Effects of Adenosine Infusion on Renal Blood Flow, Vascular Resistance and Oxygen Consumption in Patients with Heart Failure

1992 ◽  
Vol 82 (s26) ◽  
pp. 21P-21P
Author(s):  
GA Haywood ◽  
JF Sneddon ◽  
Y Bashir ◽  
S Jennison ◽  
WJ McKenna
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Adenosine Infusion ◽  
Patients With Heart Failure

scholarly journals Abnormal glomerular response to atrial natriuretic peptide in rats with aortocaval fistulas.

1996 ◽  
Vol 7 (7) ◽  
pp. 1038-1044
Author(s):  
L L Norling ◽  
B A Thornhill ◽  
R L Chevalier
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Atrial Natriuretic Peptide ◽  
Renal Blood Flow ◽  
Natriuretic Peptide ◽  
Vascular Resistance ◽  
Sprague Dawley ◽  
And Control ◽  
Atrial Natriuretic

Heart failure is characterized by a blunted natriuretic and diuretic response to atrial natriuretic peptide (ANP). To investigate this, a rat model of compensated high-output heart failure was used to determine whether glomerular response to ANP differs in animals with high cardiac output compared with control animals. An aortocaval (AC) fistula was made below the level of the renal arteries in male Sprague-Dawley rats. At 6 wk, one group of AC fistula (N = 6) and control rats (N = 6) was injected with radiolabeled microspheres for determination of hemodynamic parameters, including cardiac output, renal blood flow, and vascular resistance. Rats with AC fistulas had significant changes in cardiac output (218 +/- 17 versus 57 +/- 11 mL/min, P < or = 0.0001), renal blood flow (3.4 +/-0.7 versus 8.4 +/- 1.9 mL/min Left, P < or = 0.05; 3.0 +/- 0.4 versus 7.2 +/- 1.9 mL/min Right, P < or = 0.05), and total vascular resistance (0.6 +/- 0.1 versus 2.7 +/- 0.4 mm Hg/mL per min, P < 0.001) compared with control animals, respectively. In another group of animals, after 6 wk, glomeruli were isolated from kidneys. Extracellular (EC) and intracellular (IC) cGMP was measured as an indication of glomerular response to ANP. Early glomerular response to ANP (10(-8)mol/L) showed a similar acute 13- to 18-fold rise in IC cGMP after 30 sec exposure to ANP (P < or = 0.0001 versus no ANP; N = 4 AC fistula rats and N = 4 control rats). During 1-h incubations with ANP, glomerular response was characterized by a five- to sevenfold increase in EC cGMP. However, glomeruli of AC fistula rats produced significantly less EC cGMP than did those of control animals (21.3 +/- 2.5 versus 44 +/- 4.9 fMol cGMP/2000 glomeruli, P < = 0.005; N = 5 AC fistula rats and N = 5 control rats, respectively). Probenecid-sensitive transport of EC cGMP between AC fistula and control rats (86% decrease versus 82% decrease) was similar. However, glomeruli from AC fistula animals had significantly less phosphodiesterase activity compared with control animals (3.6 +/- 0.4 versus 5.4 +/- 0.7 nMol cGMP/mg protein per min, P < or = 0.01; N = 4 AC fistula rats and N = 5 control rats, respectively). It is speculated that reduced glomerular generation of cGMP in response to ANP contributes to sodium retention in heart failure, but may be compensated for in part by decreased phosphodiesterase-mediated hydrolysis of cGMP.

Baroreflex regulation of regional blood flow in congestive heart failure

1990 ◽  
Vol 258 (5) ◽  
pp. H1409-H1414 ◽  
Author(s):  
M. A. Creager ◽  
A. T. Hirsch ◽  
V. J. Dzau ◽  
E. G. Nabel ◽  
S. S. Cutler ◽  
...  
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Blood Flow ◽  
Vascular Resistance ◽  
Lower Body Negative Pressure ◽  
Regional Blood Flow ◽  
Venous Pressure ◽  
Normal Subjects ◽  
Splanchnic Blood Flow ◽  
Patients With 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.

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

1996 ◽  
Vol 81 (6) ◽  
pp. 2571-2579 ◽  
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.

Soothing the sleeping giant: improving skeletal muscle oxygen kinetics and exercise intolerance in HFpEF

2015 ◽  
Vol 119 (6) ◽  
pp. 734-738 ◽  
Author(s):  
Satyam Sarma ◽  
Benjamin D. Levine
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Oxygen Consumption ◽  
Functional Capacity ◽  
Oxidative Capacity ◽  
Exercise Intolerance ◽  
Aerobic Performance ◽  
Muscle Oxygen ◽  
Oxygen Kinetics ◽  
Patients With Heart Failure

Patients with heart failure with preserved ejection fraction (HFpEF) have similar degrees of exercise intolerance and dyspnea as patients with heart failure with reduced EF (HFrEF). The underlying pathophysiology leading to impaired exertional ability in the HFpEF syndrome is not completely understood, and a growing body of evidence suggests “peripheral,” i.e., noncardiac, factors may play an important role. Changes in skeletal muscle function (decreased muscle mass, capillary density, mitochondrial volume, and phosphorylative capacity) are common findings in HFrEF. While cardiac failure and decreased cardiac reserve account for a large proportion of the decline in oxygen consumption in HFrEF, impaired oxygen diffusion and decreased skeletal muscle oxidative capacity can also hinder aerobic performance, functional capacity and oxygen consumption (V̇o2) kinetics. The impact of skeletal muscle dysfunction and abnormal oxidative capacity may be even more pronounced in HFpEF, a disease predominantly affecting the elderly and women, two demographic groups with a high prevalence of sarcopenia. In this review, we 1) describe the basic concepts of skeletal muscle oxygen kinetics and 2) evaluate evidence suggesting limitations in aerobic performance and functional capacity in HFpEF subjects may, in part, be due to alterations in skeletal muscle oxygen delivery and utilization. Improving oxygen kinetics with specific training regimens may improve exercise efficiency and reduce the tremendous burden imposed by skeletal muscle upon the cardiovascular system.

Haemodynamic Assessment of Adenosine Infusion in Patients with Heart Failure

1992 ◽  
Vol 82 (s26) ◽  
pp. 17P-17P
Author(s):  
GA Haywood ◽  
JF Sneddon ◽  
Y Bashir ◽  
S Jennison ◽  
WJ McKenna
Keyword(s):  
Heart Failure ◽  
Adenosine Infusion ◽  
Patients With Heart Failure
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