Effects of Coronary Blood Flow and Perfusion Pressure on Left Ventricular Contractility in Dogs

Effects of ventricular compression on maximally dilated left circumflex coronary blood flow were investigated in seven mongrel dogs under pentobarbital anesthesia. The left circumflex artery was perfused with the animals' own blood at a constant pressure (63 mmHg) while left ventricular pressure was experimentally altered. Adenosine was infused to produce maximal vasodilation, verified by the hyperemic response to coronary occlusion. Alterations of peak left ventricular pressure from 50 to 250 mmHg resulted in a linear decrease in total circumflex flow of 1.10 ml.min-1 x 100 g heart wt-1 for each 10 mmHg of peak ventricular to coronary perfusion pressure gradient; a 2.6% decrease from control levels. Similar slopes were obtained for systolic and diastolic flows as for total mean flow, implying equal compressive forces in systole as in diastole. Increases in left ventricular end-diastolic pressure accounted for 29% of the flow changes associated with an increase in peak ventricular pressure. Doubling circumferential wall tension had a minimal effect on total circumflex flow. When the slopes were extrapolated to zero, assuming linearity, a peak left ventricular pressure of 385 mmHg greater than coronary perfusion pressure would be required to reduce coronary flow to zero. The experiments were repeated in five additional animals but at different perfusion pressures from 40 to 160 mmHg. Higher perfusion pressures gave similar results but with even less effect of ventricular pressure on coronary flow or coronary conductance. These results argue for an active storage site for systolic arterial flow in the dilated coronary system.

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Flow manipulation and the association with myocardial contractility during extracorporeal life support (FLAME)

European Heart Journal Acute Cardiovascular Care ◽

10.1093/ehjacc/zuab020.030 ◽

2021 ◽

Vol 10 (Supplement_1) ◽

Author(s):

SKT Ma ◽

WC Sin ◽

CW Ngai ◽

ASK Wong ◽

WM Chan ◽

...

Keyword(s):

Blood Flow ◽

Cardiogenic Shock ◽

Myocardial Contractility ◽

Life Support ◽

Extracorporeal Life Support ◽

Left Ventricular ◽

Left Ventricular Ejection ◽

Ventricular Contractility ◽

Left Ventricular Contractility ◽

Extracorporeal Blood

Abstract Funding Acknowledgements Type of funding sources: None. Background Veno-arterial extracorporeal membrane oxygenation (V-A ECMO) is an advanced technique in extracorporeal life support (ECLS) used to support extreme circulatory failure including patients with cardiac arrest and cardiogenic shock refractory to conventional support. It is a long-standing belief that peripheral V-A ECMO poses increased afterload to the inured heart, but conventional echocardiographic measurements are often insensitive in detecting subtle changes in loading conditions. Purpose This study aimed to evaluate the effects of varying blood flow during peripheral V-A ECMO on intrinsic myocardial contractility, using detailed echocardiographic assessment including speckle tracking echocardiography (STE). Methods Adult patients with acute cardiogenic shock who were supported by peripheral V-A ECMO from April 2019 to September 2020 were recruited. Serial hemodynamic and cardiac performance parameters were measured by transthoracic echocardiogram (TTE) within 48 hours after implementation of V-A ECMO, at different levels of extracorporeal blood flow – 100%, 120% and 50% of target blood flow (TBF). Results A total of 30 patients were included. 22 (71%) were male, and the mean (SD) age was 54 (13) years. The major indications for V-A ECMO were myocardial infarction (19, 63% patients), and myocarditis (5, 17%). With a decrease in extracorporeal blood flow from 100% to 50% of TBF, mean arterial pressure (MAP) dropped from 76+/-3 to 64+/-3mmHg (p <0.001), and cardiac index (CI) increased from 0.89+/-0.13 to 1.27+/-0.18L/min/m2 (p < 0.001). All indices of left ventricular contractility improved at a lower extracorporeal blood flow: the myocardial contractility measured by global longitudinal peak systolic strain (GLPSS) improved from -3+/-0.7% to -5+/-0.8% (p < 0.001); left ventricular ejection fraction (LVEF) increased from 21.5+/-2.6% to 30.9+/-2.7% (p < 0.001) and 19.7+/-3.1% to 28.4+/-3.2% (p < 0.001) by biplane and linear methods, respectively; left ventricular index of myocardial performance (LIMP) improved from 1.51+/-0.12 to 1.03+/-0.09 (p < 0.001). Similar findings were reproduced when comparing left ventricular contractility at extracorporeal blood flows of 120% and 50% of TBF. Conclusions The ECMO blood flow rate in peripheral V-A ECMO is inversely related to myocardial contractility, and is quantifiable by myocardial strain measured by STE.

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Muscle metaboreflex-induced coronary vasoconstriction functionally limits increases in ventricular contractility

Journal of Applied Physiology ◽

10.1152/japplphysiol.01243.2009 ◽

2010 ◽

Vol 109 (2) ◽

pp. 271-278 ◽

Cited By ~ 22

Author(s):

Matthew Coutsos ◽

Javier A. Sala-Mercado ◽

Masashi Ichinose ◽

ZhenHua Li ◽

Elizabeth J. Dawe ◽

...

