scholarly journals High Density Intramural Mapping of Post-Infarct Premature Ventricular Contractions.

2021 ◽  
Author(s):  
Eugene Downar ◽  
Michiel Janse ◽  
Abhishek Bhaskaran ◽  
Ahmed Niri ◽  
Arulalan Velluppillai ◽  
...  
Keyword(s):  
Canine Model ◽  
High Density ◽  
Ischemic Myocardium ◽  
Acute Ischemia ◽  
Ectopic Activity ◽  
Premature Ventricular Contractions ◽  
Diagonal Branch ◽  
Graded Responses ◽  
Anesthetized Dogs ◽  
Unipolar Electrograms

Background: Spontaneous ventricular premature contractions (PVCs) in the post infarct milieu is assumed to be due to automaticity. However, the mechanism has not been studied with appropriate mapping tools. Objective: To study the mechanism of spontaneous PVCs with high density intramural mapping in a canine model, to test the hypothesis that post-infarct PVCs are due to re-entry rather than automaticity. Methods: In 15 anesthetized dogs, using 768 intramural unipolar electrograms, simultaneous recordings were made. After 30 mins of stabilization, recordings were made during the first 10 minutes of ischemia, and activation maps were constructed of individual beats. Acute ischemia was produced by clamping the left anterior descending coronary artery proximal to the first diagonal branch. The analysis was limited to the activation pattern of spontaneous ventricular beats. Results: In all experiments ST-T alternans occurred. In 8 of 15 dogs spontaneous ventricular beats occurred. In all 8 of these experiment earliest, ectopic activity occurred in the endocardium, well within the ischemic zone. From there, activity spread rapidly along the subendocardium, with endo-to epicardial spread along the non ischemic myocardium. Epicardial breakthrough always occurred at the border of the ischemic myocardium. In 3 dogs, delayed potentials were observed, which were earliest at the ischemic epicardium and extended transmurally with increasing delay towards the endocardium, where they culminated in a premature beat. Conclusion: Graded responses that occur with each sinus beat intramurally, when able to propagate from epicardium to endocardium is the mechanism by which PVCs are generated in post-infarct myocardium.

Differential cardiac sympathetic activity during acute myocardial ischemia

1990 ◽  
Vol 258 (5) ◽  
pp. H1534-H1541 ◽  
Author(s):  
B. H. Neely ◽  
G. R. Hageman
Keyword(s):  
Sympathetic Activity ◽  
Coronary Occlusion ◽  
Left Ventricular ◽  
Ischemic Myocardium ◽  
Neural Responses ◽  
Ischemic Region ◽  
Innervation Patterns ◽  
Anesthetized Dogs ◽  
Increased Activity ◽  
Cardiac Nerves

Efferent sympathetic activities were simultaneously recorded from two thoracic cardiac nerves in 33 chloralose-anesthetized dogs. Efferent innervation patterns were determined by electrical stimulation prior to recording in each animal. One of the nerves selected for recording was shown to innervate the proposed ischemic region, whereas the other nerve was selected because it was shown to innervate nonischemic regions. Left ventricular ischemia was produced by occlusion of a branch of either the left anterior descending (LAD) or left circumflex (LCX) coronary arteries. Heart rate was paced. Cardiac postganglionic sympathetic efferent activities were recorded during a 30-min coronary occlusion in 22 animals. Thirty minutes after LAD occlusion (n = 10), postganglionic sympathetic activity to ischemic myocardium was decreased (84 +/- 5% of control; P less than 0.05) while activity to nonischemic myocardium was unchanged. Thirty minutes after LCX occlusion (n = 12), postganglionic sympathetic activity to ischemic myocardium was also decreased (87 +/- 3% of control; P less than 0.01); however, sympathetic activity to nonischemic myocardium was increased (159 +/- 10% of control; P less than 0.001). Thus, in the anesthetized canine, regional left ventricular ischemia elicits differential sympathetic neural responses that are dependent on the location of the ischemic myocardium as well as the efferent destinations of the nerves. Changes in cardiac postganglionic sympathetic efferent activities are characterized by decreased activity to ischemic regions, with either no change or increased activity to nonischemic regions.

scholarly journals Cardiac progenitor-derived exosomes protect ischemic myocardium from acute ischemia/reperfusion injury

