scholarly journals 830 Coronary blood flow, longitudinal function of left ventricle and cytokines' levels in hypertrophic patients

2006 ◽  
Vol 7 ◽  
pp. S132-S132
Author(s):  
E PAVLYUKOVA ◽  
T SUSLOVA ◽  
R KARPOV
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Coronary Blood Flow ◽  
Longitudinal Function

Effect of hypoxemia and hypercapnia on regional distribution of myocardial blood flow

1965 ◽  
Vol 208 (6) ◽  
pp. 1211-1216 ◽  
Author(s):  
William D. Love ◽  
Myra D. Tyler
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Coronary Blood Flow ◽  
Regional Distribution ◽  
Fick Principle ◽  
The Right ◽  
Isotope Content ◽  
Coronary Sinus Blood ◽  
Normal Difference

The effect of hypoxia and hypercapnia on regional coronary blood flow and vascular resistance (CVR) was studied in dogs without thoracotomy. Gas tensions were varied by ventilation at controlled rates with gas mixtures containing 4–100% O2 and 0–24% CO2. After 10 min intravenous infusion of Rb86, the animals were killed and the heart isotope content determined. Blood flow to the left ventricle was calculated by the Fick principle from the isotope uptake and the mean difference in radioactivity of arterial and coronary sinus blood. Patterns of flow elsewhere were estimated from the rates of regional Rb86 clearance. Myocardial Rb86 clearance in the right and left ventricles has been previously shown to be closely related to the rate of coronary blood flow. Hypoxemia and severe hypercapnia (pCO2 above 100 mm Hg) both produced a profound fall in CVR. With hypoxemia this decrease was more marked in the right ventricle. Elevation of pCO2 exaggerated the normal difference in Rb86 uptake between inner and outer thirds of the wall of the left ventricle, while hypoxemia reversed the normal gradients. Hypercapnia did not affect these gradients in the right ventricle, but hypoxemia significantly reduced them.

Role of K ATP + channels and adenosine in regulation of coronary blood flow in the hypertrophied left ventricle

1999 ◽  
Vol 277 (2) ◽  
pp. H617-H625 ◽  
Author(s):  
Peter J. Melchert ◽  
Dirk J. Duncker ◽  
Jay H. Traverse ◽  
Robert J. Bache
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Coronary Blood Flow ◽  
Coronary Flow ◽  
Rate Pressure Product ◽  
Receptor Blockade ◽  
Channel Activity ◽  
Channel Blockade ◽  
Coronary Vasodilation ◽  
Exercise Induced

In the hypertrophied heart, increased extravascular forces acting to compress the intramural coronary vessels might require augmentation of metabolic vasodilator mechanisms to maintain adequate coronary blood flow. Vascular smooth muscle ATP-sensitive potassium ([Formula: see text]) channel activity is important in metabolic coronary vasodilation, and adenosine contributes to resistance vessel dilation in the hypoperfused heart. Consequently, this study was performed to determine whether[Formula: see text] channels and adenosine have increased importance in exercise-induced coronary vasodilation in the hypertrophied left ventricle. Studies were performed in dogs in which banding of the ascending aorta had resulted in a 66% increase in left ventricular mass in comparison with historic normal animals. Treadmill exercise resulted in increases of coronary blood flow that were linearly related to the increase of heart rate or rate-pressure product. During resting conditions, [Formula: see text]channel blockade with glibenclamide caused a 17 ± 5% decrease in coronary blood flow, similar to that previously observed in normal hearts. Unlike normal hearts, however, glibenclamide blunted the increase in coronary flow that occurred during exercise, causing a significant decrease in the slope of the relationship between coronary flow and the rate-pressure product. Adenosine receptor blockade with 8-phenyltheophylline did not alter coronary blood flow at rest or during exercise. Furthermore, even after[Formula: see text] channel blockade with glibenclamide, the addition of 8-phenyltheophylline had no effect on coronary blood flow. This finding was different from normal hearts, in which the addition of adenosine receptor blockade after glibenclamide impaired exercise-induced coronary vasodilation. The data suggest that, in comparison with normal hearts, hypertrophied hearts have increased reliance on opening of [Formula: see text] channels to augment coronary flow during exercise. Contrary to the initial hypothesis, however, adenosine was not mandatory for exercise-induced coronary vasodilation in the hypertrophied hearts either during control conditions or when [Formula: see text] channel activity was blocked with glibenclamide.

