Dynamic regulation of leg vasomotor tone in patients with chronic heart failure

1991 ◽  
Vol 71 (3) ◽  
pp. 1070-1075 ◽  
Author(s):  
M. J. Sullivan ◽  
F. R. Cobb
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Chronic Heart Failure ◽  
Left Ventricular ◽  
Work Rate ◽  
Vasomotor Tone ◽  
Leg Blood Flow ◽  
Leg Exercise

We examined the central hemodynamic (n = 5) and leg blood flow (n = 9) responses to one- and two-leg bicycle exercise in nine ambulatory patients with chronic heart failure due to left ventricular systolic dysfunction (ejection fraction 17 +/- 9%). During peak one- vs. two-leg exercise, leg blood flow (thermodilution) tended to be higher (1.99 +/- 0.91 vs. 1.67 +/- 0.91 l/min, P = 0.07), whereas femoral arteriovenous oxygen difference was lower (13.6 +/- 3.1 vs. 15.0 +/- 2.9 ml/dl, P less than 0.01). Comparison of data from exercise stages matched for single-leg work rate during one- vs. two-leg exercise demonstrated that cardiac output was similar while both oxygen consumption and central arteriovenous oxygen differences were lower, indicating relative improvement in the cardiac output response at a given single-leg work rate during one-leg exercise. This was accompanied by higher leg blood flow (1.56 +/- 0.76 vs. 1.83 +/- 0.72 l/min, P = 0.02) and a tendency for leg vascular resistance to be lower (92 +/- 54 vs. 80 +/- 48 Torr.l-1.min, P = 0.08) without any change in blood lactate. These data indicate that, in patients with chronic heart failure, leg vasomotor tone is dynamically regulated, independent of skeletal muscle metabolism, and is not determined solely by intrinsic abnormalities in skeletal muscle vasodilator capacity. Our results suggest that relative improvements in central cardiac function may lead to a reflex release of skeletal muscle vasoconstrictor tone in this disorder.

Abstract 14822: Impact of Proportional Assist Ventilation on Skeletal Muscle Reoxygenation and Central Hemodynamic During Constant Work Rate Exercise in Chronic Heart Failure

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Audrey Borghi-Silva ◽  
Luiz Eduardo Nery ◽  
Dirceu R de Almeida ◽  
Jose Alberto Neder
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Cardiac Output ◽  
Infrared Spectroscopy ◽  
Chronic Heart Failure ◽  
High Intensity ◽  
Near Infrared ◽  
Work Rate ◽  
Constant Work Rate ◽  
Kinetics Of

Introduction: Progressive chronic heart failure slows the recovery of microvascular oxygen delivery and utilization, which produce deleterious implications to exercise capacity. Respiratory muscle unloading can enhance the responses to exercise thereby allowing a closer matching between skeletal muscle oxygen delivery and utilization in patients with chronic heart failure (CHF). Hypothesis: We reasoned that noninvasive ventilation administered by proportional assisted ventilation (PAV) could accelerate skeletal muscle reoxygenation after high intensity exercise in CHF humans. To test this hypothesis, we conducted a study with 12 patients with stable CHF who were randomized to receive PAV or sham ventilation during high-intensity constant work exercise and compared the effects of these interventions on oxygen pulmonary (O2p), cardiac output and [[Unable to Display Character: &#8710;]][deoxi-Hb+Mb] off kinetics. Methods: Twelve patients with CHF (NYHA class II and III and left ventricle ejection fraction= 26±9%) underwent two high-intensity, constant-work rate (80% peak) cycle ergometer tests receiving PAV or sham ventilation. Off-exercise kinetics of the primary component of oxygen uptake, an index of fractional oxygen extraction by near infrared spectroscopy (~[[Unable to Display Character: &#8710;]][deoxy-Hb+Mb]) in the vastus lateralis) and cardiac output (QT) by impedance cardiography were assessed. Results: PAV significantly accelerated the recovery of O2p when compared with sham τ = 56±22 vs. 77±42s, respectively, p<0.05). Interestingly, PAV was associated with faster fractional O2 extraction (~[[Unable to Display Character: &#8710;]][deoxy-Hb+Mb] by near-infrared spectroscopy) (τ= 31±19 vs. 42±22s, respectively, p<0.05) . In addition, kinetics of QT were significantly faster with PAV than sham (τ = 39±22 vs. 78±46s, respectively, p<0.05). Conclusions: These data indicate that PAV has beneficial effects on recovery of muscle metabolism and central hemodynamics after high-intensity exercise in CHF patients. Financial Support: FAPESP 2009-01842-0

