Impaired cholinergic peripheral vasodilation and its relationship to hyperemic calf blood flow response and exercise intolerance in patients with chronic heart failure

1995 ◽  
Vol 48 (2) ◽  
pp. 139-146 ◽  
Author(s):  
Motoyuki Nakamura ◽  
Makoto Chiba ◽  
Kenji Ueshima ◽  
Naoshi Arakawa ◽  
Hiroaki Yoshida ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Chronic Heart Failure ◽  
Exercise Intolerance ◽  
Blood Flow Response ◽  
Peripheral Vasodilation ◽  
Flow Response ◽  
Calf Blood Flow

scholarly journals Impaired skin blood flow response to environmental heating in chronic heart failure

2005 ◽  
Vol 27 (3) ◽  
pp. 338-343 ◽  
Author(s):  
Daniel J. Green ◽  
Andrew J. Maiorana ◽  
Jeffrey Ha Jin Siong ◽  
Valerie Burke ◽  
Matthew Erickson ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Chronic Heart Failure ◽  
Skin Blood Flow ◽  
Blood Flow Response ◽  
Flow Response

Myocardial Blood Flow Response to Pacing Tachycardia and to Dipyridamole Infusion in Patients With Dilated Cardiomyopathy Without Overt Heart Failure

Circulation ◽  
1995 ◽  
Vol 92 (4) ◽  
pp. 796-804 ◽  
Author(s):  
Danilo Neglia ◽  
Oberdan Parodi ◽  
Michela Gallopin ◽  
Gianmario Sambuceti ◽  
Assuero Giorgetti ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Dilated Cardiomyopathy ◽  
Blood Flow Response ◽  
Flow Response

scholarly journals Regional blood flow response to orthostasis in patients with congestive heart failure

1983 ◽  
Vol 1 (6) ◽  
pp. 1391-1395 ◽  
Author(s):  
Steven R. Goldsmith ◽  
Gary S. Francis ◽  
T. Barry Levine ◽  
Jay N. Cohn
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Blood Flow ◽  
Regional Blood Flow ◽  
Blood Flow Response ◽  
Flow Response

Hemodynamic and regional blood flow response to milrinone in patients with severe congestive heart failure: A dose-ranging study

1987 ◽  
Vol 114 (1) ◽  
pp. 97-105 ◽  
Author(s):  
Patricia G. Fitzpatrick ◽  
Michael P. Cinquegrani ◽  
Arthur R. Vakiener ◽  
Judith G. Baggs ◽  
Theodore L. Biddle ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Blood Flow ◽  
Regional Blood Flow ◽  
Severe Congestive Heart Failure ◽  
Blood Flow Response ◽  
Flow Response ◽  
Dose Ranging

EFFECTS OF MODERATE HEART FAILURE ON SKELETAL MUSCLE BLOOD FLOW RESPONSE TO CONTRACTIONS.

2002 ◽  
Vol 34 (5) ◽  
pp. S171
Author(s):  
B J. Behnke ◽  
K S. Hageman ◽  
P J. McDonough ◽  
T I. Musch ◽  
D C. Poole
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Muscle Blood Flow ◽  
Skeletal Muscle Blood Flow ◽  
Blood Flow Response ◽  
Moderate Heart Failure ◽  
Flow Response

Muscle pump-dependent self-perfusion mechanism in legs in normal subjects and patients with heart failure

2002 ◽  
Vol 92 (4) ◽  
pp. 1647-1654 ◽  
Author(s):  
Issei Shiotani ◽  
Hideyuki Sato ◽  
Hiroshi Sato ◽  
Hiroshi Yokoyama ◽  
Yozo Ohnishi ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Pressure Drop ◽  
De Novo ◽  
Venous Pressure ◽  
Normal Subjects ◽  
Muscle Pump ◽  
Blood Flow Response ◽  
Flow Response ◽  
Dependent Mechanism

Leg venous pressure markedly falls during upright exercise via a muscle pump effect, creating de novo perfusion pressure. We examined physiological roles of this mechanism in increasing femoral artery blood flow (FABF) and its alterations in chronic heart failure (CHF). In 10 normal subjects and 10 patients with CHF, standard hemodynamic variables, mean ankle vein pressure (MAVP), and FABF with Doppler techniques were obtained during graded upright bicycle exercise. To evaluate a nonspecific blood flow response, normal subjects also performed supine exercise. In normal subjects, MAVP rapidly declined by 45 mmHg and FABF correspondingly increased 5.3-fold without a systemic pressor response during 10 s of light upright exercise at 5 W. Approximately 67% of the blood flow response was attributed to the venous pressure drop-dependent mechanism. In CHF patients, MAVP declined by only 36 mmHg and FABF increased only 1.7-fold during the same upright exercise. The muscle venous pump has an ability to increase FABF at least threefold via the venous pressure drop-dependent mechanism. This mechanism is impaired in CHF patients.

Oxygen uptake kinetics during exercise in chronic heart failure: influence of peripheral vascular reserve

1999 ◽  
Vol 97 (5) ◽  
pp. 569-577 ◽  
Author(s):  
Russell T. HEPPLE ◽  
Peter. P. LIU ◽  
Michael J. PLYLEY ◽  
Jack M. GOODMAN
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Chronic Heart Failure ◽  
Healthy Subjects ◽  
Maximal Exercise ◽  
Submaximal Exercise ◽  
Work Rate ◽  
Calf Blood Flow ◽  
Relative Work Rate ◽  
Maximal Exercise Capacity

Exercise performance in chronic heart failure is severely impaired, due in part to a peripherally mediated limitation. In addition to impaired maximal exercise capacity, the O2 uptake (O2) response during submaximal exercise may be affected, with a greater reliance on anaerobiosis leading to early fatigue. However, the response of O2 kinetics to submaximal exercise in chronic heart failure has not been studied extensively; in particular, the relationship between oxygen utilization and the peripheral response to exercise has not been studied. The present investigation examined the time-constant (τ, corresponding to 63% of the total response fitted from exercise onset) of the O2 kinetics on-response to submaximal exercise and its relationship to maximal peripheral blood flow in patients with chronic heart failure, and compared responses with those in healthy sedentary subjects. Subjects were 10 patients with chronic heart failure (NYHA class II/III). The mean age was 50±12 years, with a mean resting left ventricular ejection fraction of 25±9%. Controls were 10 age-matched healthy subjects. O2(max) was first determined for all subjects. Repeated transitions from rest to exercise were performed on a cycle ergometer while measuring breath-by-breath responses of O2 at a fixed work rate of 50% of O2(max) (heart failure patients and healthy controls) and at a work rate equivalent to the average in heart failure patients (65 W; healthy controls only). On a separate occasion, post-maximal ischaemic exercise calf blood flow was measured (strain-gauge plethysmography).Whereas heart failure subjects displayed a significantly prolonged O2 kinetics response at a similar absolute workload (i.e. 65 W), as indicated by a longer τ value (42 s, compared with 22 s in controls; P< 0.01), there was no difference in τ at a similar relative work rate [50% of O2(max)]. In addition, heart failure subjects demonstrated a lower maximal calf blood flow (P< 0.05) than control subjects. These results indicate that patients with heart failure have a prolonged O2 kinetics on-response compared with healthy subjects at a similar absolute work rate (i.e. 65 W), but not at a similar relative work rate [50% of O2(max)]. Thus, despite a reduced maximal calf blood flow response associated with heart failure, it does not appear that this contributes to an impairment of the submaximal exercise response beyond that explained by a reduced maximal exercise capacity [O2(max)].

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