The Effect of Cardiomyoplasty on Coronary Blood Flow and Diastolic Dimension of the Left Ventricle

1998 ◽  
pp. 243-247
Author(s):  
M. Okada ◽  
Y. Toyoda ◽  
T. Mukai ◽  
M. A. Kashem ◽  
T. Tsukube
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Coronary Blood Flow

Alterations of coronary blood flow and reserve with aging in Fischer 344 rats

1989 ◽  
Vol 256 (1) ◽  
pp. H66-H73 ◽  
Author(s):  
R. Hachamovitch ◽  
P. Wicker ◽  
J. M. Capasso ◽  
P. Anversa
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Coronary Blood Flow ◽  
Vascular Resistance ◽  
Pressure Overload ◽  
Fischer 344 Rats ◽  
Time Intervals ◽  
Vascular Reserve ◽  
Fischer 344 ◽  
The Right

To determine whether aging affects the coronary circulation, left and right ventricular coronary blood flow and vascular resistance at rest and after maximal vasodilation were measured by left atrial injection of radioactive microspheres in conscious, unrestrained male Fischer 344 rats at 4, 12, and 20 mo of age. As a function of age, maximal coronary blood flow per 100 g of tissue decreased by 43% in the left ventricle at both 12 and 20 mo, whereas a 44 and a 47% reduction was found in the right side of the heart at the same time intervals. Minimal coronary vascular resistance per 100 g of myocardium increased by 56 and 36% in the left ventricle and by 48 and 44% in the right at 12 and 20 mo, respectively. No change was found in total minimal coronary resistance for either ventricle despite an increase in myocardial mass. Maximal coronary blood flow per 100 g to the endocardium was depressed more than epicardial flow, leading to a 24% reduction in the endocardial-to-epicardial flow ratio at 20 mo. Coronary vascular reserve per 100 g, expressed as the increase in coronary blood flow during maximal coronary vasodilation, was greater in the right than in the left ventricle at all ages. It is concluded that the changes in coronary hemodynamics associated with maturation and aging are comparable with those seen in pressure overload hypertrophy with an increased vulnerability potential of the myocardium to ischemic episodes, particularly of the subendocardial region of the left ventricle.

Quantitative study of intramyocardial compression in the fibrillating heart

1979 ◽  
Vol 237 (2) ◽  
pp. H191-H196 ◽  
Author(s):  
J. M. Downey ◽  
R. W. Chagrasulis ◽  
V. Hemphill
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Coronary Blood Flow ◽  
Quantitative Study ◽  
Coronary Arteries ◽  
Venous Pressure ◽  
Beating Heart ◽  
Flow Curves ◽  
Pressure Flow ◽  
Zero Flow

Extravascular compression inhibits coronary blood flow in fibrillating hearts. Pressure-flow curves from spontaneously fibrillating hearts whose coronary arteries were maximally dilated were examined to see whether this inhibition involves a vascular waterfall mechanism as has been found in the beating heart. Waterfall behavior is indicated when pressure-flow curves are linear and experience a zero-flow intercept at pressures greater than venous pressure. Regional pressure-flow curves revealed a zero flow intercept of 28.4 mmHg for the inner quarter of the left ventricle, indicating that compression is quite high in that region. A zero-pressure intercept of only 15.1 was found at the outer quarter, which was not significantly different from venous pressure. We conclude that the spontaneously fibrillating heart experiences a gradient of compression falling from 28 mmHg at the subendocardium to near zero at the subepicardium.

