Consequences of Coronary Occlusion on Changes in Regional Interstitial Myocardial Neuropeptide Y and Norepinephrine Concentrations

Mertès, Paul-Michel; El-Abbassi, Khalid; Jaboin, Y.; Michel, Christophe B; Beck, Bernard; Pinelli, G; Carteaux, Jean‐Pierre; Villemot, Jean Pierre; Burlet, C.

doi:10.1006/jmcc.1996.0192

Cited by 18 publications

(8 citation statements)

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“…Judging from the relations between median and IQR values for each sampling, the intraprobe variation of the relative recovery during the six consecutive samplings was high. This result differs from previous studies where low intraprobe variations were found during microdialysis of NPY (Lambert et al, 1994;Mertes et al, 1993Mertes et al, , 1996Thompson et al, 1995). The reason for the large variation in the present study is unknown, but cannot be explained by degradation of the standard solution since there was no significant difference in NPY concentration between the standard samples obtained at different times.…”

Section: Resultscontrasting

confidence: 85%

“…They found a relative in vitro NPY recovery of 23% with a 10 mm cellulose membrane and a flow rate of 2 l/min. The same group has also demonstrated a 27% relative in vitro recovery of NPY using a 12 mm polyacrylonitrile membrane at 2 l/min (Mertes et al, 1996). The higher relative recovery in these studies compared to the present study could be explained by lower flow rate and perhaps also by the different membrane material used (Hsiao et al, 1990;Ungerstedt, 1991).…”

Section: Discussioncontrasting

confidence: 44%

“…The in vivo and in vitro relative recovery has been shown to differ significantly (Alexander et al, 1988;Mertes et al, 1996). Calculation of the tissue concentration based upon the known in vitro recovery is thus not recommendable.…”

Section: Discussionmentioning

confidence: 95%

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Microdialysis of neuropeptide Y in human muscle tissue

Ernberg

Alstergren

2004

Journal of Neuroscience Methods

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Section: Resultscontrasting

confidence: 85%

Section: Discussioncontrasting

confidence: 44%

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Microdialysis of neuropeptide Y in human muscle tissue

Ernberg

Alstergren

2004

Journal of Neuroscience Methods

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“…Previous studies (18,19) have shown that, in the in vivo nonischemic pig heart, a localized subepicardial infusion of norepinephrine (NE), the permeant cyclic-AMP analog dibutyryl-cAMP, or inhibitors of cyclic nucleotide phosphodiesterase were effective in causing a sustained ventricular arrhythmia, resulting in depressed hemodynamics. In the clinical situation, highadrenergic tone is known to occur around regions of ischemia (11) or during right ventricular (RV) outflow tract dysfunction (16), both of which may facilitate spontaneous activity in the ventricular myocardium (10).…”

mentioning

confidence: 99%

Ventricular activation during sympathetic imbalance and its computational reconstruction

Nash¹,

Thornton²,

Sears

et al. 2001

Journal of Applied Physiology

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We characterized the epicardial activation sequence during a norepinephrine (NE)-induced ventricular arrhythmia in anesthetized pigs and studied factors that modulated it. Subepicardial NE infusion caused the QRS complex to invert within a single beat (n = 35 animals, 101 observations), and the earliest epicardial activation consistently shifted to the randomly located infusion site (n = 14). This preceded right atrial activation, whereas the total ventricular epicardial activation time increased from 20 +/- 4 to 50 +/- 9 ms (P < 0.01). These events were accompanied by a ventricular tachycardia and a drop in left ventricular pressure, which were fully reversed after the infusion was stopped. Epicardial pacing at the infusion site mimicked all electrical and hemodynamic changes induced by NE. The arrhythmia was prevented by propranolol and abolished by cardiac sympathetic or vagal nerve stimulation. Focal automaticity was computationally reconstructed using a two-dimensional sheet of 256 x 256 resistively coupled ventricular cells, where calcium handling was abnormally high in the central region. We conclude that adrenergic stimulation to a small region of the ventricle elicits triggered automaticity and that computational reconstruction implicates calcium overload. Interventions that reduce spatial inhomogeneities of intracellular calcium may prevent this type of arrhythmia.

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“…39 Platelet aggregation in diseased donor arteries from which collateral vessels arise would have potential to decrease blood flow to the dependent myocardial region. In addition, ischemia can cause release of other mediators of vasoconstriction such as neuropeptide Y 40 or endothelin 41 which could contribute to impaired perfusion of collateraldependent myocardium.…”

Section: Discussionmentioning

confidence: 99%

Effect of Platelet Activation on Coronary Collateral Blood Flow

Kinn

Bache

1998

Circulation

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Background-The platelet products thromboxane A 2 and serotonin have been shown to cause constriction of welldeveloped coronary collateral vessels. This study was performed to determine whether intravascular platelet activation produced with platelet activating factor (PAF) can cause a decrease in coronary collateral blood flow. Methods and Results-Collateral vessel growth was induced by embolization of a hollow stainless steel plug into the left anterior descending coronary artery (LAD) of adult dogs. The animals were returned to the laboratory 3 to 6 weeks later for surgical instrumentation and measurement of collateral blood flow. Collateral flow was assessed by measuring retrograde blood flow from the cannulated collateral-dependent artery. PAF (10 nmol) was injected into the left main coronary artery to allow products of platelet activation to reach collateral vessels arising from the left coronary system. PAF caused a vasoconstrictor response, which became maximal 3 minutes after injection and resulted in a 40.3Ϯ7.4% decrease in retrograde blood flow (32.1Ϯ2.1 to 19.6Ϯ3.2 mL/min; PϽ0.05). By 15 minutes after the PAF injection, both retrograde blood flow and transcollateral resistance had returned to normal. After pretreatment with the thromboxane A 2 receptor antagonist SQ30,741, the vasoconstrictor response to PAF was abolished and, in contrast to the decrease in retrograde blood flow from PAF alone, a weak vasodilator effect was unmasked. Conclusions-PAF caused a decrease in coronary collateral blood flow. This vasoconstrictor response required the participation of thromboxane A 2 .

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Consequences of Coronary Occlusion on Changes in Regional Interstitial Myocardial Neuropeptide Y and Norepinephrine Concentrations

Cited by 18 publications

References 0 publications

Microdialysis of neuropeptide Y in human muscle tissue

Microdialysis of neuropeptide Y in human muscle tissue

Ventricular activation during sympathetic imbalance and its computational reconstruction

Effect of Platelet Activation on Coronary Collateral Blood Flow

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