Journal of cardiovascular electrophysiology · 2011
Heart failure decreases nerve activity in the right atrial ganglionated plexus.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Shinohara Tetsuji, Shen Mark J, Han Seongwook, Maruyama Mitsunori, Park Hyung-Wook, Fishbein Michael C, Shen Changyu, Chen Peng-Sheng, Lin Shien-Fong
Аннотация
OBJECTIVE: We tested the hypothesis that heart failure (HF) results in right atrial ganglionated plexus (RAGP) denervation that contributes to sinoatrial node dysfunction.
BACKGROUND: HF is associated with sinoatrial node dysfunction. However, the detailed mechanisms remain unclear.
METHODS: We recorded nerve activity (NA) from the RAGP, right stellate ganglion (SG), and right vagal nerve in 7 ambulatory dogs at baseline and after pacing-induced HF. We also determined the effects of RAGP stimulation in isolated normal and HF canine RA.
RESULTS: NAs in both the SG and vagal were significantly higher in HF than at baseline. The relationship between 1-minute integrated NAs of vagal and RAGP showed either a positive linear correlation (Group 1, n = 4) or an L-shaped correlation (Group 2, n = 3). In all dogs, a reduced heart rate was observed when vagal-NA was associated with simultaneously increased RAGP-NA. On the other hand, when vagal-NA was not associated with increased RAGP-NA, the heart rate was not reduced. The induction of HF significantly decreased RAGP-NA in all dogs (P < 0.05). Stimulating the superior RAGP in isolated RA significantly reduced the sinus rate in normal but not the HF hearts. Immunohistochemical staining revealed lower densities of tyrosine hydroxylase- and choline acetyltransferase-positive nerve tissues in HF RAGP than normal (P < 0.001 and P = 0.001, respectively).
CONCLUSIONS: The RAGP-NA is essential for the vagal nerve to counterbalance the SG in sinus rate control. In HF, RAGP denervation and decreased RAGP-NA contribute to the sinus node dysfunction.
BACKGROUND: HF is associated with sinoatrial node dysfunction. However, the detailed mechanisms remain unclear.
METHODS: We recorded nerve activity (NA) from the RAGP, right stellate ganglion (SG), and right vagal nerve in 7 ambulatory dogs at baseline and after pacing-induced HF. We also determined the effects of RAGP stimulation in isolated normal and HF canine RA.
RESULTS: NAs in both the SG and vagal were significantly higher in HF than at baseline. The relationship between 1-minute integrated NAs of vagal and RAGP showed either a positive linear correlation (Group 1, n = 4) or an L-shaped correlation (Group 2, n = 3). In all dogs, a reduced heart rate was observed when vagal-NA was associated with simultaneously increased RAGP-NA. On the other hand, when vagal-NA was not associated with increased RAGP-NA, the heart rate was not reduced. The induction of HF significantly decreased RAGP-NA in all dogs (P < 0.05). Stimulating the superior RAGP in isolated RA significantly reduced the sinus rate in normal but not the HF hearts. Immunohistochemical staining revealed lower densities of tyrosine hydroxylase- and choline acetyltransferase-positive nerve tissues in HF RAGP than normal (P < 0.001 and P = 0.001, respectively).
CONCLUSIONS: The RAGP-NA is essential for the vagal nerve to counterbalance the SG in sinus rate control. In HF, RAGP denervation and decreased RAGP-NA contribute to the sinus node dysfunction.