Effect of intraaortic balloon counterpulsation (IABP) on myocardial infarct size and collateral flow in an experimental dog model

1982 ◽  
Vol 8 (3) ◽  
pp. 131-137 ◽  
Author(s):  
K. D. Müller ◽  
F. Lübbecke ◽  
W. Schaper ◽  
P. Walter
Keyword(s):  
Infarct Size ◽  
Myocardial Infarct ◽  
Myocardial Infarct Size ◽  
Collateral Flow ◽  
Intraaortic Balloon ◽  
Dog Model ◽  
Intraaortic Balloon Counterpulsation ◽  
Balloon Counterpulsation

Dobutamine modifies myocardial infarct size through supply-demand balance

1988 ◽  
Vol 254 (5) ◽  
pp. H855-H861 ◽  
Author(s):  
T. Miura ◽  
S. Yoshida ◽  
O. Iimura ◽  
J. M. Downey
Keyword(s):  
Coronary Artery ◽  
Infarct Size ◽  
Flow Measurement ◽  
Myocardial Infarct ◽  
Coronary Artery Occlusion ◽  
Control Group ◽  
Myocardial Infarct Size ◽  
Collateral Flow ◽  
Drug Infusion ◽  
Regional Flow

We investigated dobutamine effect on infarct size during permanent coronary artery occlusion in dogs. The coronary artery of closed-chest dog was embolized by a 2.5-mm Teflon bead. Regional flow was measured 8 min after embolization with microspheres and, in drug-treated animals, again 20 min after starting dobutamine infusion (10 micrograms.kg-1.min-1 for 5 h immediately after the first microsphere measurement). The percent of the ischemic region progressing to infarct was determined 48 h later in each animal. Percent necrosis in the control group correlated closely with collateral flow to the epicardial one-third of the ischemic zone normalized against flow to the corresponding layer in the nonischemic zone. This flow should reflect an index of supply (collateral flow) and demand (flow to the nonischemic region determined by autoregulation). Percent necrosis in the drug-treated group did not correlate with normalized collateral flow measurement made before drug infusion, indicating that dobutamine had modified the course of infarction. Percent necrosis correlated well with normalized collateral flow measured during drug infusion, and that relationship was not different from that in the control group. Dobutamine increased infarct size over that expected from the predrug flow measurement in some dogs and reduced it in others. In all cases, however, the drug effect on infarct size was clearly reflected in normalized collateral flow measurement during drug infusion. Percent necrosis correlated with absolute collateral flow but less closely than with the normalized one.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Hydralazine protects the heart against acute ischaemia/reperfusion injury by inhibiting Drp1-mediated mitochondrial fission

2021 ◽  
Author(s):  
Siavash Beikoghli Kalkhoran ◽  
Janos Kriston-Vizi ◽  
Sauri Hernandez-Resendiz ◽  
Gustavo E Crespo-Avilan ◽  
Ayeshah A Rosdah ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Infarct Size ◽  
Myocardial Infarct ◽  
Mitochondrial Fission ◽  
Vehicle Control ◽  
Myocardial Infarct Size ◽  
Ischaemia Reperfusion Injury ◽  
Ischaemia Reperfusion ◽  
Pre Treatment ◽  
Apoptotic Effects

Abstract Aims Genetic and pharmacological inhibition of mitochondrial fission induced by acute myocardial ischaemia/reperfusion injury (IRI) has been shown to reduce myocardial infarct size. The clinically used anti-hypertensive and heart failure medication, hydralazine, is known to have anti-oxidant and anti-apoptotic effects. Here, we investigated whether hydralazine confers acute cardioprotection by inhibiting Drp1-mediated mitochondrial fission. Methods and results Pre-treatment with hydralazine was shown to inhibit both mitochondrial fission and mitochondrial membrane depolarisation induced by oxidative stress in HeLa cells. In mouse embryonic fibroblasts (MEFs), pre-treatment with hydralazine attenuated mitochondrial fission and cell death induced by oxidative stress, but this effect was absent in MEFs deficient in the mitochondrial fission protein, Drp1. Molecular docking and surface plasmon resonance studies demonstrated binding of hydralazine to the GTPase domain of the mitochondrial fission protein, Drp1 (KD 8.6±1.0 µM), and inhibition of Drp1 GTPase activity in a dose-dependent manner. In isolated adult murine cardiomyocytes subjected to simulated IRI, hydralazine inhibited mitochondrial fission, preserved mitochondrial fusion events, and reduced cardiomyocyte death (hydralazine 24.7±2.5% vs. control 34.1±1.5%, P=0.0012). In ex vivo perfused murine hearts subjected to acute IRI, pre-treatment with hydralazine reduced myocardial infarct size (as % left ventricle: hydralazine 29.6±6.5% vs. vehicle control 54.1±4.9%, P=0.0083), and in the murine heart subjected to in vivo IRI, the administration of hydralazine at reperfusion, decreased myocardial infarct size (as % area-at-risk: hydralazine 28.9±3.0% vs. vehicle control 58.2±3.8%, P<0.001). Conclusion We show that, in addition to its antioxidant and anti-apoptotic effects, hydralazine, confers acute cardioprotection by inhibiting IRI-induced mitochondrial fission, raising the possibility of repurposing hydralazine as a novel cardioprotective therapy for improving post-infarction outcomes.

Sign in / Sign up

Export Citation Format

Share Document