Aortic pressure reduction redistributes transmural blood flow in dog left ventricle

1988 ◽  
Vol 254 (2) ◽  
pp. H361-H368 ◽  
Author(s):  
J. J. Smolich ◽  
P. L. Weissberg ◽  
A. Broughton ◽  
P. I. Korner
Keyword(s):  
Blood Flow ◽  
Diastolic Pressure ◽  
Blood Pressure Reduction ◽  
Wall Stress ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Pressure Reduction ◽  
Flow Ratio ◽  
Flow Reserve ◽  
Aortic Blood Pressure

We studied the effect of graded aortic blood pressure reduction on left ventricular (LV) blood flow in anesthetized, autonomically blocked, open-chest dogs at constant heart rate and mean left atrial pressure. Aortic diastolic pressure (ADP) was lowered from rest (average 116 mmHg) to 90, 75, and 60 mmHg with an arteriovenous fistula. Global and regional LV blood flow was measured with radioactive microspheres. Mean LV blood flow fell stepwise from 145 ml.min-1.100 g-1 at rest to 116 ml.min-1.100 g-1 at ADP of 60 mmHg, whereas the endocardial-to-epicardial flow ratio decreased from 1.20 to 0.84. The transmural redistribution of LV blood flow was not accompanied by increases in LV oxygen extraction, depression of LV contractility, LV dilatation or LV electrical dysfunction and also occurred in the presence of considerable coronary vasodilator flow reserve. Electrical evidence of subendocardial ischemia appeared at ADP of 32 mmHg and an endocardial-to-epicardial flow ratio of 0.41 in a subgroup of animals. We conclude that the redistribution of LV flow during moderate aortic pressure reduction was an appropriate physiological adjustment to uneven transmural alterations in regional LV wall stress and that it preceded a more pronounced redistribution evident with myocardial ischemia.

Parasympathetic control of transmural coronary blood flow in dogs

1985 ◽  
Vol 249 (2) ◽  
pp. H337-H343 ◽  
Author(s):  
J. V. Reid ◽  
B. R. Ito ◽  
A. H. Huang ◽  
C. W. Buffington ◽  
E. O. Feigl
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Vagal Stimulation ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Left Ventricular Wall ◽  
Regional Myocardial Blood Flow ◽  
Ventricular Wall ◽  
Flow Ratio ◽  
Outer Flow

The transmural distribution of coronary blood flow was studied during vagal stimulation in closed-chest, morphine- and alpha-chloralose-anesthetized dogs. The left main coronary artery was cannulated and perfused at constant pressure. Bradycardia during vagal stimulation was prevented by atrioventricular heart block and ventricular pacing. Beta-adrenergic receptors were blocked with propranolol (1 mg/kg iv), and aortic pressure was stabilized by means of a pressure reservoir. Regional myocardial blood flow was measured with 9-micron radioactive microspheres during vagal stimulation and during intracoronary acetylcholine infusion. Vagal stimulation increased coronary blood flow uniformly across the left ventricular wall. In contrast, intracoronary acetylcholine infusion, at a rate selected to increase total flow to the same degree, vasodilated the subendocardium more than the subepicardium, increasing the inner/outer blood flow ratio. It is concluded that both vagal activation and acetylcholine produce coronary vasodilation that is independent of left ventricular preload, afterload, and heart rate. Acetylcholine vasodilation preferentially vasodilates the subendocardium, increasing the inner/outer flow ratio, but vagal stimulation produces uniform vasodilation across the left ventricular wall.

Interaction of aortic pressure and left ventricular end-diastolic pressure in the dog

1977 ◽  
Vol 232 (6) ◽  
pp. H697-H704
Author(s):  
J. R. Foster ◽  
E. R. Powers ◽  
W. J. Powell
Keyword(s):  
Performance Improvement ◽  
Fiber Length ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Ventricular Performance ◽  
Aortic Blood Pressure ◽  
Mean Aortic Pressure ◽  
Right Heart Bypass

Fiber length (preload) is an important determinant of left ventricular performance. Mean aortic blood pressure also influences ventricular performance. The present study was undertaken to examine the influence of mean aortic pressure on the fiber length-ventricular performance relationship. Fifteen anesthetized, adrenergically blocked dogs were studied on right-heart bypass at constant heart rate and coronary blood flow. An increase in mean aortic pressure permitted a greater improvement in performance as evaluated by stroke work for a given increase in left ventricular end-diastolic pressure. A given increase in mean aortic pressure at a constant stroke volume produced a greater rise in stroke work over intermediate ranges of left ventricular end-diastolic pressure than occurred with higher or lower left ventricular end-diastolic pressure. Thus, the degree of afterload-induced performance improvement depended on the magnitude of the preload. External circumference-left ventricular end-diastolic pressure data suggested a possible relationship between isovolumic systolic circumferential expansion and the improvement of ventricular performance at higher mean aortic pressures.

