Nitric oxide modulates epicardial coronary basal vasomotor tone in awake dogs

1990 ◽  
Vol 258 (4) ◽  
pp. H1250-H1254 ◽  
Author(s):  
A. Chu ◽  
D. E. Chambers ◽  
C. C. Lin ◽  
W. D. Kuehl ◽  
F. R. Cobb
Keyword(s):  
Nitric Oxide ◽  
Coronary Flow ◽  
Diastolic Pressure ◽  
Coronary Vessels ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Vasomotor Tone ◽  
Coronary Vasomotor Tone ◽  
Endogenous Nitric Oxide

This study evaluates the role of endogenous nitric oxide in the modulation of basal coronary vasomotor tone by studying the effects of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of nitric oxide formation from L-arginine, on resting epicardial coronary diameter and coronary flow. L-NMMA (5 mg/kg) was infused in seven awake dogs chronically instrumented with coronary dimension crystals for measurement of epicardial coronary diameter, and Doppler flow probes for quantitation of phasic coronary flow (vasomotion of distal regulatory resistance coronary vessels). Epicardial coronary diameter decreased 5.5% from 3.47 +/- 0.17 to 3.28 +/- 0.15 mm (mean +/- SE). The diameter change was gradual, reaching a maximum at 13 +/- 2 min after infusion, and persistent, lasting greater than 90 min. Phasic coronary flow did not change. Mean aortic pressure significantly increased from 99 +/- 3 to 111 +/- 3 mmHg and heart rate decreased from 56 +/- 4 to 46 +/- 3 beats/min. Left ventricular end-diastolic pressure and contractility were not significantly altered. L-Arginine (66 mg/kg) but not D-arginine reversed all hemodynamic parameters. These data support an important role of nitric oxide in modulating basal epicardial coronary vasomotor tone and systemic vascular resistance.

Modulation of coronary flow by left ventricular volume in the presence and absence of vasomotor tone

1995 ◽  
Vol 269 (6) ◽  
pp. H2010-H2016
Author(s):  
D. Manor ◽  
S. Williams ◽  
R. Ator ◽  
K. Bryant ◽  
K. W. Scheel
Keyword(s):  
Coronary Flow ◽  
Ventricular Volume ◽  
Left Ventricular ◽  
Vasomotor Tone ◽  
Volume Loading ◽  
Wide Range ◽  
Coronary Vasomotor Tone ◽  
Left And Right ◽  
Presence And Absence ◽  
Lv Volume

This study was undertaken to determine the relationship between left ventricular (LV) volume and coronary flow in the presence and absence of coronary vasomotor tone in arrested dog hearts. We utilized an isolated, blood-perfused, potassium-arrested dog heart preparation with vascular vasomotor tone present (n = 5) or after maximal vasodilation with adenosine (n = 7). LV volume was controlled with a balloon while left and right coronary flows were recorded. Left and right coronary flows were plotted as a function of LV volume, and the degree of interdependency was quantitatively assessed by the slope of the linear regression and the correlation coefficient (r) between coronary flow and LV volume. With vasomotor tone present, both left (slope = 0.01 +/- 0.06 min-1) and right (slope = -0.01 +/- 0.01 min-1) coronary arterial flows were maintained relatively constant over a wide range of LV volumes. After maximal vasodilation, left coronary flow decreased linearly with LV volume loading (slope = -2.51 +/- 0.47 min-1, r2 = 0.96 +/- 0.02), whereas right coronary flow, similar to the response with tone present, did not change relative to control in most cases. We conclude that changes in coronary vasomotor tone may take place with LV volume loading to compensate for the mechanical vascular resistance changes secondary to myocardial stretch.

Effect of PDE5 inhibition on coronary hemodynamics in pacing-induced heart failure

2003 ◽  
Vol 284 (5) ◽  
pp. H1513-H1520 ◽  
Author(s):  
YingJie Chen ◽  
Jay H. Traverse ◽  
Mingxiao Hou ◽  
Yunfang Li ◽  
Ruisheng Du ◽  
...  
Keyword(s):  
Heart Failure ◽  
Diastolic Pressure ◽  
Time Derivative ◽  
Systolic Pressure ◽  
Coronary Vessels ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Pde5 Inhibition ◽  
Rapid Ventricular Pacing ◽  
Phosphodiesterase Type

