Derangement of autonomic nerve control in rat with right ventricular failure

Sanyal, Shamarendra; Ono, Katsushige

doi:10.1016/s0928-4680(02)00002-0

Cited by 18 publications

(20 citation statements)

References 18 publications

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“…Heart rate variability assesses autonomic nervous system activity by analyzing fluctuations in the RR interval on electrocardiography. 30 Similar to the result of this study, Sanyal et al 31 reported that total power and HF power were reduced in monocrotaline-treated rats, which indicates a decrease in parasympathetic activity. But LF/HF ratio, which reflects sympathetic activity tones in the heart, was comparable unlike our results.…”

Section: Discussionsupporting

confidence: 87%

Cervical Ganglion Block Attenuates the Progression of Pulmonary Hypertension via Nitric Oxide and Arginase Pathways

Kim²,

Ryoo³

et al. 2014

Hypertension

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Abstract-It has been recognized that the sympathetic nervous system is activated in pulmonary arterial hypertension (PAH), and abnormal sympathetic hyperactivity leads to worsening of PAH via endothelial dysfunction. The purpose of this study was to examine whether sympathetic ganglion block (SGB) can treat PAH by increasing the availability of nitric oxide (NO). PAH was induced in rats by 50 mg/kg of subcutaneous monocrotaline. After 2 weeks, daily injections of ropivacaine into the left superior cervical ganglion were repeated for 14 days (monocrotaline-SGB group). Monocrotaline group received sham SGB with saline, whereas control group received saline instead of monocrotaline. PAH was evident in monocrotaline group, with right ventricular systolic pressures (47±4 mm Hg) that were higher than those of controls (17±2 mm Hg), whereas SGB significantly attenuated monocrotalineinduced PAH (35±4 mm Hg). The right/left ventricular mass ratios exhibited similar changes to those seen with right ventricular pressures. Heart rate variability showed significantly higher sympathetic activity in the monocrotaline group. Microscopy revealed a higher proportion of muscular arteries with thicker medial walls in the monocrotaline group, which was attenuated by SGB. Monocrotaline induced arginase hyperactivity, which was in turn decreased by SGB-induced endothelial NO synthase activation. SGB restored monocrotaline-induced hypoactivity of superoxide dismutase. In conclusion, SGB could suppress PAH and the remodeling of pulmonary arteries via inactivation of arginase and reciprocal elevation of NO bioavailability, thus attenuating disproportionate hyperactivation of the have been reported to attenuate the severity of symptoms and slow the progression of cardiovascular diseases including coronary artery disease, heart failure, and arrhythmias. According to the previous reports, there is a possibility that direct sympathetic nerve blocks are effective in patients with myocardial ischemia or systemic hypertension. 17,19 Given the relationship between sympathetic nervous system hyperactivity and endothelial dysfunction in patients with PAH, blockade of sympathetic hyperactivity may improve vascular reactivity by preserving endothelial function. To date, however, there is limited amount of data on the therapeutic effects of sympathetic ganglion block (SGB) on PAH. The purpose of the present study is to assess the therapeutic effects of SGB in a monocrotaline-induced PAH rat model. In parallel, we investigated whether SGB could attenuate the changes in arginase and NO bioavailability, as well as oxidative stress caused by monocrotaline. MethodsDetailed methods about animal preparation, experimental design, SGB, heart rate variability, hemodynamic analysis, right ventricular mass, pulmonary vessel morphometry, and NO (synthase)/arginase/ cGMP/oxidative stress assay are described in the online-only Data Supplement. Results Right Ventricular Systolic Pressure and Right Ventricular/Left Ventricular Mass RatioRight ventricular systolic pr...

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Section: Discussionsupporting

confidence: 87%

Cervical Ganglion Block Attenuates the Progression of Pulmonary Hypertension via Nitric Oxide and Arginase Pathways

Kim²,

Ryoo³

et al. 2014

Hypertension

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“…More specifically, it has recently been demonstrated in an animal model of right ventricular heart failure that there is an autonomic nerve control derangement particularly of parasympathetic activity, 30 whereas it was also shown that decreased HR variability is present in rats with pulmonary hypertension and right ventricular hypertrophy from chronic hypoxia. 31 Similarly, a decreased heart variability in patients with primary pulmonary hypertension has also been reported.…”

