Time Course and Mechanism of Myocardial Catecholamine Release During Transient Ischemia In Vivo

Lameris, Thomas W.; Zeeuw, Sandra de; Alberts, Gooitzen; Boomsma, Frans; Duncker, Dirk J.; Verdouw, Pieter D.; Veld, A. J. Man In 'T; Meiracker, Anton H. van den

doi:10.1161/01.cir.101.22.2645

Cited by 126 publications

(127 citation statements)

References 25 publications

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“…Treatment, surgical procedure, and positioning of catheters and flow probes have been described previously. 19,20 In animals subjected to LAD flow reduction, a fluid-filled balloon occluder (In Vivo Metric) was placed around the LAD distal to the Doppler flow probe and attached to a bidirectional roller pump (Ismatec). The voltage output from the Doppler equipment was directed through a custom-built electrical circuit, which steered the roller pump to maintain LAD flow at 30% of baseline values.…”

Section: Animal Proceduresmentioning

confidence: 99%

“…Probes were perfused with Ringer's solution (Baxter) at a flow of 2 L/min, and dialysate was collected at 10-minute intervals, during which period blood was collected from the aorta and the interventricular coronary vein. 19,20 In group I (nϭ7), the effects of angiotensin II on basal sympathetic norepinephrine release were investigated by infusing angiotensin II (Department of Pharmacy) into the LAD at consecutive infusion rates of 0.05, 0.5, and 5 ng/kg per minute for 20 minutes each. In group II (nϭ7), we assessed the effects of angiotensin II on enhanced exocytotic norepinephrine release by stimulating the left stellate ganglion before and during infusion of angiotensin II.…”

Section: Experimental Protocolmentioning

confidence: 99%

“…22,23 Therefore, we not only investigated the modulation of NE MIF by angiotensin II under basal conditions but also during enhanced exocytotic norepinephrine release evoked by stimulation of the left stellate ganglion. In addition, we monitored norepinephrine release in MIF during reduction of left anterior descending coronary artery (LAD) flow, resulting in both exocytotic and nonexocytotic norepinephrine release, 20 while still allowing for intracoronary infusion of angiotensin II.…”

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Exogenous Angiotensin II Does Not Facilitate Norepinephrine Release in the Heart

et al. 2002

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Abstract-Studies on the effect of angiotensin II on norepinephrine release from sympathetic nerve terminals through stimulation of presynaptic angiotensin II type 1 receptors are equivocal. Furthermore, evidence that angiotensin II activates the cardiac sympathetic nervous system in vivo is scarce or indirect. In the intact porcine heart, we investigated whether angiotensin II increases norepinephrine concentrations in the myocardial interstitial fluid (NE MIF ) under basal conditions and during sympathetic activation and whether it enhances exocytotic and nonexocytotic ischemia-induced norepinephrine release. In 27 anesthetized pigs, NE MIF was measured in the left ventricular myocardium using the microdialysis technique. Key Words: norepinephrine Ⅲ angiotensin II Ⅲ renin-angiotensin system Ⅲ sympathetic nervous system A ctivation of the sympathetic nervous system simultaneously leads to activation of the renin-angiotensin system via stimulation of ␤-adrenergic receptors within the kidney, resulting in an increased renin release. There is also evidence, albeit conflicting, that the sympathetic nervous system is activated by the renin-angiotensin system. 1-13 This activation supposedly occurs through stimulation of angiotensin II receptors within the central nervous system and/or stimulation of presynaptic angiotensin II receptors located at sympathetic nerve terminals. When investigating the sympathetic nervous system and its interaction with the renin-angiotensin system, the heart is of particular interest. First of all, the mammalian heart has a dense sympathetic innervation. Second, all components of the renin-angiotensin system are present in the heart, and most angiotensin II in the heart is formed from locally synthesized angiotensin I. 14 Third, in conditions like hypertension, ischemia, and especially heart failure, the renin-angiotensin system and sympathetic nervous system are both activated, and this activation likely contributes to the deterioration of cardiac function. [15][16][17] Evidence that angiotensin II activates the cardiac sympathetic nervous system in vivo is scarce 4 or indirect. 7,18 In a recent study, Teisman et al 4 have shown with the use of the microdialysis technique that "pharmacological" (10 Ϫ6 mol/L) concentrations of locally applied angiotensin II were associated with an increase in norepinephrine concentrations in the myocardial interstitial fluid (NE MIF ) of the in vivo rat heart. In the present study, we determined whether "physiological" (10 Ϫ10 mol/L) to "pathophysiological" (10 Ϫ8 mol/L) concentrations of angiotensin II modulate NE MIF in the intact porcine heart. The pig is especially suitable as a model for studying the cardiac sympathetic nervous system because, unlike the rat, the prevailing parasympathetic control of cardiac function is very similar to that in man, which allows for a more reliable extrapolation of the experimental results to the reality of human patients.To exclude a masking effect of neuronal norepinephrine reuptake and negative feedback through pr...