2013 ◽  
Vol 431 (3) ◽  
pp. 566-571 ◽  
Author(s):  
Lijuan Chen ◽  
Yingjie Wang ◽  
Yaohua Pan ◽  
Lan Zhang ◽  
Chengxing Shen ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ischemic Myocardium ◽  
Acute Ischemia

Effect of Ibutilide, a New Class III Agent, On Sustained Atrial Fibrillation in a Canine Model of Acute Ischemia and Myocardial Dysfunction Induced By Microembolization

1993 ◽  
Vol 16 (10) ◽  
pp. 1975-1983 ◽  
Author(s):  
MERVAT A. NABIH ◽  
PETAR PRCEVSKI ◽  
BARBARA S. FROMM ◽  
STEVEN J. LAVINE ◽  
MOHAMED ELNABTITY ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Myocardial Dysfunction ◽  
Canine Model ◽  
Acute Ischemia ◽  
Class Iii ◽  
New Class

EFFECT OF THE NEW ALPHA2-ADRENERGIC AGONIST MIVAZEROL ON METABOLISM AND BLOOD FLOW OF ISCHEMIC MYOCARDIUM IN ANESTHETIZED DOGS

1994 ◽  
Vol 81 (SUPPLEMENT) ◽  
pp. A758
Author(s):  
P. M. H.J. Roekaerts ◽  
F. W. Prinzen ◽  
H. W. W. Willigers ◽  
S. De Lange
Keyword(s):  
Blood Flow ◽  
Ischemic Myocardium ◽  
Adrenergic Agonist ◽  
Anesthetized Dogs

Myocardial Gene Expression of Angiogenic Factors in Human Chronic Ischemic Myocardium: Influence of Acute Ischemia/Cardioplegia and Reperfusion

2006 ◽  
Vol 13 (3) ◽  
pp. 187-197 ◽  
Author(s):  
Yongzhong Wang ◽  
Anders Gabrielsen ◽  
Patrick R. Lawler ◽  
Gabrielle Paulsson-Berne ◽  
Daniel A. Steinbrüchel ◽  
...  
Keyword(s):  
Gene Expression ◽  
Angiogenic Factors ◽  
Ischemic Myocardium ◽  
Acute Ischemia ◽  
Myocardial Gene Expression

Anonlethal, Anesthetized Canine Model for Efficacy Evaluation of Anticyanide Therapy

1997 ◽  
Vol 16 (2) ◽  
pp. 141-149 ◽  
Author(s):  
F. M. Reid ◽  
R. G. Menton ◽  
K. K. Audet ◽  
M. Marino ◽  
T. G. Brewer ◽  
...  
Keyword(s):  
Canine Model ◽  
Respiratory Arrest ◽  
Sodium Cyanide ◽  
Repeated Testing ◽  
Efficacy Evaluation ◽  
Respiratory Effects ◽  
Anesthetized Dogs ◽  
Unanesthetized Animals ◽  
S Period ◽  
Therapeutic Compounds

Efficacy evaluations of anticyanide therapeutic compounds historically have used lethality in unanesthetized animals as the toxic endpoint, and a nonlethal, repeated-testing, anesthetized canine model has been reported. Time to respiratory arrest (TRA) induced by a continuous, slow intravenous (IV) infusion of sodium cyanide (Na CN) was shown to be a consistent, well-defined endpoint in anesthetized canines. Thirty seconds after respiratory arrest (RA), an IV bolus of a methemoglobin-forming compound reversed the respiratory effects. This study was designed to determine the variability in TRA, survivability of anesthetized dogs repeatedly infused with Na CN and treated with hydroxylamine, replicability of the procedure within an animal and between animals, and development of trends in data. Four animals were anesthetized, intubated, catheterized, and instrumented to record respiratory rate and heart rate. Immediately following baseline data collection, a 4-mgl m L. Na CN solution w as infused at a rate of 2 m Llmin. Following a 10-s period without functional respiration, infusion was stopped and this moment was designated as RA. Hydroxylamine therapy was administered 30 s after RA. There were 4 replicate experiments per animal with a 1-week washout period between replicates. Interanimal variability in TRA was significant (p = <.04). The average variability in TRA within an animal was less than 10%. Baseline heart and respiratory rates were not altered significantly. Data confirm, by replicate testing, the utility of this model.

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