Energy production, O2 consumption, and blood flow reserve in experimental aortic valve disease

1987 ◽  
Vol 252 (2) ◽  
pp. H243-H251
Author(s):  
S. F. Qian ◽  
J. M. Brum ◽  
A. A. Bove
Keyword(s):  
Blood Flow ◽  
Left Ventricular Mass ◽  
Energy Production ◽  
Left Ventricular ◽  
Total Power ◽  
Stroke Work ◽  
O2 Consumption ◽  
Flow Ratio ◽  
Flow Reserve ◽  
Ventricular Mass

Left ventricular energy production and its relation to myocardial O2 consumption and blood flow reserve were studied in 11 dogs with surgically produced valvular aortic stenosis (AS, 6 of 11) or combined stenosis and insufficiency (AS + AI, 5 of 11), and 7 dogs undergoing sham operation (S). Two months after operation the combined AS + AI group had the highest left ventricular mass (S, 4.85 +/- 0.53; AS, 6.38 +/- 0.90; AS + AI, 7.23 +/- 0.39 g/kg), left ventricular end-diastolic pressure (S, 2.1 +/- 1.6; AS, 6.3 +/- 1.7; AS + AI, 8.6 +/- 3.1 mmHg), left ventricular end-diastolic volume (S, 61.1 +/- 8.5; AS, 73.0 +/- 7.8; AS + AI, 95.8 +/- 20.9 ml), and stroke work. At rest, total left ventricular myocardial blood flow was increased in AS and AS + AI compared with sham (S, 89 +/- 8; AS, 135 +/- 19; AS + AI, 164 +/- 9 ml/min, P less than 0.05); and coronary resistance was lower in both AS and AS + AI groups. Peak-to-resting flow ratio determined by adenosine vasodilation was reduced in AS and AS + AI despite normal resting function (peak-to-resting flow ratio: S, 6.78 +/- 2.24; AS, 3.19 +/- 0.58, AS + AI, 3.99 +/- 0.84, P less than 0.02). Peak-to-resting flow ratio was inversely proportional to left ventricular mass. In turn the degree of hypertrophy correlated with the total power requirement of the left ventricle, regardless of the type of overload lesion.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of treadmill exercise on transmural distribution of blood flow in hypertrophied left ventricle

1998 ◽  
Vol 275 (4) ◽  
pp. H1274-H1282 ◽  
Author(s):  
Dirk J. Duncker ◽  
Yutaka Ishibashi ◽  
Robert J. Bache
Keyword(s):  
Blood Flow ◽  
Treadmill Exercise ◽  
Diastolic Pressure ◽  
Coronary Vessels ◽  
Weight Ratio ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Flow Ratio ◽  
Coronary Pressure ◽  
Blood Flow Ratio

Pressure-overload left ventricular (LV) hypertrophy (LVH) is associated with increased vulnerability to subendocardial hypoperfusion during exercise. Abnormal perfusion could be the result of failure of the coronary vessels to grow in proportion to the degree of myocyte hypertrophy or could be due to increased extravascular forces acting on the intramural coronary vasculature. This study assessed the contribution of extravascular forces by examining the effect of exercise on the distribution of myocardial blood flow when coronary vasomotor tone was abolished with a maximal vasodilating dose of intracoronary adenosine. One year after ascending aortic banding in six dogs, the LV-to-body weight ratio was 7.80 ± 0.38 g/kg compared with 4.57 ± 0.20 g/kg in nine normal dogs ( P < 0.01). Under awake resting conditions blood flow in LVH hearts increased from 1.17 ± 0.27 ml ⋅ min−1 ⋅ g−1during basal conditions to 5.78 ± 1.06 ml ⋅ min−1 ⋅ g−1during adenosine (at a coronary pressure of 100 ± 6 mmHg), whereas in normal dogs blood flow increased from 1.22 ± 0.17 to 5.26 ± 0.71 ml ⋅ min−1 ⋅ g−1(at a coronary pressure of 62 ± 4 mmHg). At rest the transmural distribution of blood flow during adenosine was not different between hypertrophied and normal hearts, with subendocardial-to-subepicardial (Endo-to-Epi) blood flow ratios of 1.01 ± 0.09 and 1.14 ± 0.13, respectively ( P = not significant). During adenosine infusion, treadmill exercise to produce heart rates of 200–220 beats/min caused redistribution of blood flow away from the subendocardium that was much more marked in LVH (Endo-to-Epi blood flow ratio = 0.35 ± 0.04) than in normal hearts (Endo-to-Epi blood flow ratio = 0.76 ± 0.09, P < 0.05 vs. LVH). In comparison with normal, the exaggerated decrease in subendocardial blood flow produced by exercise in LVH hearts resulted from abnormally increased extravascular compressive forces, including a greater decrease in diastolic duration and an increase in LV end-diastolic pressure.

scholarly journals Left ventricular blood flow during aortic pressure reduction in hypertensive dogs.

