scholarly journals Intracoronary Ghrelin Infusion Decreases Coronary Blood Flow in Anesthetized Pigs

Endocrinology ◽  
2007 ◽  
Vol 148 (2) ◽  
pp. 806-812 ◽  
Author(s):  
Elena Grossini ◽  
Claudio Molinari ◽  
David A. S. G. Mary ◽  
Ezio Ghigo ◽  
Gianni Bona ◽  
...  
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Coronary Blood Flow ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Ventricular Systolic Pressure ◽  
Coronary Vasoconstriction ◽  
Intracoronary Infusion ◽  
Atherosclerotic Process

The peptide ghrelin has been linked to the atherosclerotic process and coronary artery disease. We planned to study, for the first time, the primary effects of ghrelin on the intact coronary circulation and determine the mechanisms involved. In 24 sodium pentobarbitone-anesthetized pigs, changes in anterior descending coronary blood flow caused by intracoronary infusion of ghrelin at constant heart rate and arterial pressure were assessed using electromagnetic flowmeters. In 20 pigs, intracoronary infusion of ghrelin decreased coronary blood flow without affecting left ventricular maximum rate of change of left ventricular systolic pressure (dP/dtmax), filling pressures of the heart or plasma levels of GH. In four pigs, this decrease was graded by step increments of infused dose of the hormone. The mechanisms of the above response were studied in the 20 pigs by repeating the experiment after coronary flow had returned to the control values observed before infusion. The ghrelin-induced coronary vasoconstriction was not affected by iv atropine (five pigs) or phentolamine (five pigs). This response was abolished by iv butoxamine (five pigs) and intracoronary Nω-nitro-l-arginine methyl ester (five pigs), even after reversing the increase in arterial pressure and coronary vascular resistance caused by the two blocking agents with iv infusion of papaverine. The present study showed that intracoronary infusion of ghrelin primarily caused coronary vasoconstriction. The mechanisms of this response were shown to involve the inhibition of a vasodilatory β2-adrenergic receptor-mediated effect related to the release of nitric oxide.

Effects of intensive exercise training on myocardial performance and coronary blood flow

1980 ◽  
Vol 49 (3) ◽  
pp. 444-449 ◽  
Author(s):  
R. J. Barnard ◽  
H. W. Duncan ◽  
K. M. Baldwin ◽  
G. Grimditch ◽  
G. D. Buckberg
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Work Capacity ◽  
Left Ventricular ◽  
Maximum Exercise ◽  
Time Index ◽  
Significant Difference ◽  
Tension Time

Five instrumented and eight noninstrumented dogs were progressively trained for 12-18 wk on a motor-driven treadmill. Data were compared with 14 instrumented and 8 noninstrumented control dogs. Gastrocnemius malate dehydrogenase activity was significantly increased in the trained dogs (887 +/- 75 vs. 667 +/- 68 mumol . g-1 . min-1). The trained dogs also showed significant increases in maximum work capacity, cardiac output (7.1 +/- 0.5 vs. 9.1 +/- 0.7 1/min), stroke volume (25.9 +/- 2.0 vs. 32.0 +/- 2.0 ml/beat), and left ventricular (LV) positive dP/dtmax (9,242 +/- 405 vs. 11,125 +/- 550 Torr/s). Negative dP/dtmax was not significantly different. Peak LV systolic pressure increased with exercise, but there was no significant difference between the trained and control dogs. LV end-diastolic pressure did not change with exercise and was the same in both groups. Tension-time index was lower in the trained dogs at rest and submaximum exercise (9.7 km/h, 10%) but was not different at maximum exercise. Diastolic pressure-time index was significantly higher in the trained dogs at rest and during submaximum exercise but was not different at maximum exercise. LV coronary blood flow was significantly reduced at rest (84 +/- 4 vs. 67 +/- 6 mo . min-1 . 100 g-1) and during submaximum exercise (288 +/- 24 vs. 252 +/- 8 ml . min-1 . 100 g-1). During maximum exercise flow was not significantly different (401 +/- 22 vs. 432 +/- 11 ml . min-1 . 100 g-1) between the control and trained groups. The maximum potential for subendocardial flow was unchanged with training despite the development of mild hypertrophy.

