The interruption of collateral blood flow to the ischemic canine myocardium by embolization of a coronary artery with latex: effects on conduction delay and ventricular arrhythmias.

Euler, David E.; Prood, Charles; Spear, Joseph F.; Moore, E. Neil

doi:10.1161/01.res.49.1.97

Cited by 32 publications

(9 citation statements)

References 45 publications

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“…This indicates that neither improved 02 supply nor washout of metabolites from the ischemie myocardium influence this early bimodal vulnerability of the heart. These findings are confirmed by studies of Euler et al (6) in dogs and Cinca et al (4) in pigs. They compared the changes in local conduction and ectopic activity induced by coronary occlusion with those induced by coronary embolization with latex, thereby preventing any collateral flow to the ischemic myocardium.…”

Section: Importance Of Coronary Collateral Blood Flow In the First Arsupporting

confidence: 81%

Early changes in collateral blood flow to ischemic myocardium and their influence on bimodal vulnerability during the first 30 min of acute coronary artery occlusion in dogs

1988

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Coronary collateral blood flow and its changes during the first 30 min of acute coronary artery occlusion were studied in 34 anesthetized dogs to clarify its influence on the vulnerability of the heart in this first arrhythmic phase. Collateral flow was determined with 9-micron tracer microspheres (TM) injected at 1, 10 and 30 min after acute proximal occlusion of the left circumflex (LCX, n = 30) or left anterior descending (LAD, n = 4) coronary artery. The post-mortem selective retrograde coronary angiography was used to evaluate the functional extent of preexisting coronary collaterals. After acute LCX occlusions collateral flow increased significantly (p less than 0.05) from 17.8 +/- 2.7 ml.(min.100 g)-1 (mean +/- SE; n = 13) at 1 min to 29.3 +/- 5.1 ml . (min . 100 g)-1 at 30 min of occlusion in animals with well-formed preexisting coronary collaterals (group 1), whereas it was very low (4.7 +/- 0.6 ml . (min . 100 g)-1; n = 13) and changed only slightly in dogs with poor collaterals (group 2). Most of these animals died by ventricular fibrillation (VF) before a second measurement could be carried out. In four dogs with poor collaterals but an unusually small LCX area (group 3), flow remained almost constant (11.0 +/- 4.7 versus 11.0 +/- 4.4 ml . (min . 100 g)-1) during this period. Similar results were obtained in animals with acute LAD occlusion (group 4). Ventricular extrasystoles (VES) mainly developed in animals with poor collaterals and respective low and almost unchanging collateral flow (group 2,3,4) while none or only a few VES occurred in dogs in which flow initially was clearly higher and increased significantly (group 1). The animals of group 1, 3 and 4 all survived the first arrhythmic phase, whereas all the animals of group 2 died by VF, either in the arrhythmic subphase Ia (n = 7) or Ib (n = 6). The results of the present study show that only the initial magnitude of flow is decisive for the development of VES and VF during the first arrhythmic phase, whereas the subsequent increase in flow is of no importance to the bimodal vulnerability in the first arrhythmic phase (subphases Ia and Ib). The in vivo measured critical minimal collateral flow of about 5 ml . (min . 100 g)-1 corresponds well with the survival limit (border between collateral state III and IV) previously determined by post-mortem retrograde coronary angiography.

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Section: Importance Of Coronary Collateral Blood Flow In the First Arsupporting

confidence: 81%

Early changes in collateral blood flow to ischemic myocardium and their influence on bimodal vulnerability during the first 30 min of acute coronary artery occlusion in dogs

1988

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“…For example, large homogeneous infarctions are not arrhythmogenic. 12 The fact that dogs treated with phenol alone had a greater incidence of PVS-induced ventricular fibrillation than sham-operated dogs and that propranolol reduced the incidence of ventricular fibrillation supports the importance of catecholamine supersensitivity with or without infarction. Despite these limitations, it should be emphasized that in dogs in the ligation infarction plus phenol group, the incidence of induction of ventricular fibrillation was significantly greater than that in any other study group. In a recent study, nerve activity was recorded centrally in response to electrical stimulation applied to the epicardium of dogs subjected to latex-induced infarction or to ventricular fibrillation.30 However, the study did not provide any information on whether the recorded neural activity was normal or was adequate to elicit functional responses.…”

Section: Discussionmentioning

confidence: 88%

“…Because the injection of latex eliminates collateral blood flow, it is likely that dogs in the latex infarction group had infarctions that were as large or larger than those produced by ligation alone. 12 While the size of the infarction undoubtedly is important, the type of infarction is also critical. For example, large homogeneous infarctions are not arrhythmogenic.…”

Section: Discussionmentioning

confidence: 99%

Results of sympathetic denervation in the canine heart: supersensitivity that may be arrhythmogenic.