Adrenergic vasoconstriction limits coronary blood flow during exercise in hypertrophied left ventricle

1991 ◽  
Vol 260 (5) ◽  
pp. H1489-H1494 ◽  
Author(s):  
R. J. Bache ◽  
D. C. Homans ◽  
X. Z. Dai
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Ventricular Hypertrophy ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Additional Contribution ◽  
Adrenergic Blockade ◽  
Myocardial O2 Consumption

This study was carried out to test the hypothesis that alpha-adrenergic vasoconstriction limits coronary blood flow (CBF) during exercise in the chronically pressure overloaded, hypertrophied left ventricle. Studies were performed in dogs in which left ventricular hypertrophy had been produced by banding the ascending aorta at 9 wk of age. Left circumflex coronary artery blood flow and myocardial O2 consumption (MVO2) were examined at rest and during treadmill exercise during control conditions, after selective alpha 1-adrenergic blockade with prazosin, and after nonselective alpha-adrenergic blockade with phentolamine. All studies were performed after beta-adrenergic blockade with propranolol. During control conditions CBF and MVO2 increased progressively during exercise, while coronary sinus O2 tension decreased. Neither prazosin nor phentolamine altered CBF at rest but, in comparison with control measurements, both agents significantly increased CBF during exercise and abolished the decrease in coronary sinus O2 tension that normally occurred during exercise. Both prazosin and phentolamine caused similar significant increases of MVO2 relative to the heart rate times systolic left ventricular pressure during exercise, indicating that the increased CBF produced by these agents enhanced MVO2. Similar findings after prazosin and phentolamine indicate that adrenergic restraint of CBF during exercise resulted principally from alpha 1-adrenergic vasoconstrictions with little additional contribution from postjunctional alpha 2-adrenergic mechanisms.

Effect of supranormal coronary blood flow on energy metabolism and systolic function of porcine left ventricle

1992 ◽  
Vol 26 (10) ◽  
pp. 1001-1006 ◽  
Author(s):  
G. G Schwartz ◽  
S. Schaefer ◽  
S. D Trocha ◽  
J. Garcia ◽  
S. Steinman ◽  
...  
Keyword(s):  
Blood Flow ◽  
Energy Metabolism ◽  
Left Ventricle ◽  
Coronary Blood Flow ◽  
Systolic Function

Coronary flow by left atrial and left ventricular microsphere injection in the rat

1990 ◽  
Vol 259 (2) ◽  
pp. H635-H638
Author(s):  
G. D. Schrock ◽  
R. L. Krahmer ◽  
J. L. Ferguson
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Left Atrium ◽  
Coronary Blood Flow ◽  
Left Atrial ◽  
Blood Gases ◽  
Left Ventricular ◽  
Systemic Blood ◽  
Systemic Blood Flow ◽  
Blood Flows

Previous studies have reported significantly higher variability in coronary blood flow (CBF) measurements obtained by microsphere injection into the left ventricle (LV) as compared with microsphere injection into the left atrium (LA) of the rat. Questions have arisen concerning whether or not some of the variability may have been due to successive rather than simultaneous injections at the two sites, thereby giving measurements at different cardiovascular states. To address this question, we measured cardiac output (CO) and CBF as well as other systemic organ blood flows by employing simultaneous injection of two different sets of radiolabeled microspheres into the left atrium and left ventricle of semiconscious rats. Using this technique, CBF values (ml.min-1.g-1) of 5.45 +/- 0.43 and 5.24 +/- 0.46 for LA and LV injection sites, respectively, were measured (all values reported as means +/- SE). CO values (ml/min) of 67.5 +/- 3.5 for LA and 67.6 +/- 3.4 for LV were obtained. Paired left atrial and left ventricular measurements of CBF, CO, and other systemic organ blood flows using tracer microsphere methodology were not significantly different. All variabilities in these measurements by LA and LV injection were not significantly different. Our procedure did not significantly alter physiological parameters such as heart rate, mean arterial pressure, hematocrit, or blood gases. These findings indicate that, in our rat model, measurements made by LV microsphere injection are not only adequate for determining systemic blood flow at distal beds but provide coronary blood flow data with variability not significantly different from that of left atrial injection.