Cardiac response to submaximal exercise in dogs susceptible to sudden cardiac death

1985 ◽  
Vol 59 (3) ◽  
pp. 890-897 ◽  
Author(s):  
G. E. Billman ◽  
P. J. Schwartz ◽  
J. P. Gagnol ◽  
H. L. Stone
Keyword(s):  
Ventricular Fibrillation ◽  
Diastolic Pressure ◽  
Stress Test ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Submaximal Exercise ◽  
Rate Of Change ◽  
Cardiac Response ◽  
Exercise Stress ◽  
Ventricular Systolic Pressure

The hemodynamic response to submaximal exercise was investigated in 38 mongrel dogs with healed anterior wall myocardial infarctions. The dogs were chronically instrumented to measure heart rate (HR), left ventricular pressure (LVP), LVP rate of change, and coronary blood flow. A 2 min coronary occlusion was initiated during the last minute of an exercise stress test and continued for 1 min after cessation of exercise. Nineteen dogs had ventricular fibrillation (susceptible) while 19 animals did not (resistant) during this test. The cardiac response to submaximal exercise was markedly different between the two groups. The susceptible dogs exhibited a significantly higher HR and left ventricular end-diastolic pressure (LVEDP) but a significantly lower left ventricular systolic pressure (LVSP) in response to exercise than did the resistant animals. (For example, response to 6.4 kph at 8% grade; HR, susceptible 201.4 +/- 5.1 beats/min vs. resistant 176.2 +/- 5.6 beats/min; LVEDP, susceptible 19.4 +/- 1.1 mmHg vs. resistant 12.3 +/- 1.7 mmHg; LVSP, susceptible 136.9 +/- 7.9 mmHg vs. resistant 154.6 +/- 9.8 mmHg.) beta-Adrenergic receptor blockade with propranolol reduced the difference noted in the HR response but exacerbated the LVP differences (response to 6.4 kph at 8% grade; HR, susceptible 163.4 +/- 4.7 mmHg vs. resistant 150.3 +/- 6.4 mmHg; LVEDP susceptible 28.4 +/- 2.1 mmHg vs. resistant 19.6 +/- 3.0 mmHg; LVSP, susceptible 122.2 +/- 8.1 mmHg vs. resistant 142.8 +/- 10.7 mmHg). These data indicate that the animals particularly vulnerable to ventricular fibrillation also exhibit a greater degree of left ventricular dysfunction and an increased sympathetic efferent activity.

Volume expansion potentiates cardiac sympathetic afferent reflex in dogs

2001 ◽  
Vol 280 (2) ◽  
pp. H576-H581 ◽  
Author(s):  
Wei Wang ◽  
Harold D. Schultz ◽  
Rong Ma
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Coronary Blood Flow ◽  
Volume Expansion ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Blood Volume Expansion ◽  
Cardiac Sympathetic Afferent Reflex

Our previous study (27) showed that the cardiac sympathetic afferent reflex (CSAR) was enhanced in dogs with congestive heart failure. The aim of this study was to test whether blood volume expansion, which is one characteristic of congestive heart failure, potentiates the CSAR in normal dogs. Ten dogs were studied with sino-aortic denervation and bilateral cervical vagotomy. Arterial pressure, left ventricular pressure, left ventricular epicardial diameter, heart rate, and renal sympathetic nerve activity were measured. Coronary blood flow was also measured and, depending on the experimental procedure, controlled. Blood volume expansion was carried out by infusion of isosmotic dextran into a femoral vein at 40 ml/kg at a rate of 50 ml/min. CSAR was elicited by application of bradykinin (5 and 50 μg) and capsaicin (10 and 100 μg) to the epicardial surface of the left ventricle. Volume expansion increased arterial pressure, left ventricular pressure, left ventricular diameter, and coronary blood flow. Volume expansion without controlled coronary blood flow only enhanced the RSNA response to the high dose (50 μg) of epicardial bradykinin (17. 3 ± 1.9 vs. 10.6 ± 4.8%, P < 0.05). However, volume expansion significantly enhanced the RSNA responses to all doses of bradykinin and capsaicin when coronary blood flow was held at the prevolume expansion level. The RSNA responses to bradykinin (16. 9 ± 4.1 vs. 5.0 ± 1.3% for 5 μg, P < 0.05, and 28.9 ± 3.7 vs. 10.6 ± 4.8% for 50 μg, P < 0.05) and capsaicin (29.8 ± 6.0 vs. 9.3 ± 3.1% for 10 μg, P < 0.05, and 34.2 ± 2.7 vs. 15.1 ± 2.7% for 100 μg, P < 0.05) were significantly augmented. These results indicate that acute volume expansion potentiated the CSAR. These data suggest that enhancement of the CSAR in congestive heart failure may be mediated by the concomitant cardiac dilation, which accompanies this disease state.

