scholarly journals Cardiodepressant Activity of 90% Alcoholic Extract of Terminalia Arjuna and its Probable Mechanism of Action

Author(s):  
B. Jassal ◽  
B. Kumar ◽  
V. Bajaj ◽  
R. Walia

<strong>Background:</strong>Terminalia arjuna is being used in various cardiovascular diseases as cardiotonic, diuretic&amp;in hypercholesterolemia. Studies conflict each other for its mechanism of action. This study aims to investigate effect of 90% alcoholic extract of Terminalia arjuna on in vitro isolated rabbit's heart&amp;to find its probable mechanism of action.<p><strong>Objective:</strong> To study the preliminary pharmacological effects of 90% alcoholic extract of Terminalia arjuna in-vitro on isolated heart, coronary blood flow, and to study its probable mechanism of action.</p><p><strong>Material&amp;Methods:</strong> Effect of Terminalia arjuna was observed on heart rate, coronary blood flow, amplitude on in vitro isolated perfused rabbit's heart mounted on langendorff apparatus&amp;further cholinergic&amp;adrenergic blockers were used to study the mechanism of action. Six experiments were conducted for each parameter&amp;data was analysed using Student's t test.</p><p><strong>Results:</strong> Terminalia arjuna causes mean percentage decrease of 7.26%, 9.31%&amp;20.51% in heart rate, decrease of 10.34%, 16.64%, 20.51% in coronary blood flow&amp;decrease of 15.11%, 12.61%, 11.65% in amplitude at 25μg, 50μg&amp;100μg doses respectively. The decrease in heart rate, coronary blood flow&amp;amplitude persists even after cholinergic&amp;adrenergic blockers suggesting that cholinergic&amp;adrenergic receptors are not involved in mechanism of Terminalia arjuna.</p><p><strong>Conclusion:</strong> Terminalia arjuna cardiodepressant effect does not involve cholinergic&amp;adrenergic receptors.</p>

2021 ◽  
Vol 10 (22) ◽  
pp. 5333
Author(s):  
Philippe Reymond ◽  
Karim Bendjelid ◽  
Raphaël Giraud ◽  
Gérald Richard ◽  
Nicolas Murith ◽  
...  

ECMO is the most frequently used mechanical support for patients suffering from low cardiac output syndrome. Combining IABP with ECMO is believed to increase coronary artery blood flow, decrease high afterload, and restore systemic pulsatile flow conditions. This study evaluates that combined effect on coronary artery flow during various load conditions using an in vitro circuit. In doing so, different clinical scenarios were simulated, such as normal cardiac output and moderate-to-severe heart failure. In the heart failure scenarios, we used peripheral ECMO support to compensate for the lowered cardiac output value and reach a default normal value. The increase in coronary blood flow using the combined IABP-ECMO setup was more noticeable in low heart rate conditions. At baseline, intermediate and severe LV failure levels, adding IABP increased coronary mean flow by 16%, 7.5%, and 3.4% (HR 60 bpm) and by 6%, 4.5%, and 2.5% (HR 100 bpm) respectively. Based on our in vitro study results, combining ECMO and IABP in a heart failure setup further improves coronary blood flow. This effect was more pronounced at a lower heart rate and decreased with heart failure, which might positively impact recovery from cardiac failure.


1982 ◽  
Vol 242 (5) ◽  
pp. H805-H809 ◽  
Author(s):  
G. R. Heyndrickx ◽  
P. Muylaert ◽  
J. L. Pannier

alpha-Adrenergic control of the oxygen delivery to the myocardium during exercise was investigated in eight conscious dogs instrumented for chronic measurements of coronary blood flow, left ventricular (LV) pressure, aortic blood pressure, and heart rate and sampling of arterial and coronary sinus blood. After alpha-adrenergic receptor blockade a standard exercise load elicited a significantly greater increase in heart rate, rate of change of LV pressure (LV dP/dt), LV dP/dt/P, and coronary blood flow than was elicited in the unblocked state. In contrast to the response pattern during control exercise, there was no significant change in coronary sinus oxygen tension (PO2), myocardial arteriovenous oxygen difference, and myocardial oxygen delivery-to-oxygen consumption ratio. It is concluded that the normal relationship between myocardial oxygen supply and oxygen demand is modified during exercise after alpha-adrenergic blockade, whereby oxygen delivery is better matched to oxygen consumption. These results indicate that the increase in coronary blood flow and oxygen delivery to the myocardium during normal exercise is limited by alpha-adrenergic vasoconstriction.


Mathematics ◽  
2020 ◽  
Vol 8 (8) ◽  
pp. 1205
Author(s):  
Timur Gamilov ◽  
Philipp Kopylov ◽  
Maria Serova ◽  
Roman Syunyaev ◽  
Andrey Pikunov ◽  
...  

In this work we present a one-dimensional (1D) mathematical model of the coronary circulation and use it to study the effects of arrhythmias on coronary blood flow (CBF). Hydrodynamical models are rarely used to study arrhythmias’ effects on CBF. Our model accounts for action potential duration, which updates the length of systole depending on the heart rate. It also includes dependency of stroke volume on heart rate, which is based on clinical data. We apply the new methodology to the computational evaluation of CBF during interventricular asynchrony due to cardiac pacing and some types of arrhythmias including tachycardia, bradycardia, long QT syndrome and premature ventricular contraction (bigeminy, trigeminy, quadrigeminy). We find that CBF can be significantly affected by arrhythmias. CBF at rest (60 bpm) is 26% lower in LCA and 22% lower in RCA for long QT syndrome. During bigeminy, trigeminy and quadrigeminy, respectively, CBF decreases by 28%, 19% and 14% with respect to a healthy case.