Myocardial, skeletal muscle, and renal blood flow during exercise in conscious dogs with heart failure

1997 ◽  
Vol 273 (5) ◽  
pp. H2452-H2457 ◽  
Author(s):  
Till Neumann ◽  
Gerd Heusch
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Renal Blood Flow ◽  
Plasma Catecholamines ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Ventricular Pacing ◽  
Control State

The present study characterizes the hemodynamic and neurohumoral responses to moderate treadmill exercise in conscious dogs with pacing-induced heart failure. Seven dogs were instrumented with a left ventricular micromanometer, ultrasonic crystals for the measurement of systolic wall thickening, left atrial and aortic catheters for the injection of colored microspheres and reference withdrawal, respectively, and ventricular pacing leads with a subcutaneous pacemaker. Dogs were run on a treadmill at a speed of 5 km/h. After control studies, heart failure was induced by rapid left ventricular pacing at 250 beats/min for (mean ± SD) 23 ± 6 days. In the control state, cardiac output was increased from 4.5 ± 1.5 to 7.9 ± 1.4 l/min ( P < 0.05 vs. rest). With heart failure, cardiac output was decreased to 2.5 ± 0.5 l/min at rest ( P < 0.05 vs. control state) and was only 3.0 ± 0.3 l/min during exercise ( P < 0.05 vs. control state; not significant vs. rest). Myocardial and, more so, skeletal muscle blood flows at rest were reduced in heart failure; their increases with exercise were attenuated. An increase in renal blood flow during exercise in the control state was no longer seen in heart failure. Increases in plasma catecholamines and lactate during exercise were more pronounced in heart failure. In conclusion, in heart failure, the increase in cardiac output during exercise was largely attenuated. Increased catecholamine levels may have contributed to splanchnic vasoconstriction and preferential distribution of cardiac output into the working skeletal muscle.

scholarly journals Beneficial haemodynamic effects of insulin in chronic heart failure

Heart ◽  
2001 ◽  
Vol 85 (5) ◽  
pp. 508-513
Author(s):  
W A Parsonage ◽  
D Hetmanski ◽  
A J Cowley
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Chronic Heart Failure ◽  
Insulin Infusion ◽  
Muscle Blood Flow ◽  
Haemodynamic Effects ◽  
High Dose ◽  
Skeletal Muscle Blood Flow

OBJECTIVETo characterise the central and regional haemodynamic effects of insulin in patients with chronic heart failure.DESIGNSingle blind, placebo controlled study.SETTINGUniversity teaching hospital.PATIENTSTen patients with stable chronic heart failure.INTERVENTIONSHyperinsulinaemic euglycaemic clamp and non-invasive haemodynamic measurements.MAIN OUTCOME MEASURESChange in resting heart rate, blood pressure, cardiac output, and regional splanchnic and skeletal muscle blood flow.RESULTSInsulin infusion led to a dose dependent increase in skeletal muscle blood flow of 0.36 (0.13) and 0.73 (0.14) ml/dl/min during low and high dose insulin infusions (p < 0.05 and p < 0.005 v placebo, respectively). Low and high dose insulin infusions led to a fall in heart rate of 4.6 (1.4) and 5.1 (1.3) beats/min (p < 0.05 and p < 0.005 v placebo, respectively) and a modest increase in cardiac output. There was no significant change in superior mesenteric artery blood flow.CONCLUSIONIn patients with chronic heart failure insulin is a selective skeletal muscle vasodilator that leads to increased muscle perfusion primarily through redistribution of regional blood flow rather than by increased cardiac output. These results provide a rational haemodynamic explanation for the apparent beneficial effects of insulin infusion in the setting of heart failure.

scholarly journals Metabolic abnormality of calf skeletal muscle is improved by localised muscle training without changes in blood flow in chronic heart failure

Heart ◽  
1997 ◽  
Vol 78 (5) ◽  
pp. 437-443 ◽  
Author(s):  
M. Ohtsubo ◽  
K. Yonezawa ◽  
H. Nishijima ◽  
K. Okita ◽  
A. Hanada ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Chronic Heart Failure ◽  
Metabolic Abnormality ◽  
Muscle Training

