Circulation, Vol 89, 2070-2078, Copyright © 1994 by American Heart Association
WJ Paulus, PJ Vantrimpont and AM Shah
BACKGROUND: In isolated mammalian cardiomyocytes, papillary muscle
preparations, and ejecting hearts, nitric oxide (NO) or other cyclic
GMP-elevating interventions increase diastolic cell length and reduce peak
contractile performance by hastening onset of myocardial relaxation. In the
present study, the effect of NO on left ventricular (LV) relaxation and
diastolic distensibility was investigated in humans. METHODS AND RESULTS:
The NO donor substance sodium nitroprusside was infused during cardiac
catheterization in the global coronary bed of the LV of patients (n = 13)
investigated for chest pain who were without evidence of obstructive
coronary artery or other cardiac disease. Sodium nitroprusside was infused
intracoronarily at a dosage (< or = 4 micrograms/min) that was
previously shown to be devoid of systemic effects when infused into the
brachial artery to investigate the reactivity of the forearm vascular bed.
The effect of this global intracoronary infusion of the NO donor sodium
nitroprusside was assessed by sequential LV angiograms and
tip-micromanometer pressure recordings. During global intracoronary
nitroprusside infusion, there was a decrease in heart rate from 78 +/- 11
to 76 +/- 12 beats per minute (P < .05), in LV peak systolic pressure
from 161 +/- 18 to 146 +/- 18 mm Hg (P < .001), and in time to onset of
LV relaxation (interval from Q wave on the ECG to LV dP/dtmin) from 432 +/-
36 to 419 +/- 36 milliseconds (P < .01). In 7 patients in whom adequate
sequential LV angiograms could be obtained, LV end-diastolic volume
increased from 158 +/- 34 to 165 +/- 40 mL (P < .05), whereas LV end-
diastolic pressure fell from 18 +/- 5 to 12 +/- 3 mm Hg (P < .02), and
in 5 of these 7 patients, a downward shift of the diastolic LV pressure-
volume relation was observed. In 5 patients, a right atrial infusion of
sodium nitroprusside was performed either before (n = 2) or after the
global intracoronary infusion. The decrease in LV peak systolic pressure
observed during right atrial infusion was significantly smaller (P <
.01) than during global intracoronary infusion. CONCLUSIONS: The present
study reveals reduced LV pressure development, an LV relaxation-hastening
effect, and improved LV diastolic distensibility during global
intracoronary infusion of the NO donor substance sodium nitroprusside.
These effects appeared to be unrelated to systemic vasodilation or to
pericardial constraint and could be explained by a direct myocardial effect
of NO, probably through activation of guanylyl cyclase to increase cyclic
GMP or through modification of other cellular proteins.
ARTICLES
Acute effects of nitric oxide on left ventricular relaxation and diastolic distensibility in humans. Assessment by bicoronary sodium nitroprusside infusion
Cardiovascular Center, O.L.V. Ziekenhuis, Aalst, Belgium.
