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

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.

1991 ◽  
Vol 71 (3) ◽  
pp. 1070-1075 ◽  
Author(s):  
M. J. Sullivan ◽  
F. R. Cobb

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.


1996 ◽  
Vol 90 (4) ◽  
pp. 269-276 ◽  
Author(s):  
U. Høst ◽  
H. Kelbaek ◽  
H. Rasmusen ◽  
M. Court-Payen ◽  
N. Juel Christensen ◽  
...  

1. The purpose of this study was to investigate the effect of fractional meal stimulation on postprandial haemodynamic changes, the possible correlation between these changes and the potential mediating role of circulating catecholamines and insulin. 2. Healthy young subjects were studied before and after ingestion of isocaloric, isovolumetric high-protein, carbohydrate or fat meals (80–85% of total energy), 60 kJ per kg of body weight. Multigated radionuclide cardiography with autologous 99mTc-labelled erythrocytes was performed for assessment of cardiac output, venous occlusion plethysmography to obtain forearm blood flow and Doppler-ultrasonography for portal vein flow. Plasma levels of catecholamines and insulin were determined by radioimmunoassay. 3. Cardiac output increased considerably after each meal, including the control meal (water) with only minor differences in extent and timing. Left ventricular volumes increased after food intake, most pronounced after carbohydrate and protein. Forearm blood flow increased only after carbohydrate and protein. Portal vein flow increased after all meals, especially after fat, but also after the control meal. There was a significant correlation between the increment in cardiac output and changes in forearm and portal vein flow, but no correlation between either haemodynamic response and plasma catecholamines or insulin. 4. Postprandial cardiovascular changes are not substantially different after various isocaloric and isovolumic meal compositions. Gastric distension seems to play a role in the increase in cardiac output, accomplished by ventricular dilatation. These changes seem to some extent to be linked to changes in muscle and splanchnic flow.


2012 ◽  
Vol 302 (8) ◽  
pp. H1584-H1590
Author(s):  
Thor Allan Stenberg ◽  
Anders Benjamin Kildal ◽  
Ole-Jakob How ◽  
Truls Myrmel

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.


1980 ◽  
Vol 238 (5) ◽  
pp. H736-H739 ◽  
Author(s):  
J. Bhattacharya ◽  
L. J. Beilin

When cannulation of the left ventricle and the left atrium were compared as methods for measuring for measuring renal blood flow distribution with radioactive microspheres in 9 conscious and 6 anesthetized rabbits, there were no differences between the two injection routes. Left ventricular cannulation per se did not affect cardiac output, nor the percentage of the cardiac output supplying the kidneys; but cardiac outputs estimated by thermodilution by injections via this route were up to 10% greater than those from left atrial injection. The advantages of left ventricular cannulation for experiments on regional blood flow distribution in conscious animals are discussed.


Heart ◽  
2001 ◽  
Vol 85 (5) ◽  
pp. 508-513
Author(s):  
W A Parsonage ◽  
D Hetmanski ◽  
A J Cowley

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.


1993 ◽  
Vol 265 (4) ◽  
pp. H1119-H1131 ◽  
Author(s):  
K. Komamura ◽  
R. P. Shannon ◽  
T. Ihara ◽  
Y. T. Shen ◽  
I. Mirsky ◽  
...  

