Key result
Larger hypoperfused areas during reperfusion proportionally correlate with greater norepinephrine release and sustained VT.
In a canine model, the magnitude of norepinephrine release and the incidence of sustained ventricular tachycardia during reperfusion are proportionally related to the size of the hypoperfused ventricular area.
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May link larger ischemic zones to greater reperfusion VT risk via norepinephrine in dogs; hypothesis-generating for human arrhythmia mechanisms and targets.
In anesthetized dogs, 60-min occlusions of either the proximal (n = 14), distal (n = 8) left circumflex (LCX), or left anterior descending (LAD, n = 10) arteries were followed by reperfusion. Coronary sinus and aortic norepinephrine and epinephrine plasma concentrations were measured. The ventricular arrhythmias were ventricular premature depolarizations (VPDs), unsustained ventricular tachycardia (VT) ([Formula: see text] and <20 VPDs), sustained VT ([Formula: see text] VPDs), and ventricular fibrillation (VF). A gradual twofold increase (p < 0.05) in myocardial norepinephrine overflow followed occlusion in all three groups. The increases in the amounts of norepinephrine released in the coronary sinus blood during reperfusion were significant and proportional to the size of the occluded area: proximal LCX, from 0.236 ± 0.038 to 1.528 ± 0.490 ng/mL of plasma (p < 0.001); LAD, from 0.180 ± 0.027 to 0.795 ± 0.286 ng/mL (p < 0.05); distal LCX, from 0.215 ± 0.039 to 0.404 ± 0.110 ng/mL (p < 0.05). Aortic epinephrine concentrations were significantly increased only by LAD occlusion; at 15 min, the value had increased to 0.187 ± 0.053 ng/mL from an initial value of 0.069 ± 0.029 ng/mL (p < 0.001). Two phases of ventricular arrhythmias followed both occlusion and reperfusion. Phase 1 postocclusion was characterized by VPDs and phase 2 by VPDs and unsustained VT. Sustained VT was seen only in phase 1 postreperfusion, whereas unsustained VT was seen in phase 2. VF was seen in 50, 35, and 25% of the dogs with proximal LCX, LAD, and distal LCX occlusion and reperfusion. Sustained VT occurred in 90, 45, and 30% of the dogs during proximal LCX, LAD, and distal LCX reperfusion. In conclusion, postocclusion and phase-2 reperfusion arrhythmias did not appear to be related to either increased coronary sinus norepinephrine or aortic epinephrine concentrations. However, the occurrence and time course of reperfusion-sustained VT closely followed those of norepinephrine washout. Furthermore, both the magnitude of norepinephrine release and the incidence of sustained VT appeared to be proportionally related to the size of the hypoperfused ventricular area.
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Godin‐Ribuot et al. (1985) studied Myocardial ischemia and reperfusion (n=32). 60-minute coronary occlusion and reperfusion vs. Baseline / different occlusion sites was evaluated on Myocardial norepinephrine overflow and ventricular arrhythmias. In anesthetized dogs, the magnitude of norepinephrine release and the incidence of sustained ventricular tachycardia during reperfusion were proportionally related to the size of the hypoperfused area.
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