scholarly journals Arterial baroreflex sensitivity is a good predictor of inotropic responses to a phosphodiesterase inhibitor in human heart failure

2006 ◽  
Vol 29 (6) ◽  
pp. 263-267 ◽  
Author(s):  
Naoki Sato ◽  
Takeshi Yamamoto ◽  
Koichi Akutsu ◽  
Nobuhiko Fujita ◽  
Kuniya Asai ◽  
...  
Keyword(s):  
Heart Failure ◽  
Good Predictor ◽  
Human Heart ◽  
Baroreflex Sensitivity ◽  
Phosphodiesterase Inhibitor ◽  
Arterial Baroreflex ◽  
Human Heart Failure ◽  
Inotropic Responses ◽  
Arterial Baroreflex Sensitivity

scholarly journals Slow Breathing Increases Arterial Baroreflex Sensitivity in Patients With Chronic Heart Failure

Circulation ◽  
2002 ◽  
Vol 105 (2) ◽  
pp. 143-145 ◽  
Author(s):  
Luciano Bernardi ◽  
Cesare Porta ◽  
Lucia Spicuzza ◽  
Jerzy Bellwon ◽  
Giammario Spadacini ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Baroreflex Sensitivity ◽  
Arterial Baroreflex ◽  
Slow Breathing ◽  
Arterial Baroreflex Sensitivity

Nitric oxide and cardiac parasympathetic control in human heart failure

2002 ◽  
Vol 102 (4) ◽  
pp. 397-402 ◽  
Author(s):  
Saqib CHOWDHARY ◽  
G. Andre NG ◽  
Sarah L. NUTTALL ◽  
John H. COOTE ◽  
Hamish F. ROSS ◽  
...  
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
High Frequency ◽  
Human Heart ◽  
Baroreflex Sensitivity ◽  
No Production ◽  
Human Heart Failure ◽  
Heart Failure Patients ◽  
Parasympathetic Control

Cardiac parasympathetic control has prognostic significance in heart failure, but the control mechanisms of this system remain poorly defined. We have demonstrated previously a facilitatory role for nitric oxide (NO) in the parasympathetic control of heart rate in young healthy human subjects. In view of the complex abnormalities of regional NO activity observed in chronic heart failure, we now aim to establish if this mechanism is active in subjects with this condition. Groups of 12heart failure patients [NYHA class II-III; mean age 52 years (range 38-67 years)] and 12 age/sex-matched healthy control subjects [mean age 50 years (range 36-62 years)] were studied. Heart rate variability and baroreflex sensitivity were measured during inhibition of endogenous NO production with NG-monomethyl-l-arginine (l-NMMA; 3mgċh-1ċkg-1) and during administration of an equipressor dose of the control vasoconstrictor phenylephrine (12-36μgċh-1ċkg-1). Basal levels of nitrate+nitrite were measured in the plasma as an indication of systemic NO production. In the heart failure patients, despite an equal rise in blood pressure with both drugs, high-frequency indices of heart rate variability increased less with l-NMMA than with phenylephrine: RMSSD (root mean square of successive RR-interval differences) increased by 4±2 compared with 26±8ms (P < 0.001) and high-frequency power increased by 97±62 compared with 1372±861ms2 (P < 0.001). The increases in cross-spectral baroreflex sensitivity were also lower with l-NMMA than with phenylephrine [high-frequency α-index, 2.2±1.3 and 12.6±3.8ms/mmHg respectively (P < 0.001); low-frequency α-index, 1.3±0.9 and 4.3±1.7ms/mmHg respectively (P < 0.05)]. Healthy subjects showed a similar discrepancy in the response of high-frequency indices of heart rate variability to the two drugs, although baroreflex sensitivity responses were significantly different only for the high-frequency α-index. Levels of plasma nitrate+nitrite were significantly higher in the heart failure patients compared with controls. These data demonstrate that baroreflex-mediated cardiac parasympathetic activation in human heart failure, as in health, is dependent upon endogenous NO synthesis.

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