Training-induced changes in skeletal muscle Na+-K+ pump number and isoform expression in rats with chronic heart failure

2003 ◽  
Vol 94 (6) ◽  
pp. 2225-2236 ◽  
Author(s):  
Bryan Helwig ◽  
Katherine M. Schreurs ◽  
Joslyn Hansen ◽  
K. Sue Hageman ◽  
Michael G. Zbreski ◽  
...  
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Chronic Heart Failure ◽  
Exercise Training ◽  
Left Ventricular ◽  
Β Subunit ◽  
Severe Left Ventricular Dysfunction ◽  
Subunit Expression ◽  
Run Time ◽  
Isoform Expression

The mechanisms responsible for the decrements in exercise performance in chronic heart failure (CHF) remain poorly understood, but it has been suggested that sarcolemmal alterations could contribute to the early onset of muscular fatigue. Previously, our laboratory demonstrated that the maximal number of ouabain binding sites (Bmax) is reduced in the skeletal muscle of rats with CHF (Musch TI, Wolfram S, Hageman KS, and Pickar JG. J Appl Physiol 92: 2326–2334, 2002). These reductions may coincide with changes in the Na+-K+-ATPase isoform (α and β) expression. In the present study, we tested the hypothesis that reductions in Bmax would coincide with alterations in the α- and β-subunit expression of the sarcolemmal Na+-K+-ATPase of rats with CHF. Moreover, we tested the hypothesis that exercise training would increase Bmax along with producing significant changes in α- and β-subunit expression. Rats underwent a sham operation (sham; n = 10) or a surgically induced myocardial infarction followed by random assignment to either a control (MI; n = 16) or exercise training group (MI-T; n = 16). The MI-T rats performed exercise training (ET) for 6–8 wk. Hemodynamic indexes demonstrated that MI and MI-T rats suffered from severe left ventricular dysfunction and congestive CHF. Maximal oxygen uptake (V˙o 2 max) and endurance capacity (run time to fatigue) were reduced in MI rats compared with sham. Bmax in the soleus and plantaris muscles and the expression of the α2-isoform of the Na+-K+-ATPase in the red portion of the gastrocnemius (gastrocnemiusred) muscle were reduced in MI rats. After ET, V˙o 2 max and run time to fatigue were increased in the MI-T group of rats. This coincided with increases in soleus and plantaris Bmax and the expression of the α2-isoform in the gastrocnemiusred muscle. In addition, the expression of the β2-isoform of the gastrocnemiusred muscle was increased in the MI-T rats compared with their sedentary counterparts. This study demonstrates that CHF-induced alterations in skeletal muscle Na+-K+-ATPase, including Bmax and isoform expression, can be partially reversed by ET.

Effects of chronic heart failure on skeletal muscle capillary hemodynamics at rest and during contractions

2003 ◽  
Vol 95 (3) ◽  
pp. 1055-1062 ◽  
Author(s):  
Troy E. Richardson ◽  
Casey A. Kindig ◽  
Timothy I. Musch ◽  
David C. Poole
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Chronic Heart Failure ◽  
Muscle Function ◽  
Muscle Blood Flow ◽  
Rat Skeletal Muscle ◽  
Exercise Onset ◽  
Final Response ◽  
Microscopy Techniques

Chronic heart failure (CHF) reduces muscle blood flow at rest and during exercise and impairs muscle function. Using intravital microscopy techniques, we tested the hypothesis that the speed and amplitude of the capillary red blood cell (RBC) velocity ( VRBC) and flux (FRBC) response to contractions would be reduced in CHF compared with control (C) spinotrapezius muscle. The proportion of capillaries supporting continuous RBC flow was less ( P < 0.05) in CHF (0.66 ± 0.04) compared with C (0.84 ± 0.01) muscle at rest and was not significantly altered with contractions. At rest, VRBC (C, 270 ± 62; CHF, 179 ± 14 μm/s) and FRBC (C, 22.4 ± 5.5 vs. CHF, 15.2 ± 1.2 RBCs/s) were reduced (both P < 0.05) in CHF vs. C muscle. Contractions significantly (both P < 0.05) elevated VRBC (C, 428 ± 47 vs. CHF, 222 ± 15 μm/s) and FRBC (C, 44.3 ± 5.5 vs. CHF, 24.0 ± 1.2 RBCs/s) in C and CHF muscle; however, both remained significantly lower in CHF than C. The time to 50% of the final response was slowed (both P < 0.05) in CHF compared with C for both VRBC (C, 8 ± 4; CHF, 56 ± 11 s) and FRBC (C, 11 ± 3; CHF, 65 ± 11 s). Capillary hematocrit increased with contractions in C and CHF muscle but was not different ( P > 0.05) between CHF and C. Thus CHF impairs diffusive and conductive O2 delivery across the rest-to-contractions transition in rat skeletal muscle, which may help explain the slowed O2 uptake on-kinetics manifested in CHF patients at exercise onset.