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Left Ventricular ◽

Ventricular Contractility ◽

Left Ventricular Contractility ◽

Coronary Vasodilation ◽

Cardiac Work ◽

Vascular Conductance ◽

Muscle Metaboreflex ◽

Coronary Vasoconstriction

Muscle metaboreflex activation during dynamic exercise induces a substantial increase in cardiac work and oxygen demand via a significant increase in heart rate, ventricular contractility, and afterload. This increase in cardiac work should cause coronary metabolic vasodilation. However, little if any coronary vasodilation is observed due to concomitant sympathetically induced coronary vasoconstriction. The purpose of the present study is to determine whether the restraint of coronary vasodilation functionally limits increases in left ventricular contractility. Using chronically instrumented, conscious dogs ( n = 9), we measured mean arterial pressure, cardiac output, and circumflex blood flow and calculated coronary vascular conductance, maximal derivative of ventricular pressure (dp/d tmax), and preload recruitable stroke work (PRSW) at rest and during mild exercise (2 mph) before and during activation of the muscle metaboreflex. Experiments were repeated after systemic α1-adrenergic blockade (∼50 μg/kg prazosin). During prazosin administration, we observed significantly greater increases in coronary vascular conductance (0.64 ± 0.06 vs. 0.46 ± 0.03 ml·min−1·mmHg−1; P < 0.05), circumflex blood flow (77.9 ± 6.6 vs. 63.0 ± 4.5 ml/min; P < 0.05), cardiac output (7.38 ± 0.52 vs. 6.02 ± 0.42 l/min; P < 0.05), dP/d tmax (5,449 ± 339 vs. 3,888 ± 243 mmHg/s; P < 0.05), and PRSW (160.1 ± 10.3 vs. 183.8 ± 9.2 erg·103/ml; P < 0.05) with metaboreflex activation vs. those seen in control experiments. We conclude that the sympathetic restraint of coronary vasodilation functionally limits further reflex increases in left ventricular contractility.

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Alpha 1-adrenergic blockade increases coronary blood flow during coronary hypoperfusion

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1985.249.6.h1070 ◽

1985 ◽

Vol 249 (6) ◽

pp. H1070-H1077 ◽

Cited By ~ 1

Author(s):

I. Y. Liang ◽

C. E. Jones

Keyword(s):

Blood Flow ◽

Oxygen Consumption ◽

Coronary Blood Flow ◽

Coronary Flow ◽

Perfusion Pressure ◽

Coronary Perfusion Pressure ◽

Left Ventricular ◽

Coronary Perfusion ◽

Adrenergic Blockade ◽

Adrenergic Antagonist

Coronary hypoperfusion was elicited in alpha-chloralose-anesthetized open-chest dogs by reducing left coronary perfusion pressure to 50 mmHg. Left coronary blood flow, as well as left ventricular oxygen extraction, oxygen consumption, and contractile force were measured. The reduction in perfusion pressure caused significant reductions in coronary flow, oxygen consumption, and peak reactive hyperemic flow. During hypoperfusion in 11 dogs, intracoronary infusion of the specific alpha 1-adrenergic antagonist prazosin (0.1 mg/min) increased coronary flow and oxygen consumption by 22 and 16%, respectively. Peak increases were observed after 6–8 min of prazosin infusion (0.6–0.8 mg prazosin), and both increases were statistically significant (P less than 0.05). In seven additional dogs, beta-adrenergic blockade with propranolol (1.0 mg ic) did not significantly affect the actions of prazosin. In five additional dogs, the specific alpha 2-adrenergic antagonist yohimbine (1.3 mg ic) in the presence of propranolol (1.0 mg ic) did not affect coronary flow or oxygen consumption during coronary hypoperfusion. Those results suggest that an alpha 1- but not an alpha 2-adrenergic constrictor tone was operative in the left coronary circulation under the conditions of these experiments.

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Effects of intracoronary felodipine versus nifedipine on left ventricular contractility and coronary sinus blood flow in stable angina pectoris

The American Journal of Cardiology ◽

10.1016/0002-9149(94)90320-4 ◽

1994 ◽

Vol 74 (7) ◽

pp. 730-732 ◽

Cited By ~ 5

Author(s):

Jacques J. Koolen ◽

Harry B. Van Wezel ◽

Jan Piek ◽

Rob van Liebergen ◽

Astrid Swaan ◽

...

Keyword(s):

Blood Flow ◽

Angina Pectoris ◽

Coronary Sinus ◽

Stable Angina ◽

Left Ventricular ◽

Ventricular Contractility ◽

Left Ventricular Contractility ◽

Stable Angina Pectoris ◽

Coronary Sinus Blood ◽

Coronary Sinus Blood Flow

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

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00417.2016 ◽

2017 ◽

Vol 312 (1) ◽

pp. H68-H79 ◽

Cited By ~ 10

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/ .

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