Inhibition of phosphodiesterase type 5 (PDE5) can relax systemic and coronary vessels by causing accumulation of cGMP. Both the endothelial dysfunction with decreased nitric oxide production and increased natriuretic peptide levels in congestive heart failure (CHF) have the potential to alter cGMP production, thereby influencing the response to PDE5 inhibition. Consequently, this study examined the effects of PDE5 inhibition with sildenafil in dogs with CHF produced by rapid ventricular pacing. CHF resulted in decreases of left ventricular (LV) systolic pressure, coronary blood flow, and the maximal first time derivative of LV pressure (LV dP/d t max) at rest and during treadmill exercise compared with normal, whereas resting LV end-diastolic pressure increased from 10 ± 1.4 to 23 ± 1.4 mmHg. Sildenafil (2 and 10 mg/kg per os) caused a 5- to 6-mmHg decrease of aortic pressure ( P < 0.05), with no change of heart rate, LV systolic pressure, or LV dP/d t max. Sildenafil caused no change in coronary flow or myocardial oxygen consumption in animals with CHF at rest or during exercise. In contrast to findings in normal animals, sildenafil did not augment endothelium-dependent coronary vasodilation in response to acetylcholine in animals with CHF. Furthermore, Western blotting showed decreased PDE5 protein expression in myocardium from failing hearts. These findings demonstrate that PDE5 contributes little to regulation of coronary hemodynamics in CHF.

Adrenal contribution to coronary regulation in the newborn

1978 ◽  
Vol 234 (2) ◽  
pp. H173-H179
Author(s):  
S. E. Downing ◽  
W. E. Hellenbrand ◽  
J. C. Lee ◽  
D. B. Nudel
Keyword(s):  
Diastolic Pressure ◽  
Coronary Vessels ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Beta Blockade ◽  
Sham Operation ◽  
Metabolic Demand ◽  
Adrenergic Control ◽  
Alpha Blockade ◽  
Myocardial O2 Consumption

Evidence for adrenergic regulation of the coronary vessels was sought in 27 newborn lambs. Sympathetic activity was altered by temporarily lowering cephalic perfusion pressure (CPP) from 90 to 20 mmHg while aortic pressure was held constant. Heart rate (HR) and left ventricular dP/dt max increased markedly, while end-diastolic pressure and stroke volume fell. These changes were accompanied by an increase in coronary blood flow (CBF), myocardial O2 consumption (MVO2), and reduced coronary resistance (CF) (P less than 0.005). After beta blockade, which prevented an augmentation of metabolic demand, the same maneuver resulted in coronary vasoconstriction, reflected by reduced CBF and increased CR (P less than 0.02). This response was eliminated by alpha blockade with phentolamine (2 mg/kg). In 13 lambs subjected to bilateral adrenalectomy or sham operation, lowering CPP elicited similar positive chronotropic and inotropic changes, increases of MVO2 and CBF, and reduced CR. Following beta blockade, lowering CPP in the sham group caused coronary constriction. However, no changes in CBF or CR were elicited in the adrenalectomized lambs. These observations indicate that integrity of the adrenal glands is required for adrenergic control of the coronary vessels in the newborn. Chronotropic and inotropic regulation is mediated by direct neural action and is not dependent on adrenal function.

scholarly journals Estrogen restores role of basal nitric oxide in control of vascular tone in rats with chronic heart failure

1998 ◽  
Vol 274 (6) ◽  
pp. H2094-H2099 ◽  
Author(s):  
Ali Akbar Nekooeian ◽  
Catherine C. Y. Pang
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Chronic Heart Failure ◽  
Diastolic Pressure ◽  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ovariectomized Rats ◽  
17Β Estradiol

This study examined the cardiovascular effects of 17β-estradiol in ovariectomized rats with heart failure. Two groups (50–60 days old) were implanted with 60-day-release pellets containing 17β-estradiol (25 μg/day) or vehicle at 7 days before ligation of the left coronary artery. Another group was sham operated and given vehicle pellets. After 7 wk, they were studied under pentobarbital anesthesia. Relative to sham-operated rats, ligated rats had reduced mean arterial pressure (MAP, −24 ± 6 mmHg), cardiac output (−27 ± 4 ml/min), left ventricular (LV) end-systolic pressure (−29 ± 8 mmHg), depressor responses to ACh (−6 ± 4 mmHg at 7.2 μg/kg) and sodium nitroprusside (SNP, −22 ± 6 mmHg at 9 μg/kg), and pressor responses to N G-nitro-l-arginine methyl ester (l-NAME, −14 ± 6 mmHg at 8 mg/kg) and increased LV end-diastolic pressure (LVEDP, 10.3 ± 0.8 mmHg) but no change in total peripheral resistance (TPR). Treatment of ligated rats with 17β-estradiol reduced TPR (−0.19 ± 0.06 mmHg ⋅ min ⋅ ml−1), LVEDP (−3.6 ± 1 mmHg), and responses to ACh (−16 ± 4 mmHg) and augmented responses tol-NAME (14 ± 3 mmHg) but did not alter other variables. Therefore, 17β-estradiol reduces preload and afterload and restores the vasodilator role of basal nitric oxide in ovariectomized rats with chronic heart failure.