Augmented catecholamine uptake by the heart during hemorrhage in the conscious dog

1986 ◽  
Vol 250 (1) ◽  
pp. H76-H81 ◽  
Author(s):  
O. L. Woodman ◽  
J. Amano ◽  
T. H. Hintze ◽  
S. F. Vatner
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Nerve Stimulation ◽  
Left Ventricular ◽  
Sympathetic Nerve Stimulation ◽  
Net Release

Changes in arterial and coronary sinus concentrations of norepinephrine (NE) and epinephrine (E) in response to hemorrhage were examined in conscious dogs. Hemorrhage (45 +/- 3.2 ml/kg) decreased mean arterial pressure by 47 +/- 6%, left ventricular (LV) dP/dt by 38 +/- 6%, and mean left circumflex coronary blood flow by 47 +/- 6%, while heart rate increased by 44 +/- 13%. Increases in concentrations of arterial NE (5,050 +/- 1,080 from 190 +/- 20 pg/ml) and E (12,700 +/- 3,280 from 110 +/- 20 pg/ml) were far greater than increases in coronary sinus NE (1,700 +/- 780 from 270 +/- 50 pg/ml) and E (4,300 +/- 2,590 from 90 +/- 10 pg/ml). Net release of NE from the heart at rest was converted to a fractional extraction of 66 +/- 9% after hemorrhage. Fractional extraction of E increased from 16 +/- 6% at rest to 73 +/- 8% after hemorrhage. In cardiac-denervated dogs, hemorrhage (46 +/- 2.8 ml/kg) decreased mean arterial pressure by 39 +/- 15%, LV dP/dt by 36 +/- 10%, and mean left circumflex coronary blood flow by 36 +/- 13%, while heart rate increased by 24 +/- 10%. Hemorrhage increased arterial NE (1,740 +/- 150 from 210 +/- 30 pg/ml) and E (3,050 +/- 880 from 140 +/- 20 pg/ml) more than it increased coronary sinus NE (460 +/- 50 from 150 +/- 30 pg/ml) and E (660 +/- 160 from 90 +/- 20 pg/ml) but significantly less (P less than 0.05) than observed in intact dogs. These experiments indicate that hemorrhage, unlike exercise and sympathetic nerve stimulation, does not induce net overflow of NE from the heart.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of sympathetic stimulation during cooling on hypothermic as well as posthypothermic hemodynamic function

2006 ◽  
Vol 84 (10) ◽  
pp. 985-991 ◽  
Author(s):  
T.V. Kondratiev ◽  
T. Tveita
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Saline Solution ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Left Ventricular ◽  
Mechanical Function ◽  
Ventricular Systolic Pressure ◽  
Hemodynamic Variables ◽  
Left Ventricular Systolic Pressure