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 M. Argenziano, D. A. Dean, N. Moazami, D. J. Goldstein, E. A. Rose, H. M. Spotnitz, D. Burkhoff, M. C. Oz, and M. L. Dickstein Inhaled Nitric Oxide Is Not A Myocardial Depressant In A Porcine Model Of Heart Failure J. Thorac. Cardiovasc. Surg., March 1, 1998; 115(3): 700 - 704. [Abstract] [Full Text] [PDF]
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J. D. Sadoff, P. M. Scholz, J. Tse, and H. R. Weiss Reduced myocardial cyclic GMP increases myocardial O2 consumption in control but not renal hypertension-induced cardiac hypertrophy Cardiovasc Res, December 1, 1997; 36(3): 453 - 459. [Abstract] [Full Text] [PDF]
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W. J. Paulus, S. Kastner, P. Pujadas, A. M. Shah, H. Drexler, and M. Vanderheyden Left Ventricular Contractile Effects of Inducible Nitric Oxide Synthase in the Human Allograft Circulation, November 18, 1997; 96(10): 3436 - 3442. [Abstract] [Full Text]
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B. Preckel, G. Kojda, W. Schlack, D. Ebel, K. Kottenberg, E. Noack, V. Thamer, E. Noack, and V. Thämer Inotropic Effects of Glyceryl Trinitrate and Spontaneous NO Donors in the Dog Heart Circulation, October 21, 1997; 96(8): 2675 - 2682. [Abstract] [Full Text]
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 A. J. Kanai, S. Mesaros, M. S. Finkel, C. V. Oddis, L. A. Birder, and T. Malinski beta -Adrenergic regulation of constitutive nitric oxide synthase in cardiac myocytes Am J Physiol Cell Physiol, October 1, 1997; 273(4): C1371 - C1377. [Abstract] [Full Text] [PDF]
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M. Booke, R. Waurick, H. Van Aken, H.-G. Bone, Andreas Meissner, T. Prien, and J. Meyer Effects of sympathetic nerve blockade on vasoconstrictive properties of nitric oxide synthase inhibition in sheep Cardiovasc Res, October 1, 1997; 36(1): 111 - 117. [Abstract] [Full Text] [PDF]
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B. D. Prendergast, B M. Sci, V. F. Sagach, and A. M. Shah Basal Release of Nitric Oxide Augments the Frank-Starling Response in the Isolated Heart Circulation, August 19, 1997; 96(4): 1320 - 1329. [Abstract] [Full Text]
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P. Musialek, M. Lei, H. F. Brown, D. J. Paterson, and B. Casadei Nitric Oxide Can Increase Heart Rate by Stimulating the Hyperpolarization-Activated Inward Current, If Circ. Res., July 19, 1997; 81(1): 60 - 68. [Abstract] [Full Text]
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 M. Flesch, H. Kilter, B. Cremers, O. Lenz, M. Südkamp, F. Kuhn-Regnier, and M. Böhm J. Pharmacol. Exp. Ther., June 1, 1997; 281(3): 1340 - 1349. [Abstract] [Full Text]
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N. Ito, J. Bartunek, K. W. Spitzer, and B. H. Lorell Effects of the Nitric Oxide Donor Sodium Nitroprusside on Intracellular pH and Contraction in Hypertrophied Myocytes Circulation, May 6, 1997; 95(9): 2303 - 2311. [Abstract] [Full Text]
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P. Mankad and M. Yacoub INFLUENCE OF BASAL RELEASE OF NITRIC OXIDE ON SYSTOLIC AND DIASTOLIC FUNCTION OF BOTH VENTRICLES J. Thorac. Cardiovasc. Surg., April 1, 1997; 113(4): 770 - 776. [Abstract] [Full Text]
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E. O. Weinberg, M. A. Lee, M. Weigner, K. Lindpaintner, S. P. Bishop, C. R. Benedict, K. K. L. Ho, P. S. Douglas, E. Chafizadeh, and B. H. Lorell Angiotensin AT1 Receptor Inhibition : Effects on Hypertrophic Remodeling and ACE Expression in Rats With Pressure-Overload Hypertrophy due to Ascending Aortic Stenosis Circulation, March 18, 1997; 95(6): 1592 - 1600. [Abstract] [Full Text]
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J. Bartunek, A. M. Shah, M. Vanderheyden, and W. J. Paulus Dobutamine Enhances Cardiodepressant Effects of Receptor-Mediated Coronary Endothelial Stimulation Circulation, January 7, 1997; 95(1): 90 - 96. [Abstract] [Full Text]
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B. D Prendergast, P. B Anning, M. J Lewis, and A. M Shah Regulation of left ventricular relaxation in the isolated guinea-pig heart by endogenous endothelin Cardiovasc Res, January 1, 1997; 33(1): 131 - 138. [Abstract] [Full Text] [PDF]
