Baroreflex regulation of regional blood flow in congestive heart failure

In patients with congestive heart failure (CHF), the distribution of the cardiac output is altered. Cardiopulmonary and arterial baroreceptors normally can regulate regional blood flow, but their contribution in heart failure is not known. To examine the role of baroreceptors in the regulation of regional blood flow in CHF, the effect of lower body negative pressure (LBNP) on forearm, renal, and splanchnic blood flow was evaluated in 12 patients with heart failure. Incremental LBNP at -10 and -40 mmHg decreased central venous pressure but had not effect on systolic blood pressure or pulse pressure. Renal blood flow decreased from 505 +/- 63 to 468 +/- 66 ml/min during LBNP -10 mmHg (P less than 0.05) and to 376 +/- 74 ml/min during LBNP -40 mmHg (P less than 0.01). Splanchnic blood flow decreased from 564 +/- 76 to 480 +/- 62 ml/min during LBNP -10 mmHg (P less than 0.01) and to 303 +/- 45 ml/min during LBNP -40 mmHg (P less than 0.01). Forearm blood flow did not decrease during LBNP -10 mmHg or -40 mmHg. To determine whether the absence of limb vasoconstriction during LBNP was confined to abnormalities in the baroreflex arc or was secondary to impaired end-organ responsiveness, six patients with heart failure and six normal subjects received an intrabrachial artery infusion of phenylephrine. Phenylephrine increased forearm vascular resistance comparably in each group. These data demonstrate that baroreceptors can regulate splanchnic and renal but not limb vascular resistance in patients with congestive heart failure and may contribute to the redistribution of blood flow that occurs in this disorder.

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Effects of supplemental oxygen on forearm vasodilation in humans

Journal of Applied Physiology ◽

10.1152/jappl.1997.82.5.1601 ◽

1997 ◽

Vol 82 (5) ◽

pp. 1601-1606 ◽

Cited By ~ 47

Author(s):

Paul Crawford ◽

Peter A. Good ◽

Eric Gutierrez ◽

Joshua H. Feinberg ◽

John P. Boehmer ◽

...

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Vascular Resistance ◽

Peak Flow ◽

Lower Body Negative Pressure ◽

Normal Subjects ◽

Supplemental Oxygen ◽

Lower Body ◽

Minimal Resistance ◽

Minimum Resistance

Crawford, Paul, Peter A. Good, Eric Gutierrez, Joshua H. Feinberg, John P. Boehmer, David H. Silber, and Lawrence I. Sinoway.Effects of supplemental oxygen on forearm vasodilation in humans. J. Appl. Physiol. 82(5): 1601–1606, 1997.—Supplemental O2 reduces cardiac output and raises systemic vascular resistance in congestive heart failure. In this study, 100% O2 was given to normal subjects and peak forearm flow was measured. In experiment 1, 100% O2 reduced blood flow and increased resistance after 10 min of forearm ischemia (flow 56.7 ± 7.9 vs. 47.8 ± 6.7 ml ⋅ min−1 ⋅ 100 ml−1; P < 0.02; vascular resistance 1.7 ± 0.2 vs. 2.4 ± 0.4 mmHg ⋅ min ⋅ 100 ml ⋅ ml−1; P < 0.03). In experiment 2, lower body negative pressure (LBNP; −30 mmHg) and venous congestion (VC) simulated the high sympathetic tone and edema of congestive heart failure. Postischemic forearm flow and resistance were measured under four conditions: room air breathing (RA); LBNP+RA; RA+LBNP+VC; and 100% O2+LBNP+VC. LBNP and VC did not lower peak flow. However, O2raised minimal resistance (2.3 ± 0.4 RA; 2.8 ± 0.5 O2+LBNP+VC, P < 0.04). When O2 alone ( experiment 1) was compared with O2+LBNP+VC ( experiment 2), no effect of LBNP+VC on peak flow or minimum resistance was noted, although the return rate of flow and resistance toward baseline was increased. O2 reduces peak forearm flow even in the presence of LBNP and VC.