Inoue

Zipes²

1987

Circulation

242

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Latex-induced transmural myocardial infarction or epicardial application of phenol interrupts sympathetic fibers innervating myocardium apical to the infarction or to the phenol-painted area. These denervated regions subsequently show supersensitive shortening of effective refractory period (ERP) in response to the infusion of norepinephrine (denervation supersensitivity). The purpose of this study was to test the hypothesis that such denervation supersensitivity is arrhythmogenic. Ventricular arrhythmias were elicited by programmed ventricular stimulation (PVS) during a control period, during bilateral stimulation of the ansae subclaviae (4 msec pulses, 4 Hz and 3 mA), and during the infusion of norepinephrine (0.5 gg/kg/min). Study groups consisted of 14 sham-operated dogs, 16 dogs with phenol painted over a diagonal branch, 13 dogs with latex embolization of a diagonal branch that resulted in transmural myocardial infarction, 14 dogs with a one-stage ligation of a diagonal branch producing nontransmural myocardial infarction, and 12 dogs undergoing both phenol painting and onestage ligation of a diagonal branch. Four to 22 days after the first operation, PVS was performed in anesthetized, open-chest dogs after neural decentralization of the heart. Dogs with phenol painting on the epicardium and dogs in which latex was injected into a diagonal branch showed supersensitive shortening of ERP to infused norepinephrine at apical sites. PVS resulted in ventricular fibrillation more often during stimulation of the ansae subclaviae (p < .001) and infusion of norepinephrine (p < .001) than during the control state in dogs treated with phenol alone. The incidence of ventricular fibrillation was highest in dogs with ligation-induced infarction that received phenol compared with all other groups during control (p < .001), stimulation of the ansae subclaviae (p < .002), and the infusion of norepinephrine (p < .01). Propranolol (0.5 mg/kg or 10 mg iv at maximum) attenuated supersensitive shortening of ERP and decreased the incidence of induction of ventricular fibrillation. We conclude that (1) the canine heart with phenol-induced sympathetic supersensitivity, but without myocardial infarction, is more vulnerable to PVS-induced ventricular fibrillation during the infusion of norepinephrine compared with the control group, (2) the canine heart with latex-induced myocardial infarction shows sympathetic supersensitivity, but is not more vulnerable to PVS-induced ventricular fibrillation during stimulation of the ansae subclaviae and infusion of norepinephrine, (3) phenolinduced sympathetic supersensitivity combined with nontransmural myocardial infarction makes the canine heart more vulnerable to PVS-induced ventricular fibrillation than any of the other study conditions. Circulation 75, No. 4, 877-887, 1987

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“…One of the goals of the present study was to produce a localized transmural myocardial infarction in the region of a diagonal branch of the LAD that would involve both the endocardial and epicardial layers, where it has been postulated that the afferent nerve fibers course. Euler et al 14 showed that embolization of coronary arteries effectively and reproducibly resulted in transmural myocardial infarction within the distribution of the artery. Histochemical and histologic analyses of the infarcts studied in our own laboratory'2 demonstrated similar findings.…”

Section: Resultsmentioning

confidence: 99%

Interruption of sympathetic and vagal-mediated afferent responses by transmural myocardial infarction.

et al. 1985

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We have demonstrated previously that sympathetic and vagal afferents travel in an apical-to-basal course in the heart, and can be stimulated selectively with epicardial applications of bradykinin and nicotine, respectively. In this study we tested the hypothesis that transmural myocardial infarction interrupts sympathetic and vagal afferent fibers traveling through the infarction and produces regions of afferent denervation in areas apical to the infarction. In open-chest, chloralose-anesthetized dogs, transmural myocardial infarction was created by embolizing a diagonal branch of the left anterior descending coronary artery with a vinyl latex solution that was injected directly into the artery and hardened rapidly. The transmural nature of the infarction was verified by the nitro blue tetrazolium staining technique for dehydrogenase enzymes. Epicardial applications of bradykinin (5 jig) and nicotine (50 ,g) were used to stimulate chemically sensitive sympathetic and vagal afferent nerve endings, respectively. Twenty-nine dogs were studied before and 90 min after creation of transmural myocardial infarction. In 20 dogs, epicardial bradykinin applied before production of transmural myocardial infarction produced a maximal pressor response of 13 3

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The interruption of collateral blood flow to the ischemic canine myocardium by embolization of a coronary artery with latex: effects on conduction delay and ventricular arrhythmias.

Cited by 32 publications

References 45 publications

Early changes in collateral blood flow to ischemic myocardium and their influence on bimodal vulnerability during the first 30 min of acute coronary artery occlusion in dogs

Early changes in collateral blood flow to ischemic myocardium and their influence on bimodal vulnerability during the first 30 min of acute coronary artery occlusion in dogs

Results of sympathetic denervation in the canine heart: supersensitivity that may be arrhythmogenic.

Interruption of sympathetic and vagal-mediated afferent responses by transmural myocardial infarction.

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