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Section: Animal Proceduresmentioning

confidence: 99%

Section: Experimental Protocolmentioning

confidence: 99%

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Exogenous Angiotensin II Does Not Facilitate Norepinephrine Release in the Heart

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“…The early stage of acute ischemia is characterized by abrupt metabolic and electrophysiological changes in the affected area (11). Among them, the more prominent are increased extracellular potassium ([K ϩ ] o ) (25,26), decreased creatine phosphate (43,63), elevated intracellular inorganic phosphate (63), acidosis (27,46), catecholamine release (39), and partial depolarization of transmembrane potential (V m ) (28,36).…”

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Regional increase of extracellular potassium leads to electrical instability and reentry occurrence through the spatial heterogeneity of APD restitution

Sidorov¹,

Uzelac

Wikswo

2011

American Journal of Physiology-Heart and Circulatory Physiology

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Sidorov VY, Uzelac I, Wikswo JP. Regional increase of extracellular potassium leads to electrical instability and reentry occurrence through the spatial heterogeneity of APD restitution. Am J Physiol Heart Circ Physiol 301: H209 -H220, 2011. First published May 2, 2011; doi:10.1152/ajpheart.01141.2010.-The heterogeneities of electrophysiological properties of cardiac tissue are the main factors that control both arrhythmia induction and maintenance. Although the local increase of extracellular potassium ([K ϩ ]o) due to coronary occlusion is a well-established metabolic response to acute ischemia, the role of local [K ϩ ]o heterogeneity in phase 1a arrhythmias has yet to be determined. In this work, we created local [K ϩ ]o heterogeneity and investigated its role in fast pacing response and arrhythmia induction. The left marginal vein of a Langendorff-perfused rabbit heart was cannulated and perfused separately with solutions containing 4, 6, 8, 10, and 12 mM of K ϩ . The fluorescence dye was utilized to map the voltage distribution. We tested stimulation rates, starting from 400 ms down to 120 ms, with steps of 5-50 ms. We found that local [K ϩ ]o heterogeneity causes action potential (AP) alternans, 2:1 conduction block, and wave breaks. The effect of [K ϩ ]o heterogeneity on electrical stability and vulnerability to arrhythmia induction was largest during regional perfusion with 10 mM of K ϩ . We detected three concurrent dynamics: normally propagating activation when excitation waves spread over tissue perfused with normal K ϩ , alternating 2:2 rhythm near the border of [K ϩ ]o heterogeneity, and 2:1 aperiodicity when propagation was within the high [K ϩ ]o area. [K ϩ ]o elevation changed the AP duration (APD) restitution and shifted the restitution curve toward longer diastolic intervals and shorter APD. We conclude that spatial heterogeneity of the APD restitution, created with regional elevation of [K ϩ ]o, can lead to AP instability, 2:1 block, and reentry induction. restitution heterogeneity; regional perfusion; optical mapping THE STATIONARY AND DYNAMIC heterogeneities of electrophysiological properties of cardiac tissue play a key role in the induction and maintenance of cardiac arrhythmias (1,10,16,59). Cardiac tissue heterogeneities increase drastically when acute regional ischemia occurs. The early stage of acute ischemia is characterized by abrupt metabolic and electrophysiological changes in the affected area (11). Among them, the more prominent are increased extracellular potassium ([K ϩ ] o ) (25, 26), decreased creatine phosphate (43, 63), elevated intracellular inorganic phosphate (63), acidosis (27, 46), catecholamine release (39), and partial depolarization of transmembrane potential (V m ) (28,36).Since an early change in V m closely relates to [K ϩ ] o accumulation (34, 60), the K ϩ imbalance is considered to be the major factor affecting excitability and is responsible for slow impulse propagation and induction of reentry (51) Although numerous studies have been devoted to investigation ...

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“…Myocardial ischemia and infarction may induce serious ventricular arrhythmias early within the first hour of ischemia (Perron 2005). During myocardial ischemia, concentrations of catecholamines may rise in the ischemic tissue (Lameris 2000). This may impose a risk of further damage (Opie 1975, Kübler 1994.…”

Section: Myocardial Ischemiamentioning

confidence: 99%

Myocardial ischemia-reperfusion and cardioprotection: a study with microdialysis in a porcine model

Metzsch

2011

Acta Anaesthesiologica Scandinavica

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Time Course and Mechanism of Myocardial Catecholamine Release During Transient Ischemia In Vivo

Cited by 126 publications

References 25 publications

Exogenous Angiotensin II Does Not Facilitate Norepinephrine Release in the Heart

Exogenous Angiotensin II Does Not Facilitate Norepinephrine Release in the Heart

Regional increase of extracellular potassium leads to electrical instability and reentry occurrence through the spatial heterogeneity of APD restitution

Myocardial ischemia-reperfusion and cardioprotection: a study with microdialysis in a porcine model

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