Hypertension ◽  
1991 ◽  
Vol 18 (5) ◽  
pp. 665-673 ◽  
Author(s):  
J J Smolich ◽  
P L Weissberg ◽  
P Friberg ◽  
A Broughton ◽  
P I Korner
Keyword(s):  
Blood Flow ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Pressure Reduction

Myocardial responses to alpha-adrenoceptor stimulation with methoxamine hydrochloride in lambs

1982 ◽  
Vol 242 (3) ◽  
pp. H405-H410 ◽  
Author(s):  
J. C. Lee ◽  
R. R. Fripp ◽  
S. E. Downing
Keyword(s):  
Blood Flow ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Aortic Pressure ◽  
Atropine Sulfate ◽  
Left Ventricular ◽  
Inotropic Action ◽  
Ventricular Performance ◽  
Positive Inotropic Action ◽  
Alpha Adrenergic Receptors

This study was undertaken to evaluate the effects of methoxamine on left ventricular performance, coronary blood flow (CBF), and myocardial oxygen consumption (MVO2) in lambs. Measurement of maximum rate of rise of left ventricular pressure (LV dP/dtmax), left ventricular end-diastolic pressure (LVEDP), CBF, and MVO2 were made in nine lambs using a hemodynamically controlled preparation. The lambs were given atropine sulfate (1 mg), tetraethylammonium chloride (100 mg), and practolol (4 mg/kg) to provide parasympathetic, ganglionic, and beta-adrenergic blockades. Aortic pressure and blood flow and heart rate were held constant in each lamb. Dose-related increases in LV dP/dtmax and decreases in LVEDP were observed after progressively larger doses of methoxamine ranging from 0.4 to 6.0 mg/kg were given. These positive inotropic responses were eliminated by giving phentolamine (2 mg/kg). CBF, myocardial O2 extraction, and MVO2 did not change significantly. A positive inotropic action of methoxamine was also demonstrated in five additional animals by obtaining ventricular function curves. Initially the mean stroke volume at LVEDP 10 cmH2O (SV10) was 4.11 +/- 0.16 (SE) ml. This value increased to 5.09 +/- 0.28 ml after methoxamine (P less than 0.01). After phentolamine, SV 10 fell to 4.37 +/- 0.08 ml (P less than 0.05). These observations support the hypothesis that alpha-adrenergic receptors are present and mediate a substantial positive inotropic action on neonatal lamb myocardium.

Similarities in coronary flow between external counterpulsation and intra-aortic balloon pumping

1976 ◽  
Vol 230 (6) ◽  
pp. 1616-1621 ◽  
Author(s):  
JT Watson ◽  
MR Platt ◽  
DE Rogers ◽  
WL Sugg ◽  
JT Willerson
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Ischemic Myocardium ◽  
Atrial Pacing ◽  
External Counterpulsation ◽  
Pressure Peak

The ability of external counterpulsation (Cardiassist) and intra-aortic balloon pumping (AVCO) to influence collateral coronary blood flow in ischemic myocardium was measured in anesthetized dogs. Cardiac output and heart rate (atrial pacing) were held constant on right-heart bypass. Both external counterpulsation and balloon pumping augmented peak diastolic pressure (30 mmHg and 38 mmHg, respectively), while mean aortic pressure, peak left-ventricular pressure, left-ventricular end-diastolic pressure, maximum left-ventricular dp/dt, hematocrit, and osmolality remained unchanged. Regional coronary blood flow was measured using 9-mum radioactive microspheres. External counterpulsation and balloon pumping begun immediately following ligation of the left-anterior descending coronary artery significantly increased collateral coronary blood flow 29 +/- 7.5% (SE, P is less than .01) and 20 +/- 8% (P is less than .05), respectively, to ischemic myocardium. This redistribution of collateral coronary blood flow produced by both methods of counterpulsation was primarily to the subepicardial region of the ischemic myocardium. The mechanism responsible for the measured increases in collateral coronary blood flow appears most likely to be an increased pressure gradient produced by diastolic augmentation.

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.

Sign in / Sign up

Export Citation Format

Share Document