A new rabbit model of myocardial infarction without endotracheal intubation

Fujita, Masanori; Morimoto, Yuji; Shimizu, Mitsuaki; Takase, Bonpei; Maehara, Tadaaki; Kikuchi, Makoto

doi:10.1016/s0022-4804(03)00304-4

Cited by 37 publications

(30 citation statements)

References 17 publications

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“…The MI rabbit model was established as previous described [20]. In total, 50 male New Zealand white rabbits (2-2.5 kg) were anesthetized with an intraperitoneal injection of 3% sodium pentobarbital (40 mg/kg; Sigma-Aldrich, St. Louis, Mo., USA).…”

Section: Methodsmentioning

confidence: 99%

Metoprolol-Mediated Amelioration of Sympathetic Nerve Sprouting after Myocardial Infarction

Wang

Liu²,

Suo³

et al. 2013

Cardiology

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Objectives: Systemic or local inflammation causes cardiac nerve sprouting and consequent arrhythmia. Metoprolol can prevent sympathetic nerve remodeling after myocardial infarction (MI), but the underlying mechanism is unclear. In this study, we evaluated the role of metoprolol in ameliorating sympathetic sprouting. Methods: Rabbits underwent ligation of the coronary artery for MI. MI rabbits received metoprolol or saline for 7 days. Immunohistochemistry was used to measure cardiac nerve sprouting and sympathetic innervations. Nuclear factor-κB (NF-κB) DNA binding activity was analyzed by electrophoretic mobility shift assay. The protein levels of NF-κB p65, inhibitor κBa (IκBa) and nerve growth factor (NGF) were detected by Western blot analysis. The mRNA levels of NGF, interleukin-1ß (IL-1ß) and tumor necrosis factor-a (TNF-a) were examined by quantitative real-time PCR. Results: MI rabbits showed nerve sprouting and sympathetic hyperinnervation. In MI rabbits, as compared with saline treatment, metoprolol reduced NF-κB DNA binding activity and NF-κB p65 level, and increased IκBa level. Moreover, metoprolol downregulated IL-1ß, TNF-a and NGF levels, and reduced the density of sympathetic nerve fibers. Conclusions: Metoprolol ameliorates sympathetic nerve sprouting in rabbits after MI and is associated in part with inhibiting NF-κB activity.

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Section: Methodsmentioning

confidence: 99%

Metoprolol-Mediated Amelioration of Sympathetic Nerve Sprouting after Myocardial Infarction

Wang

Liu²,

Suo³

et al. 2013

Cardiology

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“…Electrodes were attached to the 4 limbs for electrocardiography. MI and DI animals underwent thoracotomy and pericardiotomy, and the left anterior descending coronary artery was ligated to create MI as described [13]. Successful creation of MI was verified by ST-segment elevation on electrocardiography and color changes in the epicardium in affected areas.…”

Section: Methodsmentioning

confidence: 99%

Risk of Ventricular Arrhythmias after Myocardial Infarction with Diabetes Associated with Sympathetic Neural Remodeling in Rabbits

Wang

Xuan²,

Hu³

et al. 2012

Cardiology

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Background: Abnormal sympathetic innervation underlies both long-term hyperglycemia and myocardial infarction (MI). The incidence of ventricular arrhythmias (VAs) after MI is higher in diabetic than in nondiabetic patients. However, the exact mechanism remains unclear. In this study, we aimed to explore sympathetic neural remodeling after MI in diabetic rabbits and its relationship with VAs. Methods: Rabbits were randomly assigned to 4 groups: control, diabetes mellitus (DM), MI and diabetic myocardial infarction (DI). After electrophysiological experiments in vivo, immunohistochemistry and real-time RT-PCR were used to measure sympathetic innervations. To test the function of sympathetic nerve fibers, norepinephrine levels were measured by high-performance liquid chromatography. Results: The corrected QT interval and QT dispersion were significantly more prolonged with DI than other conditions. The density of tyrosine hydroxylase-positive fibers and corresponding mRNA abundance was significantly higher with DI than with DM and under control conditions, but was lower than with the MI group. Moreover, the distribution and structure of regenerated nerve was heterogeneous in DI rabbits. Norepinephrine content was higher in the DI group, and accompanied by an increased quantity of tyrosine hydroxylase-positive fibers. Conclusion: MI results in sympathetic neural remodeling in diabetic rabbits, which may be responsible in part for the increased occurrence of VAs.

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“…We believe the selective CVBG should be considered in cases of coronary artery disease not amenable to traditional revascularization strategies [42][43][44][45]. Indications of selective CVBG include the patients with tenuous right coronary artery or diffuse lesions.…”

Section: Resultsmentioning

confidence: 99%