Section: Discussionmentioning

confidence: 99%

Impairment of Autonomic Nervous System Activity in Patients With Pulmonary Arterial Hypertension: A Case Control Study

Dimopoulos¹,

Anastasiou-Nana²,

Katsaros³

et al. 2009

Journal of Cardiac Failure

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“…However, the monocrotaline model exhibits alterations in the ␤-adrenergic system that resemble those in human PH; others have previously demonstrated that in monocrotaline-treated rats with RHF, heart rate variability is reduced, 35 plasma norepinephrine levels are increased, and ␤ 1 -adrenergic receptor density of the right ventricle is decreased, 36 similar to clinical PH. 3 Despite bisoprolol treatment all PH rats eventually developed right heart failure.…”

Section: De Man Et Al Bisoprolol In Experimental Pulmonary Hypertensimentioning

confidence: 99%

Bisoprolol Delays Progression Towards Right Heart Failure in Experimental Pulmonary Hypertension

Man

Handoko

Ballegoij

et al. 2012

Circ: Heart Failure

180

137

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Background-In pulmonary arterial hypertension (PH), sympathetic adrenergic activity is highly elevated. Sympathetic overactivity is a compensatory mechanism at first, but might be detrimental for cardiac function in the long run. We therefore investigated whether chronic low-dose treatment with bisoprolol (a cardioselective ␤-blocker) has beneficial effects on cardiac function in experimental PH. Methods and Results-PH was induced in rats by a single injection of monocrotaline (60 mg/kg). Pressure telemetry in PH rats revealed that 10 mg/kg bisoprolol was the lowest dose that blunted heart rate response during daily activity. Ten days after monocrotaline injection, echocardiography was performed and PH rats were randomized for bisoprolol treatment (oral gavage) or vehicle (nϭ7/group). At end of study (body mass loss Ͼ5%), echocardiography was repeated, with additional pressure-volume measurements and histomolecular analyses. Compared with control, right ventricular (RV) systolic pressure and arterial elastance (measure of vascular resistance) more than tripled in PH. Bisoprolol delayed time to right heart failure (PϽ0.05). RV afterload was unaffected, however, bisoprolol treatment increased RV contractility and filling (both PϽ0.01), and partially restored right ventriculo-arterial coupling and cardiac output (both PϽ0.05). Bisoprolol restored RV ␤-adrenergic receptor signaling. Histology revealed significantly less RV fibrosis and myocardial inflammation in bisoprolol treated PH rats. Conclusions-In experimental PH, treatment with bisoprolol delays progression toward right heart failure, and partially preserves RV systolic and diastolic function. These promising results suggest a therapeutic role for ␤-blockers in PH that warrants further clinical investigation. (Circ Heart Fail. 2012;5:97-105.)Key Words: pulmonary hypertension Ⅲ right ventricular dysfunction Ⅲ ␤-adrenergic receptor blocker Ⅲ pressure-volume relationship Ⅲ Wistar rats P ulmonary arterial hypertension (PH) is a fatal disease, characterized by progressive vascular remodeling and increased right ventricular (RV) afterload, which eventually leads to manifest right heart failure (RHF) and premature death. Current available medical treatments aim to reduce RV afterload, thereby secondarily improving RV function. 1 No treatment is currently available that improves RV function directly, partially because it was not considered a therapeutic target in PH. 2 Clinical Perspective on p 105Recently, several reports have shown that sympathetic activity is increased in patients with PH. [3][4][5][6][7] Similar to left heart failure (LHF), "ventricle-specific" down regulation of ␤ 1 -adrenergic receptors was observed in RV samples of PH patients. 8 In addition, we recently demonstrated that exercise training was detrimental in experimental and progressive PH. 9 The deleterious effects could be related to bouts of exercise-induced sympathetic stimulation.Although increased adrenergic activity is a compensatory mechanism to maintain cardiac function by increasi...

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Derangement of autonomic nerve control in rat with right ventricular failure

Cited by 18 publications

References 18 publications

Cervical Ganglion Block Attenuates the Progression of Pulmonary Hypertension via Nitric Oxide and Arginase Pathways

Cervical Ganglion Block Attenuates the Progression of Pulmonary Hypertension via Nitric Oxide and Arginase Pathways

Impairment of Autonomic Nervous System Activity in Patients With Pulmonary Arterial Hypertension: A Case Control Study

Bisoprolol Delays Progression Towards Right Heart Failure in Experimental Pulmonary Hypertension

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