Local myocardial perfusion and epicardial NADH-fluorescence after coronary artery ligation in the isolated guinea pig heart

Rösen, R.; Marsen, A.; Klaus, W.

doi:10.1007/bf01935807

Cited by 9 publications

(3 citation statements)

References 18 publications

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“…The guinea pig has a well-characterized autonomic neural phenotype (27,41) and has been successfully used to model ventricular fibrillation (18). However, guinea pigs have considerable cardiac arterial collateralization (39,45), and evidence has been presented that the guinea pig is impossible to infarct with a single coronary artery ligation (39), although others report variable success with this approach (30). For this reason, the arterial supply of the anterior left ventricle was ligated in four separate locations.…”

Section: Methodsmentioning

confidence: 99%

Cardiac cholinergic NO-cGMP signaling following acute myocardial infarction and nNOS gene transfer

Dawson¹,

Li²,

Woodward³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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DJ. Cardiac cholinergic NO-cGMP signaling following acute myocardial infarction and nNOS gene transfer. Am J Physiol Heart Circ Physiol 295: H990 -H998, 2008. First published July 11, 2008 doi:10.1152/ajpheart.00492.2008 is associated with oxidative stress, which may cause cardiac autonomic impairment. We tested the hypothesis that acute MI disrupts cardiac cholinergic signaling by impairing nitric oxide (NO)-cGMP modulation of acetylcholine (ACh) release and whether the restoration of this pathway following cardiac neuronal NO synthase (nNOS) gene transfer had any bearing on the neural phenotype. Guinea pigs underwent four ligature coronary artery surgery (n ϭ 50) under general anesthesia to induce MI or sham surgery (n ϭ 32). In a separate group, at the time of MI surgery, adenovirus encoding nNOS (n ϭ 29) or enhanced green fluorescent protein (eGFP; n ϭ 30) was injected directly into the right atria, where the postganglionic cholinergic neurons reside. In vitro-evoked right atrial [ 3 H]ACh release, right atrial NOS activity, and cGMP levels were measured at 3 days. Post-MI 24% of guinea pigs died compared with 9% in the sham-operated group. Evoked right atrial [ 3 H]ACh release was significantly (P Ͻ 0.05) decreased in the MI group as was NOS activity and cGMP levels. Tetrahydrobiopterin levels were not significantly different between the sham and MI groups. Infarct sizes between genetransferred groups were not significantly different. The nNOS transduced group had significantly increased right atrial [ 3 H]ACh release, right atrial NOS activity, cGMP levels, and decreased cAMP levels. Fourteen percent of the nNOS transduced animals died compared with 31% mortality in the MI ϩ eGFP group at 3 days. In conclusion, cardiac nNOS gene transfer partially restores the defective NO-cGMP cholinergic pathway post-MI, which was associated with a trend of improved survival at 3 days. autonomic nervous system; gene therapy; sudden death; neuronal nitric oxide synthase; nitric oxide; guanosine 3Ј,5Ј-cyclic monophosphate MYOCARDIAL INFARCTION (MI) is associated with increased oxidative stress (40, 50), which may disrupt nitric oxide (NO) cyclic nucleotide signaling. This process has been implicated in impaired autonomic control in a number of chronic cardiovascular diseases (25,32,37,43). In the peripheral nervous system under normal conditions, neuronal NO synthase (nNOS) facilitates the release of cardiac acetylcholine (ACh) (15,26,42), inhibits the release of cardiac norepinephrine (47), and decreases heart rate (10) by the modulation of intracellular calcium handling (53). Postsynaptically, nNOS is positioned in discrete subcellular domains where it assists in the regulation of sarcoplasmic reticulum calcium handling (49), excitationcontraction coupling (48), and ␤-adrenergic and muscarinic regulation of the L-type calcium channel current (ICa L ) (16,22,24) in cardiac pacemaking.In the spontaneously hypertensive rat (SHR), both NOS activity and cGMP levels are decreased in the right atria, where cholinergic intracar...

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Section: Methodsmentioning

confidence: 99%

Cardiac cholinergic NO-cGMP signaling following acute myocardial infarction and nNOS gene transfer

Dawson¹,

Li²,

Woodward³

et al. 2008

American Journal of Physiology-Heart and Circulatory Physiology

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“…Some previous studies demonstrated that tying a single vessel off for a few days to weeks did not cause myocardial infarction in guinea pig hearts (14,15). However, other researchers showed that LCA ligation in guinea pigs resulted in infarction within 3 days of surgery (16)(17)(18).…”

Section: Discussionmentioning

confidence: 99%

Thrombin and Its Receptor Enhance ST-Segment Elevation in Acute Myocardial Infarction by Activating the KATP Channel

Long

Yang

Huang

et al. 2010

Mol Med

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“…Preparation of guinea pig hearts according to Langendorff. Hearts of adult guinea pigs were prepared as previously described (16). Briefly, the guinea pigs were heparinized (1,000 IU heparin/kg), and the hearts were excised.…”

Section: Calibration Of the No Electrodementioning

confidence: 99%

A new method to measure nitrate/nitrite with a NO-sensitive electrode

Berkels

Purol-Schnabel

Roesen

2001

Journal of Applied Physiology

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There are different methods to measure the unstable molecule nitric oxide (NO). We will describe a new sensitive method to measure NO by reconversion of nitrate/nitrite to NO, which will be determined with an amperometric Clark-type electrode. Nitrate and nitrite are the degradation products of NO. First, nitrate is enzymatically converted to nitrite with the use of the nitrate reductase. Second, nitrite is reduced to equimolar NO concentrations by an acidic iodide solution. The detection limit of the electrode in an aqueous solution was 2 nmol/l NO (meaning the threshold was depending on the volume added: 500 microl of a 0.2 micromol/l nitrite solution added to a 10-ml bath). This method provides the ability to assess basal and agonist-stimulated NO releases of different biological models. We measured basal and carbachol-stimulated NO release of native endothelial cells from porcine coronary arteries and porcine aortic endothelial cell cultures. Moreover, it was possible to measure the nitrate/nitrite concentration in the coronary effluent of a guinea pig heart. In conclusion, we present a valid, highly sensitive new method of measuring nitrite/NO in biological systems with a commercially available electrode.

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Local myocardial perfusion and epicardial NADH-fluorescence after coronary artery ligation in the isolated guinea pig heart

Cited by 9 publications

References 18 publications

Cardiac cholinergic NO-cGMP signaling following acute myocardial infarction and nNOS gene transfer

Cardiac cholinergic NO-cGMP signaling following acute myocardial infarction and nNOS gene transfer

Thrombin and Its Receptor Enhance ST-Segment Elevation in Acute Myocardial Infarction by Activating the KATP Channel

A new method to measure nitrate/nitrite with a NO-sensitive electrode

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