Effects of Digitalis and Hypoxia on Potassium Transfer and Distribution in the Dog Heart

1956 ◽  
Vol 184 (3) ◽  
pp. 548-552 ◽  
Author(s):  
Hadley L. Conn
Keyword(s):  
Blood Flow ◽  
Exchange Rate ◽  
Steady State ◽  
Left Ventricle ◽  
Coronary Blood Flow ◽  
Rate Constants ◽  
Myocardial Cell ◽  
Transfer Rates ◽  
Moderate Reduction ◽  
Potassium Exchange

The effects of moderately severe hypoxia and moderately large doses of digitalis on potassium kinetics and distribution in the left ventricle of the normal intact dog were studied after the apparent establishment of a new steady state. Digitalis and hypoxia, more so, caused reduction in interstitial-intracellular potassium transfer rates and rate constants, and modest to moderate reduction in cell and interstitial potassium. Hypoxia also caused marked increase in plasma-interstitial potassium exchange rate and rate constants apparently due to the increased coronary blood flow resulting from hypoxia. The effects of digitalis on ISF-ICF transfer are compatible with the thesis that a major action of digitalis is the partial inhibition of of potassium transfer into the myocardial cell. The results from the steady state hypoxia experiments show that aerobic metabolism is necessary for at least a considerable fraction of potassium transfer in the heart.

Effects of cardiac sympathetic nerve stimulation on regional coronary blood flow

1987 ◽  
Vol 252 (2) ◽  
pp. H269-H274
Author(s):  
C. W. Haws ◽  
L. S. Green ◽  
M. J. Burgess ◽  
J. A. Abildskov
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Coronary Blood Flow ◽  
Nerve Stimulation ◽  
Sympathetic Nerve ◽  
Beta Blockade ◽  
Cardiac Sympathetic Nerve ◽  
Sympathetic Nerve Stimulation ◽  
Cardiac Nerve

The purpose of this study was to examine the effects of cardiac sympathetic nerve stimulation on regional coronary blood flow following beta-blockade. In 17 anesthetized dogs treated with propranolol (2 mg/kg iv) regional myocardial perfusion was measured (microspheres) during control and during stimulation of the ventrolateral, ventromedial, or recurrent cardiac nerve (8–10 V, 4-ms pulses at 10 Hz for 30 s). Ventrolateral nerve stimulation produced 25.5 +/- 3.4 and 23.5 +/- 3.1% (mean +/- SE) decreases in coronary blood flow in the posterior and lateral quadrants of the left ventricle. These changes were significantly greater than the 8.5 +/- 2.9, 11.5 +/- 3.0, and 3.7 +/- 2.8% decreases in the anterior and septal left ventricle and right ventricle, respectively (P less than 0.01). Ventromedial nerve stimulation produced 18.6 +/- 2.8, 15.4 +/- 2.8, and 10.1 +/- 3.2% decreases in flow in the anterior, septal, and lateral left ventricle, respectively. These changes were significantly greater than the 5.3 +/- 3.8 and 9.9 +/- 3.6% decrease in the posterior left ventricle and right ventricle (P less than 0.01). Recurrent cardiac nerve stimulation produced 16.4 +/- 2.1, 15.6 +/- 2.2, and 13.6 +/- 2.5% decreases in flow in the anterior and septal left ventricle and right ventricle, respectively. These changes were significantly greater than the 5.2 +/- 3.2 and 5.4 +/- 3.0% changes in the posterior and lateral quadrants (P less than 0.01). Ventrolateral nerve stimulation resulted in a small but significant increase in the endocardial-to-epicardial blood flow ratio in the posterolateral left ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)

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