Role of endogenous nitric oxide (NO) and NO synthases in healing of indomethacin-induced intestinal ulcers in rats

Life Sciences ◽  
2007 ◽  
Vol 80 (4) ◽  
pp. 329-336 ◽  
Author(s):  
Koji Takeuchi ◽  
Ryo Hatazawa ◽  
Mayu Tanigami ◽  
Akiko Tanaka ◽  
Ryoko Ohno ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endogenous Nitric Oxide ◽  
Intestinal Ulcers

Nitric oxide: a new role in intensive care

2020 ◽  
Vol 22 (1) ◽  
pp. 72-79
Author(s):  
Alexandra Lee ◽  
◽  
Warwick Butt ◽  
◽  
◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Potential Role ◽  
Nitric Oxide Donors ◽  
Ischaemia Reperfusion Injury ◽  
Surface Receptors ◽  
The Past ◽  
Ischaemia Reperfusion ◽  
Human Experiments ◽  
Endogenous Nitric Oxide

Inhaled nitric oxide has been used for 30 years to improve oxygenation and decrease pulmonary vascular resistance. In the past 15 years, there has been increased understanding of the role of endogenous nitric oxide on cell surface receptors, mitochondria, and intracellular processes involving calcium and superoxide radicals. This has led to several animal and human experiments revealing a potential role for administered nitric oxide or nitric oxide donors in patients with systemic inflammatory response syndrome or ischaemia–reperfusion injury, and in patients for whom exposure of blood to artificial surfaces has occurred.

INFLUENCE OF ACIDEMIA ON LEFT VENTRICULAR FUNCTION IN THE NEWBORN LAMB

PEDIATRICS ◽  
1966 ◽  
Vol 38 (3) ◽  
pp. 457-464
Author(s):  
Norman S. Talner ◽  
Thomas H. Gardner ◽  
S. Evans Downing
Keyword(s):  
Left Ventricle ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Newborn Lamb ◽  
Precise Control ◽  
Significant Impairment ◽  
Ph Range

The performance of the left ventricle in 20 newborn lambs was examined in a preparation which allowed precise control of aortic pressure, cardiac output, heart rate, and temperature. Reduction of arterial pH from a normal range (7.35 to 7.5) to severe acidemia (6.8 to 7.0) by hydrochloric or lactic acid infusion resulted in no significant impairment of left ventricular function. Prolonged acidemia (over 2 hours) failed to produce a reduction in left ventricular stroke volume or mean ejection rate for a given left ventricular end-diastolic pressure. Responsiveness of the left ventricle of the lamb to catecholamine stimulation was not diminished over the pH range 7.5 to 6.8. Under conditions of these investigations the apparent resistance of the myocardium of the newborn lamb, as well as the adult cat, to wide variations in pH may reflect a buffering capacity of cardiac muscle which would allow minimal change in intracellular pH, even though extracellular pH may indicate the presence of severe metabolic acidosis.

Interaction of interval-force relationship with aortic pressure and stroke volume

1976 ◽  
Vol 230 (4) ◽  
pp. 893-900 ◽  
Author(s):  
ER Powers ◽  
Foster ◽  
Powell WJ
Keyword(s):  
Heart Rate ◽  
Stroke Volume ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Cardiac Performance ◽  
Right Heart ◽  
Anesthetized Dogs ◽  
Right Heart Bypass ◽  
Force Relationship

The modification by aortic pressure and stroke volume of the response in cardiac performance to increases in heart rate (interval-force relationship) has not been previously studied. To investigate this interaction, 30 adrenergically blocked anesthetized dogs on right heart bypass were studied. At constant low aortic pressure and stroke volume, increasing heart rate (over the entire range 60-180) is associated with a continuously increasing stroke power, decreasing systolic ejection period, and an unchanging left ventricular end-diastolic pressure and circumference. At increased aortic pressure or stroke volume at low rates (60-120), increases in heart rate were associated with an increased performance. However, at increased aortic pressure or stroke volume at high rates (120-180), increases in heart rate were associated with a leveling or decrease in performance. Thus, an increase in aortic pressure or stroke volume results in an accentuation of the improvement in cardiac performance observed with increases in heart rate, but this response is limited to a low heart rate range. Therefore, the hemodynamic response to given increases in heart rate is critically dependent on aortic pressure and stroke volume.

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