This experimental study was performed to explore hemodynamic effects of a moderate dose epinephrine (Epi) during hypothermia and to test the hypothesis whether sympathetic stimulation during cooling affects myocardial function following rewarming. Two groups of male Wistar rats (each, n = 7) were cooled to 15 °C, maintained at this temperature for 1 h, and then rewarmed. Group 1 received 1 μg/min Epi, i.v., for 1 h during cooling to 28 °C, a dose known to elevate cardiac output (CO) by approximately 25% at 37 °C. Group 2 served a saline solution control. At 37 °C, Epi infusion elevated CO, left ventricular systolic pressure, maximum rate of left ventricle pressure rise, and mean arterial pressure. During cooling to 28 °C, these variables, with the exception of mean arterial pressure, decreased in parallel to those in the saline solution group. In contrast, in the Epi group, mean arterial pressure remained increased and total peripheral resistance was significantly elevated at 28 °C. Compared with corresponding prehypothermic values, most hemodynamic variables were lowered after 1 h at 15 °C in both groups (except for stroke volume). After rewarming, alterations in hemodynamic variables in the Epi-treated group were more prominent than in saline solution controls. Thus, before cooling, continuous Epi infusion predominantly stimulates myocardial mechanical function, materialized as elevation of CO, left ventricular systolic pressure, and maximum rate of left ventricle pressure rise. Cooling, on the other hand, apparently eradicates central hemodynamic effects of Epi and during stable hypothermia, elevation of peripheral vascular vasopressor effects seem to take over. In contrast to temperature-matched, non-Epi stimulated control rats, a significant depression of myocardial mechanical function occurs during rewarming following a moderate sympathetic stimulus during initial cooling.

Coronary physiology

1983 ◽  
Vol 63 (1) ◽  
pp. 1-205 ◽  
Author(s):  
E. O. Feigl
Keyword(s):  
Blood Flow ◽  
Metabolic Control ◽  
Coronary Blood Flow ◽  
Oxygen Tension ◽  
Nerve Stimulation ◽  
Left Ventricular ◽  
Strenuous Exercise ◽  
Unexpected Finding ◽  
Coronary Vasoconstriction ◽  
Coronary Physiology

The major areas of normal coronary physiological research since Berne's 1964 review have been the measurement of ventricular transmural blood flow distribution with microspheres, the adenosine hypothesis of local metabolic control of coronary blood flow, and the autonomic control of coronary blood flow. There is an improved understanding of intramyocardial tissue pressure and extravascular compressive forces on coronary vessels. However, the unexpected finding of zero flow during a prolonged diastole with a coronary artery pressure of 40 mmHg (PZF) is a reminder that the physical forces, including vascular smooth muscle contraction, that determine coronary vascular resistance are incompletely understood. During normal circumstances, the left ventricular subendocardium probably receives more blood flow than the subepicardium does, but the difference is small. When the coronary circulation is compromised by stenosis or aortic valve lesions, the subendocardium is much more vulnerable to underperfusion than is the subepicardium. The coronary vasodilating effect of arterial hypoxia has been confirmed in many studies, but the role of tissue oxygen tension in local metabolic control of coronary blood flow during normoxia is unknown. The coronary vasodilating action of carbon dioxide has received renewed attention, but its role in local control is also unknown. The adenosine hypothesis has passed several critical tests, but despite much research the importance of adenosine in normal coronary regulation is not established. Local metabolic control of coronary blood flow probably involves more than just one factor, but a unified hypothesis has not been put forward. Sympathetic alpha-receptor-mediated coronary vasoconstriction has been demonstrated by nerve stimulation and during a carotid sinus baroreceptor reflex. Sympathetic coronary vasoconstriction is capable of competing with local metabolic control to lower coronary venous oxygen tension under experimental circumstances, but its importance during normal resting conditions is not established. Parasympathetic muscarinic coronary vasodilation has been shown by vagal nerve stimulation, but a role for it during normal blood flow regulation has yet to be demonstrated. There have been elegant descriptive studies of the coronary blood flow response during excitement and exercise, where coronary blood flow increases pari passu with myocardial metabolism; however, there are also data that indicate a concomitant sympathetic vasoconstrictor effect during strenuous exercise. Overall there has been encouraging progress in coronary physiology. Inevitably new knowledge has focused old questions and presented new ones.

scholarly journals Exaggerated coronary vasoconstriction limits muscle metaboreflex-induced increases in ventricular performance in hypertension

