Carotid Chemoreceptor Modulation of Regional Blood Flow Distribution During Exercise in Health and Chronic Heart Failure

We sought to determine whether the normal inspiratory intrathoracic pressures (PITP) produced during exercise contribute to the blunted cardiac output and locomotor limb blood flow responses observed in chronic heart failure (CHF). Five chronically instrumented dogs exercised on a treadmill at 2.5 mile/h at 5% grade while healthy or after the induction of tachycardia-induced CHF. We observed several key differences in the cardiovascular responses to changes in the inspiratory PITP excursion between health and CHF; namely, 1) removing ∼70% of the normally produced inspiratory PITP excursion during exercise (with 15 cmH2O inspiratory positive pressure ventilation) significantly reduced stroke volume (SV) in healthy animals by 5 ± 2% ( P < 0.05) but significantly increased SV and cardiac output (QTOT) in animals with CHF by 5 ± 1% ( P < 0.05); 2) doubling the magnitude of the inspiratory PITP excursion had no effect on SV or QTOT in healthy animals but significantly reduced steady-state QTOT and SV in animals with CHF by −4 ± 3% and −10 ± 3%, respectively; 3) removing the majority of the normally produced inspiratory PITP excursion had no effect on blood flow distribution in healthy animals but increased hindlimb blood flow (9 ± 3%, P < 0.05) out of proportion to the increases in QTOT; and 4) the only similarity between healthy and CHF animals was that increasing the inspiratory PITP excursion significantly reduced steady-state locomotor limb blood flow by 5 ± 2% and 6 ± 3%, respectively ( P < 0.05 for both). We conclude that 1) the normally produced inspiratory PITP excursions are required for a maximal SV response to submaximal exercise in healthy animals but detrimental to the SV and QTOT responses to submaximal exercise in CHF, 2) the respiratory muscle ergoreflex tonically restrains locomotor limb blood flow during submaximal exercise in CHF, and 3) excessive inspiratory muscle work further compromises cardiac function and blood flow distribution in both health and CHF.

Download Full-text

Felodipine in severe chronic congestive heart failure: Acute effects on central hemodynamics and regional blood flow distribution

Cardiovascular Drugs and Therapy ◽

10.1007/bf01869580 ◽

1989 ◽

Vol 3 (6) ◽

pp. 903-911 ◽

Cited By ~ 1

Author(s):

Giorgio Binetti ◽

Ida Rubino ◽

Elisabetta Varani ◽

Roberto Spadoni ◽

Rossella Maria Ferretti ◽

...

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Blood Flow ◽

Regional Blood Flow ◽

Flow Distribution ◽

Chronic Congestive Heart Failure ◽

Blood Flow Distribution ◽

Central Hemodynamics ◽

Acute Effects

Download Full-text

Blood flow distribution within skeletal muscle during exercise in the presence of chronic heart failure: effect of milrinone.

Circulation ◽

10.1161/01.cir.76.6.1344 ◽

1987 ◽

Vol 76 (6) ◽

pp. 1344-1352 ◽

Cited By ~ 37

Author(s):

H Drexler ◽

F Faude ◽

S Höing ◽

H Just

Keyword(s):

Heart Failure ◽

Skeletal Muscle ◽

Blood Flow ◽

Chronic Heart Failure ◽

Flow Distribution ◽

Blood Flow Distribution

Download Full-text

Comparison of cardiovascular effects of mu- and delta-opioid receptor antagonists in dogs with congestive heart failure

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.267.3.h912 ◽

1994 ◽

Vol 267 (3) ◽

pp. H912-H917

Author(s):

N. Imai ◽

M. Kashiki ◽

P. D. Woolf ◽

C. S. Liang

Keyword(s):

Heart Failure ◽

Blood Flow ◽

Receptor Antagonist ◽

Opioid Receptor ◽

Regional Blood Flow ◽

Flow Distribution ◽

Cardiovascular Effects ◽

Blood Flow Distribution ◽

Blood Flows ◽

Delta Opioid Receptors

We have shown previously that right heart failure (RHF) in dogs is associated with activated endogenous opiate systems, and that administration of the opioid receptor antagonist, naloxone, increases arterial pressure, cardiac contractile function and organ blood flows. To study whether the cardiovascular effects of naloxone are mediated via the mu- or delta-opioid receptors, we administered ICI-154,129, a delta-receptor antagonist, and naloxonazine, a mu-receptor antagonist, to 10 conscious dogs with RHF on 2 separate days. Like naloxone, ICI-154,129 increased mean aortic pressure, cardiac output, peak positive first derivative of left ventricular pressure, and blood flows to the myocardium, kidneys, splanchnic beds, and skeletal muscle. These changes were associated with increases in plasma epinephrine and norepinephrine. In contrast, naloxonazine had no effects on systemic hemodynamics, regional blood flow distribution, and plasma catecholamines in RHF. These findings suggest that the increased endogenous opioids during heart failure act on the delta-opioid receptors to decrease myocardial mechanical performance and alter regional blood flow distribution. Opioid receptor-blocking agents may exert beneficial cardiovascular effects in heart failure.

Download Full-text