1980 ◽  
Vol 49 (1) ◽  
pp. 28-33 ◽  
Author(s):  
G. R. Heyndrickx ◽  
J. L. Pannier ◽  
P. Muylaert ◽  
C. Mabilde ◽  
I. Leusen

The effects of beta-adrenergic blockade upon myocardial blood flow and oxygen balance during exercise were evaluated in eight conscious dogs, instrumented for chronic measurements of coronary blood flow, left ventricular pressure, aortic blood pressure, heart rate, and sampling of arterial and coronary sinus venous blood. The administration of propranolol (1.5 mg/kg iv) produced a decrease in heart rate, peak left ventricular (LV) dP/dt, LV (dP/dt/P, and an increase in LV end-diastolic pressure during exercise. Mean coronary blood flow and myocardial oxygen consumption were lower after propranolol than at the same exercise intensity in control conditions. The oxygen delivery-to-oxygen consumption ratio and the coronary sinus oxygen content were also significantly lower. It is concluded that the relationship between myocardial oxygen supply and demand is modified during exercise after propranolol, so that a given level of myocardial oxygen consumption is achieved with a proportionally lower myocardial blood flow and a higher oxygen extraction.


2003 ◽  
Vol 95 (1) ◽  
pp. 81-88 ◽  
Author(s):  
Antonio Rodríguez-Sinovas ◽  
Josep Bis ◽  
Inocencio Anivarro ◽  
Javier de la Torre ◽  
Antoni Bayés-Genís ◽  
...  

This study tested whether ischemia-reperfusion alters coronary smooth muscle reactivity to vasoconstrictor stimuli such as those elicited by an adventitial stimulation with methacholine. In vitro studies were performed to assess the reactivity of endothelium-denuded infarct-related coronary arteries to methacholine ( n = 18). In addition, the vasoconstrictor effects of adventitial application of methacholine to left anterior descending (LAD) coronary artery was assessed in vivo in pigs submitted to 2 h of LAD occlusion followed by reperfusion ( n = 12), LAD deendothelization ( n = 11), or a sham operation ( n = 6). Endothelial-dependent vasodilator capacity of infarct-related LAD was assessed by intracoronary injection of bradykinin ( n = 13). In vitro, smooth muscle reactivity to methacholine was unaffected by ischemia-reperfusion. In vivo, baseline methacholine administration induced a transient and reversible drop in coronary blood flow (9.6 ± 4.6 to 1.9 ± 2.6 ml/min, P < 0.01), accompanied by severe left ventricular dysfunction. After ischemia-reperfusion, methacholine induced a prolonged and severe coronary blood flow drop (9.7 ± 7.0 to 3.4 ± 3.9 ml/min), with a significant delay in recovery ( P < 0.001). Endothelial denudation mimics in part the effects of methacholine after ischemia-reperfusion, and intracoronary bradykinin confirmed the existence of endothelial dysfunction. Infarct-related epicardial coronary artery shows a delayed recovery after vasoconstrictor stimuli, because of appropriate smooth muscle reactivity and impairment of endothelial-dependent vasodilator capacity.


1989 ◽  
Vol 257 (3) ◽  
pp. H954-H960
Author(s):  
G. C. Haidet ◽  
T. I. Musch ◽  
D. B. Friedman ◽  
G. A. Ordway

To test the hypothesis that stimulation of adrenergic receptors in the heart is maximal during maximal exercise, and to determine whether generalized stimulation of adrenergic receptors during strenuous exercise produces significant alterations in the normal regional distribution of blood flow that occurs during exercise, we evaluated the cardiovascular effects of the infusion of dobutamine (40 micrograms.kg-1.min-1) in mongrel dogs during treadmill running. During maximal exercise, the dobutamine infusion resulted in a significant (P less than 0.05) increase in heart rate. Exercise capacity, total body O2 consumption (VO2), and maximal arteriovenous O2 difference, however, each were reduced during the infusion of this drug. A concomitant reduction in maximal blood flow to locomotive skeletal muscle occurred. The infusion of dobutamine also resulted in an increase in heart rate at a strenuous level of submaximal exercise. However, unlike during maximal exercise, VO2 was unchanged. Blood flow to locomotive skeletal muscle increased, and there was a concomitant reduction in arteriovenous O2 difference. Blood flow reductions that normally occur in splanchnic circulations during strenuous and during maximal exercise were generally somewhat attenuated during the infusion of this drug. Thus, dobutamine, a sympathomimetic agent, produces significant cardiovascular effects when infused in high doses during exercise. Our results demonstrate that beta-adrenergic receptor reserve exists in the heart during maximal exercise in dogs. In addition, the peripheral responses that occur during the infusion of the drug provide additional evidence that different degrees of adrenergic receptor reserve normally appear to be present within different regional circulations during strenuous and during maximal exercise.


1986 ◽  
Vol 250 (1) ◽  
pp. H76-H81 ◽  
Author(s):  
O. L. Woodman ◽  
J. Amano ◽  
T. H. Hintze ◽  
S. F. Vatner

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)


1981 ◽  
Vol 642 (1) ◽  
pp. 96-105 ◽  
Author(s):  
Efrain Toro-Goyco ◽  
Matilde B. Rodriguez ◽  
Alan M. Preston ◽  
Arthur F. Rosenthal

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