2017 ◽  
Vol 312 (1) ◽  
pp. H68-H79 ◽  
Author(s):  
Marty D. Spranger ◽  
Jasdeep Kaur ◽  
Javier A. Sala-Mercado ◽  
Abhinav C. Krishnan ◽  
Rania Abu-Hamdah ◽  
...  
Keyword(s):  
Blood Flow ◽  
Ventricular Function ◽  
Coronary Blood Flow ◽  
Muscle Afferents ◽  
Left Ventricular ◽  
Adrenergic Blockade ◽  
Ventricular Contractility ◽  
Ventricular Performance ◽  
Muscle Metaboreflex ◽  
Coronary Vasoconstriction

Increases in myocardial oxygen consumption during exercise mainly occur via increases in coronary blood flow (CBF) as cardiac oxygen extraction is high even at rest. However, sympathetic coronary constrictor tone can limit increases in CBF. Increased sympathetic nerve activity (SNA) during exercise likely occurs via the action of and interaction among activation of skeletal muscle afferents, central command, and resetting of the arterial baroreflex. As SNA is heightened even at rest in subjects with hypertension (HTN), we tested whether HTN causes exaggerated coronary vasoconstriction in canines during mild treadmill exercise with muscle metaboreflex activation (MMA; elicited by reducing hindlimb blood flow by ~60%) thereby limiting increases in CBF and ventricular performance. Experiments were repeated after α1-adrenergic blockade (prazosin; 75 µg/kg) and in the same animals following induction of HTN (modified Goldblatt 2K1C model). HTN increased mean arterial pressure from 97.1 ± 2.6 to 132.1 ± 5.6 mmHg at rest and MMA-induced increases in CBF, left ventricular dP/d tmax, and cardiac output were markedly reduced to only 32 ± 13, 26 ± 11, and 28 ± 12% of the changes observed in control. In HTN, α1-adrenergic blockade restored the coronary vasodilation and increased in ventricular function to the levels observed when normotensive. We conclude that exaggerated MMA-induced increases in SNA functionally vasoconstrict the coronary vasculature impairing increases in CBF, which limits oxygen delivery and ventricular performance in HTN. NEW & NOTEWORTHY We found that metaboreflex-induced increases in coronary blood flow and ventricular contractility are attenuated in hypertension. α1-Adrenergic blockade restored these parameters toward normal levels. These findings indicate that the primary mechanism mediating impaired metaboreflex-induced increases in ventricular function in hypertension is accentuated coronary vasoconstriction. Listen to this article’s corresponding podcast at http://ajpheart.podbean.com/e/metaboreflex-induced-functional-coronary-vasoconstriction/ .

Distribution of cardiac output during static exercise in the conscious cat

1982 ◽  
Vol 52 (3) ◽  
pp. 642-646 ◽  
Author(s):  
G. Diepstra ◽  
W. Gonyea ◽  
J. H. Mitchell
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Left Kidney ◽  
Isometric Exercise ◽  
Systolic Pressure ◽  
Neural Mechanism ◽  
Left Ventricular ◽  
Static Exercise ◽  
Ventricular Systolic Pressure ◽  
Distribution Of Cardiac Output

Blood flows to major organs were measured in conscious cats to study the changes in the distribution of cardiac output during voluntary static (isometric) exercise. Five animals were operantly conditioned to hold a bar against a fixed resistance for 30 s. Organ flows were measured during rest and exercise by injecting 25-micrometer radioactive microspheres into the left atrium or left ventricle. Increases were observed during exercise in heart rate (18%), mean arterial pressure (25%), left ventricular systolic pressure (17%), and rate of left ventricular development (26%). Static exercise produced significant changes in flow (ml . min-1 .g-1) to the kidneys (-1.09 +/- 0.24), spleen (-0.85 +/- 0.21), and exercising muscles (+0.13 +/- 0.08), while flows to liver, heart, brain, and nonexercising muscle were not significantly changed from control levels. Denervation of the left kidney abolished the decrease in flow to that kidney during exercise. Thus, static exercise appears to produce a significant increase in blood flow to exercising muscles and significant reductions in blood flow to spleen and kidneys. The reduction in renal blood flow is mediated by a neural mechanism.