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M. Thompson, L. Becker, D. Bryant, G. Williams, D. Levin, L. Margraf, and B. P. Giroir Expression of the inducible nitric oxide synthase gene in diaphragm and skeletal muscle J Appl Physiol, December 1, 1996; 81(6): 2415 - 2420. [Abstract] [Full Text] [PDF]
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R. A. Kelly, J.-L. Balligand, and T. W. Smith Nitric Oxide and Cardiac Function Circ. Res., September 1, 1996; 79(3): 363 - 380. [Full Text]
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M.-C. Seghaye, MD, J. Duchateau, R. G. Grabitz, T. Wolffb, C. Marcus, W. Engelhardt, H. Hornchen, B. J. Messmer, and G. von Bernuth EFFECT OF SODIUM NITROPRUSSIDE ON COMPLEMENT ACTIVATION INDUCED BY CARDIOPULMONARY BYPASS: A CLINICAL AND EXPERIMENTAL STUDY J. Thorac. Cardiovasc. Surg., April 1, 1996; 111(4): 882 - 892. [Abstract] [Full Text]
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P. Mohan, D. L. Brutsaert, W. J. Paulus, and S. U. Sys Myocardial Contractile Response to Nitric Oxide and cGMP Circulation, March 15, 1996; 93(6): 1223 - 1229. [Abstract] [Full Text]
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N. P. Lewis, P. S. Tsao, P. R. Rickenbacher, C. Xue, R. A. Johns, G. A. Haywood, H. von der Leyen, P. T. Trindade, J. P. Cooke, S. A. Hunt, et al. Induction of Nitric Oxide Synthase in the Human Cardiac Allograft Is Associated With Contractile Dysfunction of the Left Ventricle Circulation, February 15, 1996; 93(4): 720 - 729. [Abstract] [Full Text]
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D. M. Kaye, S. D. Wiviott, J.-L. Balligand, W. W. Simmons, T. W. Smith, and R. A. Kelly Frequency-Dependent Activation of a Constitutive Nitric Oxide Synthase and Regulation of Contractile Function in Adult Rat Ventricular Myocytes Circ. Res., February 1, 1996; 78(2): 217 - 224. [Abstract] [Full Text]
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K. Node, M. Kitakaze, H. Kosaka, K. Komamura, T. Minamino, M. Inoue, M. Tada, M. Hori, and T. Kamada Increased Release of NO During Ischemia Reduces Myocardial Contractility and Improves Metabolic Dysfunction Circulation, January 15, 1996; 93(2): 356 - 364. [Abstract] [Full Text]
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G. Kojda, K. Kottenberg, P. Nix, K. D. Schluter, H. M. Piper, and E. Noack Low Increase in cGMP Induced by Organic Nitrates and Nitrovasodilators Improves Contractile Response of Rat Ventricular Myocytes Circ. Res., January 1, 1996; 78(1): 91 - 101. [Abstract] [Full Text]
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P. B. Anning, R. M. Grocott-Mason, M. J. Lewis, and A. M. Shah Enhancement of Left Ventricular Relaxation in the Isolated Heart by an Angiotensin-Converting Enzyme Inhibitor Circulation, November 1, 1995; 92(9): 2660 - 2665. [Abstract] [Full Text]
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W. J. Paulus, P. J. Vantrimpont, and A. M. Shah Paracrine Coronary Endothelial Control of Left Ventricular Function in Humans Circulation, October 15, 1995; 92(8): 2119 - 2126. [Abstract] [Full Text]
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J. M. Hare, E. Loh, M. A. Creager, and W. S. Colucci Nitric Oxide Inhibits the Positive Inotropic Response to ß-Adrenergic Stimulation in Humans With Left Ventricular Dysfunction Circulation, October 15, 1995; 92(8): 2198 - 2203. [Abstract] [Full Text]
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N. Paolocci, W. F. Saavedra, K. M. Miranda, C. Martignani, T. Isoda, J. M. Hare, M. G. Espey, J. M. Fukuto, M. Feelisch, D. A. Wink, et al. Nitroxyl anion exerts redox-sensitive positive cardiac inotropy in vivo by calcitonin gene-related peptide signaling PNAS, August 28, 2001; 98(18): 10463 - 10468. [Abstract] [Full Text] [PDF]
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J. Layland, J.-M. Li, and A. M Shah Role of cyclic GMP-dependent protein kinase in the contractile response to exogenous nitric oxide in rat cardiac myocytes J. Physiol., April 15, 2002; 540(2): 457 - 467. [Abstract] [Full Text] [PDF]
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