Cardiac adrenergic innervation after instrumentation of the coronary artery in dog

Dolezel, S; Gerová, M; Hartmannová, B; Dostál, Miroslav; Janečková, Hana; Vasků, J

doi:10.1152/ajpheart.1984.246.3.h459

Cited by 16 publications

(7 citation statements)

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“…Dolezel et al 45 have shown that 2 weeks after surgical isolation of the LAD there is a 33% decrease in ventricular sympathetic neurons when compared with those in unoperated animals. Therefore, the possibility must be raised that the control group of sham-operated dogs represents a partially denervated group.…”

Section: Discussionmentioning

confidence: 99%

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Denervation supersensitivity of refractoriness in noninfarcted areas apical to transmural myocardial infarction.

et al. 1987

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Denervation supersensitivity was demonstrated in anesthetized dogs 5 to 10 days after transmural myocardial infarction produced by latex embolization of a diagonal branch of the left anterior descending coronary artery. Sympathetic efferent denervation in noninfarcted myocardium apical to the infarction was demonstrated by a 90% depletion of myocardial norepinephrine content in the apical (45 ± 15 pg norepinephrine/g tissue) vs basal (437 ± 76 pg/g tissue) regions and by the lack of effective refractory period (ERP) shortening during bilateral ansae subclaviae stimulation in 34% of sites apical to the infarction. Supersensitivity in the area apical to the infarction was manifested by an exaggerated shortening of the ERP during both norepinephrine and isoproterenol infusions, with an upward and leftward shift in the dose-response curves in the apical vs basal regions (p < .001). The cellular mechanism for denervation supersensitivity did not involve detectable changes in the ,Badrenergic receptor adenylate cyclase system. There was no difference in the density of /3-adrenergic receptors ([1251]-cyanopindolol) in the apical (268.6 ± 22.7 fmol/mg protein) vs the basal (253.5 ± 24.8 fmol/mg protein) regions. Adenylate cyclase activity stimulated by guanosine triphosphate plus isoproterenol was slightly greater in the apical (58.7 ± 17.4%) than in the basal (49.6 ± 10.9%) region, but this difference did not reach statistical significance (p = .068). Muscarinic modulation of fl-receptor coupling (oxotremorine attenuation of guanosine triphosphate plus isoproterenol-stimulated adenylate cyclase activity) also was not significantly different at the apical (31.6 ± 17.5% inhibition) and basal (21.4 ± 20.9% inhibition) sites. These data show that a transmural myocardial infarction produces denervation supersensitivity in areas apical to the infarction, but in this preparation no differences in the total number or a redistribution of ,B-adrenergic receptors or adenylate cyclase activity were detected. Data from several studies indicate that efferent sympathetic nerves of the left ventricle course in the superficial subepicardium before diving transmurally, and travel in a basal-to-apical direction.0 15. 16 We have demonstrated that transmural myocardial infarction, presumably by affecting the postganglionic sympathetic nerves that traverse the area of infarction, produces sympathetic denervation in viable myocardium apical to the infarction. 7 We therefore reasoned that this area of myocardium might exhibit an exaggerated response to infused norepinephrine. We chose to investigate an electrophysiologic end point, shortening of effective refractory period (ERP), because it may be important in the development of arrhythmias.'`The purpose of this study was to test the hypothesis that transmural myocardial infarction produces sympathetic denervation supersensitivity in noninfarcted myocardium apical to the infarction.

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Section: Discussionmentioning

confidence: 99%

“…Ventilation was adjusted and sodium bicarbonate was administered to maintain Po2 at greater than 85 mm Hg and pH at between 7.35 and 7. 45.…”

Section: Methodsmentioning

confidence: 99%

Denervation supersensitivity of refractoriness in noninfarcted areas apical to transmural myocardial infarction.

et al. 1987

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“…In the dog, ablation of discrete areas of the ventricular epicardium revealed the presence of sympathetic fibres running in the epicardium occasionally along the main coronary arteries (21). The presence of major bundles of adrenergic fibres running along the LAD in the dog was confirmed by Dolezel et al (8).…”

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confidence: 80%

Adrenergic innervation of coronary arteries and ventricular myocardium in the pig: fluorescence microscopic appearance in the normal state and after ischemia