Myocardial perfusion in compensated and failing hypertrophied left ventricle

1985 ◽  
Vol 249 (3) ◽  
pp. H534-H539 ◽  
Author(s):  
D. G. Parrish ◽  
W. S. Ring ◽  
R. J. Bache
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Systolic Pressure ◽  
Weight Ratio ◽  
Wall Stress ◽  
Left Ventricular ◽  
Ventricular Systolic Pressure ◽  
Ventricular Wall Thickness ◽  
Left Ventricular Systolic Pressure ◽  
Increased Blood Flow

This study examined blood flow in the hypertrophied left ventricle with and without failure. Left ventricular hypertrophy was produced in 20 dogs by banding the ascending aorta at 6-7 wk of age; studies were performed after animals reached adulthood. Sixteen dogs had compensated hypertrophy, while four dogs had cardiac failure manifested by left ventricular dilatation and end-diastolic pressures greater than 18 mmHg. The degree of hypertrophy, assessed by left ventricular-to-body weight ratio, was similar in animals with compensated hypertrophy (7.29 +/- 0.26 g/kg) and failure (8.45 +/- 0.15); both were greater than control (4.50 +/- 0.15, P less than 0.01). Left ventricular systolic pressure was similar in compensated hypertrophy (184 +/- 9 mmHg) and failure (226 +/- 29), as compared with control (130 +/- 4; P less than 0.01). Left ventricular blood flow measured with microspheres was 0.89 +/- 0.07 ml X min-1 X g-1 in control animals, was increased to 1.34 +/- 0.05 with compensated hypertrophy (P less than 0.001), and was further increased with failure to 1.86 +/- 0.40 (P less than 0.05). The left ventricular wall thickness-to-cavity diameter ratio was increased to 0.63 +/- 0.04 with compensated hypertrophy but was only 0.40 +/- 0.05 in dogs with failure (P less than 0.01), suggesting that wall stress was greater in hearts with failure. These data suggest that increased blood flow rates in dogs with failure resulted from increased myocardial O2 requirements due to increased systolic wall stress. Need for increased blood flow during resting conditions in dogs with failure would impair the ability for further coronary vasodilation during periods of cardiac stress.

Effect of NO on transmural distribution of blood flow in hypertrophied left ventricle during exercise

1999 ◽  
Vol 276 (4) ◽  
pp. H1305-H1312 ◽  
Author(s):  
Dirk J. Duncker ◽  
Jay H. Traverse ◽  
Yutaka Ishibashi ◽  
Robert J. Bache
Keyword(s):  
Blood Flow ◽  
Myocardial Blood Flow ◽  
Ventricular Hypertrophy ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Aortic Banding ◽  
No Donor ◽  
Subendocardial Ischemia ◽  
Intracoronary Infusion ◽  
Control Exercise

When exercise in the presence of a coronary artery stenosis results in subendocardial ischemia, administration of a nitric oxide (NO) donor increases subendocardial blood flow, whereas NO synthesis blockade worsens subendocardial hypoperfusion. Because left ventricular hypertrophy (LVH) is also associated with subendocardial hypoperfusion during exercise, this study tested the hypothesis that alterations of NO availability can similarly influence subendocardial blood flow in the hypertrophied heart. Studies were performed in seven dogs in which ascending aortic banding resulted in an 80% increase in LV weight. Myocardial blood flow was measured with microspheres during treadmill exercise that increased heart rates to 216 ± 8 beats/min. During control exercise, mean myocardial blood flow in animals with LVH was similar to that in historic controls, but the ratio of subendocardial to subepicardial blood flow was lower in animals with hypertrophy (0.88 ± 0.07) than in controls (1.36 ± 0.08; P < 0.05). Blockade of NO synthesis with N G-nitro-l-arginine (l-NNA; 1.5 mg/kg ic) caused no change in heart rate or LV systolic pressure during exercise. Furthermore, l-NNA did not worsen subendocardial hypoperfusion during exercise. Intracoronary infusion of nitroglycerin (0.4 μg ⋅ kg−1 ⋅ min−1) did not significantly alter either mean blood flow or the transmural distribution of perfusion during exercise in the hypertrophied hearts. Thus, unlike the subendocardial underperfusion that occurs when a stenosis limits coronary blood flow, alterations of NO availability did not alter subendocardial hypoperfusion in the hypertrophied hearts.

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