ-123 reduces infarct size in a canine model of coronary occlusion and reperfusion

1993 ◽  
Vol 27 (9) ◽  
pp. 1613-1618 ◽  
Author(s):  
G. J Grover ◽  
S. Dzwonczyk ◽  
C. S Parham
Keyword(s):  
Infarct Size ◽  
Receptor Antagonist ◽  
Coronary Occlusion ◽  
Canine Model ◽  
Endothelin 1

Progression of myocardial injury during coronary occlusion in the collateral-deficient heart: a non-wavefront phenomenon

2007 ◽  
Vol 293 (3) ◽  
pp. H1799-H1804 ◽  
Author(s):  
Bradley G. Leshnower ◽  
Hiroaki Sakamoto ◽  
Hirotsugu Hamamoto ◽  
Ahmad Zeeshan ◽  
Joseph H. Gorman ◽  
...  
Keyword(s):  
Infarct Size ◽  
Functional Capacity ◽  
Collateral Circulation ◽  
Coronary Occlusion ◽  
Regional Blood Flow ◽  
Microvascular Dysfunction ◽  
Canine Model ◽  
Ischemic Time ◽  
Coronary Collaterals ◽  
Wide Range

It is widely accepted that, during acute coronary occlusion, ischemic cell death progresses from the subendocardium to the subepicardium in a wavefront fashion. This concept, which implies that the subendocardium is the most susceptible myocardial region to ischemic injury, was established using a canine model with an extensive system of subepicardial coronary collaterals. In humans, particularly in those with coronary artery disease, there is a wide range in the distribution and functional capacity of the collateral circulation, which may affect the pattern of infarct evolution. Using an ovine model with a limited system of preformed subendocardial coronary collaterals, we characterized the effect of increasing lengths of ischemia on regional blood flow and infarct size in three regions of the ventricular wall: subendocardium, midmyocardium, and subepicardium. Our results demonstrate that the myocardium and microvasculature in these three regions are equally susceptible to injury after 45 min of ischemia. When ischemic time is increased to 1 h, infarct size in the midmyocardium (90 ± 2%) is greater than in the subendocardium (76 ± 4%, P = 0.004) and subepicardium (84 ± 3%, P = 0.13). Microvascular dysfunction as assessed as a percentage of baseline flow is also greater in the midmyocardium (14 ± 5%) compared with the subendocardium (20 ± 3%, P = 0.23) and subepicardium (51 ± 9%, P = 0.007). These findings suggest that, in subjects with a limited system of coronary collateral circulation, the midmyocardium is the most susceptible myocardial region to ischemia and the subendocardium is the most resistant. Myocardial viability during coronary occlusion appears to be primarily determined by the distribution and functional capacity of the collateral circulation.

Reduction in Myocardial Infarct Size by Basic Fibroblast Growth Factor After Temporary Coronary Occlusion in a Canine Model

Circulation ◽  
1996 ◽  
Vol 94 (8) ◽  
pp. 1927-1933 ◽  
Author(s):  
Mark C.G. Horrigan ◽  
Andrew I. MacIsaac ◽  
Francesca A. Nicolini ◽  
D. Geoffrey Vince ◽  
Philmo Lee ◽  
...  
Keyword(s):  
Growth Factor ◽  
Infarct Size ◽  
Fibroblast Growth Factor ◽  
Basic Fibroblast Growth Factor ◽  
Coronary Occlusion ◽  
Myocardial Infarct ◽  
Canine Model ◽  
Myocardial Infarct Size ◽  
Fibroblast Growth

The Selective Endothelin-A-Receptor Antagonist LU 135.252 Inhibits the Direct Arrhythmogenic Action of Endothelin-1

2000 ◽  
Vol 36 ◽  
pp. S314-S316 ◽  
Author(s):  
Béla Merkely ◽  
Tamás Szabó ◽  
László Gellér ◽  
Orsolya Kiss ◽  
Ferenc Horkay ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Endothelin 1 ◽  
Endothelin A Receptor ◽  
Endothelin A

BQ123, an ETA Receptor Antagonist, Attenuates Endothelin-1-Induced Vasoconstriction in Rat Pulmonary Circulation

1993 ◽  
Vol 22 (1) ◽  
pp. 39-43 ◽  
Author(s):  
S. T. Bonvallet ◽  
M. Oka ◽  
M. Yano ◽  
M. R. Zamora ◽  
I. F. McMurtry ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Pulmonary Circulation ◽  
Endothelin 1 ◽  
Eta Receptor ◽  
Eta Receptor Antagonist

scholarly journals The xanthine oxidase inhibitor oxypurinol does not limit infarct size in a canine model of 40 minutes of ischemia with reperfusion

1988 ◽  
Vol 12 (1) ◽  
pp. 209-217 ◽  
Author(s):  
James M Kinsman ◽  
Charles E Murry ◽  
Vincent J Richard ◽  
Robert B Jennings ◽  
Keith A Reimer
Keyword(s):  
Infarct Size ◽  
Xanthine Oxidase ◽  
Canine Model ◽  
Oxidase Inhibitor ◽  
Xanthine Oxidase Inhibitor

Inhibition of nonexocytotic norepinephrine release by desipramine reduces myocardial infarction size

2006 ◽  
Vol 84 (11) ◽  
pp. 1185-1189 ◽  
Author(s):  
Doreen Richardt ◽  
Andreas Dendorfer ◽  
Ralph Tölg ◽  
Peter Dominiak ◽  
Gert Richardt
Keyword(s):  
Myocardial Infarction ◽  
Myocardial Ischemia ◽  
Infarct Size ◽  
Coronary Occlusion ◽  
Tricyclic Antidepressant ◽  
In Vivo Model ◽  
Norepinephrine Release ◽  
Area At Risk ◽  
Transport Direction

During myocardial ischemia, a substantial accumulation of norepinephrine occurs in the ischemic zone due to a local nonexocytotic release of norepinephrine. Norepinephrine release is driven by the neuronal monoamine transporter (NET), which reverses its usual transmembrane transport direction. We investigated whether this local accumulation of norepinephrine contributes to irreversible myocardial injury in an in vivo model of myocardial infarction. Male, anaesthetized Wistar rats were subjected to 30 min coronary occlusion and subsequent 120 min reperfusion. Five minutes prior to coronary occlusion, the NET inhibitor desipramine was administered intravenously. Infarct size (IS) was determined by TTC-staining and was related to the area at risk (AAR). The influence of desipramine on cardiac norepinephrine release was investigated in isolated perfused hearts with 30 min of regional ischemia. Norepinephrine was measured in the effluent from the hearts by HPLC and electrochemical detection. Desipramine (0.1–0.8 mg/kg) dose-dependently reduced infarct size (IS/AAR) from 0.54 to 0.21 and suppressed postischemic norepinephrine release from 245 to 108 pg/mL. In summary, the data indicate that nonexocytotic release of norepinephrine in myocardial ischemia exaggerates acute ischemic damage, because suppression of ischemia-induced release of norepinephrine by the tricyclic antidepressant desipramine effectively reduces infarct size in an in vivo model of myocardial ischemia.

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