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A Comparison of Regional Blood Flow and Oxygen Utilization During Dynamic Forearm Exercise in Normal Subjects and Patients with Congestive Heart Failure

Circulation ◽

10.1161/01.cir.50.1.137 ◽

1974 ◽

Vol 50 (1) ◽

pp. 137-143 ◽

Cited By ~ 151

Author(s):

ROBERT ZELIS ◽

JOHN LONGHURST ◽

ROBERT J. CAPONE ◽

DEAN T. MASON ◽

Robert Kleckner

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Blood Flow ◽

Regional Blood Flow ◽

Normal Subjects ◽

Oxygen Utilization ◽

Forearm Exercise

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Relationship between central hemodynamics and regional blood flow in normal subjects and in patients with congestive heart failure.

Circulation ◽

10.1161/01.cir.69.1.57 ◽

1984 ◽

Vol 69 (1) ◽

pp. 57-64 ◽

Cited By ~ 120

Author(s):

M E Leithe ◽

R D Margorien ◽

J B Hermiller ◽

D V Unverferth ◽

C V Leier

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Blood Flow ◽

Regional Blood Flow ◽

Normal Subjects ◽

Central Hemodynamics

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Muscular blood flow response to submaximal leg exercise in normal subjects and in patients with heart failure

Journal of Applied Physiology ◽

10.1152/jappl.1996.81.6.2571 ◽

1996 ◽

Vol 81 (6) ◽

pp. 2571-2579 ◽

Cited By ~ 27

Author(s):

Richard Isnard ◽

Philippe Lechat ◽

Hanna Kalotka ◽

Hafida Chikr ◽

Serge Fitoussi ◽

...

Keyword(s):

Heart Failure ◽

Skeletal Muscle ◽

Blood Flow ◽

Vascular Resistance ◽

Normal Subjects ◽

Submaximal Exercise ◽

Control Subjects ◽

Flow Response ◽

Patients With Heart Failure ◽

Leg Exercise

Isnard, Richard, Philippe Lechat, Hanna Kalotka, Hafida Chikr, Serge Fitoussi, Joseph Salloum, Jean-Louis Golmard, Daniel Thomas, and Michel Komajda. Muscular blood flow response to submaximal leg exercise in normal subjects and in patients with heart failure. J. Appl. Physiol. 81(6): 2571–2579, 1996.—Blood flow to working skeletal muscle is usually reduced during exercise in patients with congestive heart failure. An intrinsic impairment of skeletal muscle vasodilatory capacity has been suspected as a mechanism of this muscle underperfusion during maximal exercise, but its role during submaximal exercise remains unclear. Therefore, we studied by transcutaneous Doppler ultrasonography the arterial blood flow in the common femoral artery at rest and during a submaximal bicycle exercise in 12 normal subjects and in 30 patients with heart failure. Leg blood flow was lower in patients than in control subjects at rest [0.29 ± 0.14 (SD) vs. 0.45 ± 0.14 l/min, P < 0.01], at absolute powers and at the same relative power (2.17 ± 1.06 vs. 4.39 ± 1.4 l/min, P< 0.001). Because mean arterial pressure was maintained, leg vascular resistance was higher in patients than in control subjects at rest (407 ± 187 vs. 247 ± 71 mmHg ⋅ l−1 ⋅ min, P < 0.01) and at the same relative power (73 ± 49 vs. 31 ± 13 mmHg ⋅ l−1 ⋅ min, P < 0.01) but not at absolute powers. Although the magnitude of increase in leg blood flow corrected for power was similar in both groups (31 ± 10 vs. 34 ± 10 ml ⋅ min−1 ⋅ W−1), the magnitude of decrease of leg vascular resistance corrected for power was higher in patients than in control subjects (5.9 ± 3.3 vs. 1.9 ± 0.94 mmHg ⋅ l−1 ⋅ min ⋅ W−1, P < 0.001). These results suggest that the ability of skeletal muscle vascular resistance to decrease is not impaired and that intrinsic vascular abnormalities do not limit vasodilator response to submaximal exercise in patients with heart failure.

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