The goal of this study was to elucidate the ability of the left ventricle to accommodate an increase in preload (Frank-Starling mechanism) in the presence of congestive heart failure (CHF) but in the absence of the complicating effects of hypertrophy and fibrosis. To accomplish this, the effects of volume loading were examined in eight conscious dogs during the control state and after 3 wk of right ventricular pacing (240 beats/min). CHF increased heart rate (by 16 +/- 5 from 92 +/- 5 beats/min), left ventricular (LV) end-diastolic pressure (by 17 +/- 2 from 10 +/- 1 mmHg), and LV end-diastolic volume (EDV; by 23 +/- 4 from 57 +/- 3 ml). Despite reduced LV ejection fraction (from 54 +/- 3 to 31 +/- 3%), there was no significant change in cardiac output (2.5 +/- 0.3 l/min) compared with control (2.7 +/- 0.2 l/min). Stroke volume was preserved (control 19 +/- 2 ml; CHF 18 +/- 2 ml) at a constant heart rate by a shift to the right in the relationship between LV stroke volume and EDV, indicating the importance of chronic ventricular dilatation in maintaining pump performance. In the control state, acute volume load increased LV EDV (by 17 +/- 2 ml) and stroke volume (by 11 +/- 2 ml), whereas in CHF it did not increase LV EDV or stroke volume. Scanning electron microscopy revealed areas of reduced collagen weave pattern surrounding myofibers. Myocyte cross-sectional area by transmission electron microscopy was significantly reduced, and there were multiple electron-dense expansions of the Z lines with disruption of the normal lateral sarcomere alignment. These morphological findings suggest that chronic ventricular dilatation utilized in CHF results from myocyte stretch and morphological intracellular rearrangement. Furthermore, the failing heart cannot further augment stroke volume by acutely increasing EDV in CHF, suggesting that the Frank-Starling reserve is essentially exhausted.


Circulation ◽  
1996 ◽  
Vol 94 (9) ◽  
pp. 2260-2267 ◽  
Author(s):  
Gregory A. Helmer ◽  
M. Dan McKirnan ◽  
Ralph Shabetai ◽  
Gerry R. Boss ◽  
John Ross ◽  
...  

1991 ◽  
Vol 260 (6) ◽  
pp. H1903-H1911 ◽  
Author(s):  
R. P. Shannon ◽  
K. Komamura ◽  
B. S. Stambler ◽  
M. Bigaud ◽  
W. T. Manders ◽  
...  

We investigated the changes in left ventricular (LV) geometry and myocardial contractility in eight conscious chronically instrumented dogs studied before and after the development of dilated cardiomyopathy induced by rapid ventricular pacing. Significant increases (P less than 0.01) were observed in cardiac dimensions in both the LV long and short axes and in end-diastolic volume (control: 53 +/- 1 ml; cardiomyopathy: 76 +/- 2 ml) and end-systolic volume (control: 27 +/- 2 ml; cardiomyopathy: 56 +/- 7 ml). This was associated with the left ventricle assuming a more spherical shape with LV long-to-short axis ratio falling from 1.59 +/- 0.05 to 1.47 +/- 0.04 (P less than 0.05). Both isovolumic (LV dP/dt) and ejection phase indexes (LV mean velocity of circumferential fiber shortening, corrected LV short-axis diameter at point of maximum shortening, and LV ejection fraction) were depressed by 50%. The end-systolic elastance was also depressed significantly (control: 16.6 +/- 0.7 g.cm-2.ml-1; cardiomyopathy: 10.1 +/- 1.7 g.cm-2.ml-1, P less than 0.02). However, cardiac output was maintained at 3 wk due to a compensatory tachycardia (+31 +/- 3 beats/min), plasma volume expansion (+295 +/- 68 ml, P less than 0.05), and greater reliance on the Frank-Starling mechanism. However, in an additional four dogs studied at 4-5 wk, cardiac output fell significantly (P less than 0.05). Thus rapid ventricular pacing results in dilated congestive cardiomyopathy in conscious dogs characterized by globally depressed myocardial systolic function and changes in LV shape.


1977 ◽  
Vol 84 (2) ◽  
pp. 429-438 ◽  
Author(s):  
Uffe Bang Olsen

ABSTRACT Ten μg/min glucagon infused intravenously for 30 min in conscious dogs (weight 15–25 kg) is shown to increase renal prostaglandin activity and to produce a natriuretic effect, which is impaired by indomethacin pretreatment. Cardiac output, heart rate, renal blood flow and urine cAMP excretion are similarly increased in non-pre-treated and indomethacin pre-treated dogs. Glucagon infusion does not consistently change plasma renin activity in non-pre-treated dogs, while the renin secretion is almost totally blocked when glucagon is administered to dogs that are pre-treated with indomethacin. The results are consistent with the view that the natriuretic response to glucagon is largely dependent upon increased renal blood flow. An addition tubular prostaglandin mediated and possible anti-aldosterone effect is, however, also involved.


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