scholarly journals Tumour necrosis factor alpha as a predictor of impaired peak leg blood flow in patients with chronic heart failure

QJM ◽  
1998 ◽  
Vol 91 (3) ◽  
pp. 199-203 ◽  
Author(s):  
S. D. Anker ◽  
M. Volterrani ◽  
K. R. Egerer ◽  
C. V. Felton ◽  
W. J. Kox ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Chronic Heart Failure ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Alpha ◽  
Necrosis Factor Alpha ◽  
Leg Blood Flow ◽  
Factor Alpha ◽  
Necrosis Factor

Leg blood flow and increased potassium release during exercise in chronic heart failure: Effect of physical training

1998 ◽  
Vol 4 (2) ◽  
pp. 105-114 ◽  
Author(s):  
Clifford W. Barlow ◽  
Patrick P. Davey ◽  
Mohammed S. Qayyum ◽  
James Conway ◽  
David J. Paterson ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Chronic Heart Failure ◽  
Physical Training ◽  
Leg Blood Flow ◽  
Potassium Release

Adrenomedullin-epinephrine cotreatment enhances cardiac output and left ventricular function by energetically neutral mechanisms

2012 ◽  
Vol 302 (8) ◽  
pp. H1584-H1590
Author(s):  
Thor Allan Stenberg ◽  
Anders Benjamin Kildal ◽  
Ole-Jakob How ◽  
Truls Myrmel
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Acute Heart Failure ◽  
Coronary Blood Flow ◽  
Drug Effects ◽  
Left Ventricular ◽  
Experimental Myocardial Infarction ◽  
Energetic Cost ◽  
Lv Function

Adrenomedullin (AM) used therapeutically reduces mortality in the acute phase of experimental myocardial infarction. However, AM is potentially deleterious in acute heart failure as it is vasodilative and inotropically neutral. AM and epinephrine (EPI) are cosecreted from chromaffin cells, indicating a physiological interaction. We assessed the hemodynamic and energetic profile of AM-EPI cotreatment, exploring whether drug interaction improves cardiac function. Left ventricular (LV) mechanoenergetics were evaluated in 14 open-chest pigs using pressure-volume analysis and the pressure-volume area-myocardial O2 consumption (PVA-MV˙o2) framework. AM (15 ng·kg−1·min−1, n = 8) or saline (controls, n = 6) was infused for 120 min. Subsequently, a concurrent infusion of EPI (50 ng·kg−1·min−1) was added in both groups (AM-EPI vs. EPI). AM increased cardiac output (CO) and coronary blood flow by 20 ± 10% and 39 ± 14% (means ± SD, P < 0.05 vs. baseline), whereas controls were unaffected. AM-EPI increased CO and coronary blood flow by 55 ± 17% and 75 ± 16% ( P < 0.05, AM-EPI interaction) compared with 13 ± 12% ( P < 0.05 vs. baseline) and 18 ± 31% ( P = not significant) with EPI. LV systolic capacitance decreased by −37 ± 22% and peak positive derivative of LV pressure (dP/d tmax) increased by 32 ± 7% with AM-EPI ( P < 0.05, AM-EPI interaction), whereas no significant effects were observed with EPI. Mean arterial pressure was maintained by AM-EPI and tended to decrease with EPI (+2 ± 13% vs. −11 ± 10%, P = not significant). PVA-MV˙o2 relationships were unaffected by all treatments. In conclusion, AM-EPI cotreatment has an inodilator profile with CO and LV function augmented beyond individual drug effects and is not associated with relative increases in energetic cost. This can possibly take the inodilator treatment strategy beyond hemodynamic goals and exploit the cardioprotective effects of AM in acute heart failure.

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