Holmgren

Abrahamsson²,

Almgren³

1985

Basic Res Cardiol

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A fluorescence histochemical study was performed to describe the adrenergic innervation of the coronary arteries and the left ventricular myocardium in the pig. Large bundles of adrenergic nerve fibres were almost exclusively found running along the large coronary arteries. The arteries usually show a dense innervation of the vessel wall, evenly distributed throughout the adventitia in the larger arteries and more concentrated to the adventitia-medial border in the smaller arteries and arterioles. Most parts of the left ventricular myocardium showed a dense adrenergic innervation, however, a moderate dense and in some areas even sparse innervation was observed towards the apex of the left ventricle. Following 10 or 20 min of ischemia a small reduction in fluorescence intensity was observed in 2 out of 6 hearts. In 4 of the hearts other changes of the appearance of the adrenergic terminals were found, e.g., an unsharp, spread-out or interrupted appearance.

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“…67 Second, this method obviates the need for surgical dissection, required for circumferential probes, and possible attendant denervation. 15 - 16 However, significant changes in large coronary vessel diameter during sympathetic activation could influence the flow measurements. For several reasons, we believe that this would not alter the interpretation of this study.…”

Section: Methods Of Measuring Coronary Blood Flowmentioning

confidence: 99%

Coronary vascular response to the cerebral ischemia reflex.

Boel

Gutterman

1993

Hypertension

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Most centrally mediated sympathoexcitatory reflexes produce increases in arterial pressure, heart rate, and peripheral vascular resistance, including coronary vasoconstriction. Cerebral ischemia also causes large increases in arterial pressure and peripheral vasoconstriction but with modest or variable changes in heart rate. To examine the effect of cerebral ischemia on coronary vascular resistance, we produced cerebral ischemia in 14 cats by occluding the right brachiocephalic and left subclavian arteries for 30 seconds. After vagotomy and ^-blockade, a marked increase in arterial pressure (89±14%) and coronary vascular resistance (52 ±7%) was seen. After inhibition of the carotid baroreceptor reflex by surgical denervation and application of topical lidocaine, the increase in arterial pressure to cerebral ischemia was not affected, but the increase in coronary vascular resistance was attenuated (33 ±6%; p<0.05 versus before denervation) to a level expected with autoregulation. To evaluate the possible contribution of the chemoreflex on coronary blood flow during cerebral ischemia, we conducted separate experiments in which nicotine was injected into both carotid arteries. Coronary constriction was not observed. Adrenalectomy and upper extremity ischemia likewise did not alter coronary vascular resistance. We conclude that cerebral ischemia elicits neurally mediated coronary vasoconstriction as a result of baroreceptor hypotension rather than directly. The relative absence of neurogenic coronary constriction and changes in heart rate suggest that sympathoexcitation during cerebral ischemia is directed more toward the peripheral vasculature than the heart. {Hypertension 1993;21:216-221) KEY WORDS • vasoconstriction • pressoreceptors • sympathetic nervous system • cerebral ischemiaA variety of reflex stimuli produce a-adrenergicmediated coronary vasoconstriction. Barore->. ceptor hypotension, 1 activation of carotid chemoreceptors, 2 and nociceptive reflexes, 3 as well as static 4 and dynamic exercise, 5 all increase systemic arterial pressure, heart rate, and coronary vascular resistance through sympathetic activation.Cerebral ischemia, produced by interruption of perfusion to the head, is a potent stimulus for sympathetic discharge. However, unlike most sympathoexcitatory reflexes, tachycardia is not a consistent feature of the ischemic response. The effect of cerebral ischemia on coronary flow is difficult to predict. The large pressor response to cerebral ischemia suggests that neurogenic coronary constriction accompanies the sympathoexcitation. However, other sympathoexcitatory reflexes producing coronary constriction include tachycardia. BradyFrom the Veterans Administration

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Cardiac adrenergic innervation after instrumentation of the coronary artery in dog

Cited by 16 publications

References 0 publications

Denervation supersensitivity of refractoriness in noninfarcted areas apical to transmural myocardial infarction.

Denervation supersensitivity of refractoriness in noninfarcted areas apical to transmural myocardial infarction.

Adrenergic innervation of coronary arteries and ventricular myocardium in the pig: fluorescence microscopic appearance in the normal state and after ischemia

Coronary vascular response to the cerebral ischemia reflex.

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