The importance of the perfusion pressure in the coronary arteries for the contractility and the oxygen consumption of the heart

Arnold, G.; Kosche, F.; Miessner, E.; Neitzert, A; Lochner, W.

doi:10.1007/bf00602910

Cited by 215 publications

(68 citation statements)

References 31 publications

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“…This could be explained by increased coronary micro-vascular filling and thus stretch of the sarcomeres and/or release of positive inotropic factors, leading to increased contractility. [38][39][40] Also the nitroprusside experiments support the theory that coronary vasodilation could improve RV function. We found that nitroprusside, which can be considered a "pure" vasodilator, improved RV contractility in the control hearts and the hypertrophic hearts where the coronary flow was increased.…”

Section: A C C E P T E Dmentioning

confidence: 64%

Inotropic Effects of Prostacyclins on the Right Ventricle Are Abolished in Isolated Rat Hearts With Right-Ventricular Hypertrophy and Failure

Holmboe

Andersen

Johnsen

et al. 2017

Journal of Cardiovascular Pharmacology

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Background:Prostacyclin mimetics are vasodilatory agents used in the treatment of pulmonary arterial hypertension. The direct effects of prostanoids on right ventricular (RV) function are unknown.We aimed to investigate the direct effects of prostacyclin mimetics on RV function in hearts with and without RV hypertrophy and failure. Methods:Wistar rats were subjected to pulmonary trunk banding to induce compensated RV hypertrophy (n=32) or manifest RV failure (n=32). Rats without banding served as healthy controls (n=30).The hearts were excised and perfused in a Langendorff system and subjected to iloprost, treprostinil, epoprostenol or MRE-269 in increasing concentrations. The effect on RV function was evaluated using a balloon-tipped catheter inserted into the RV. Results:In control hearts iloprost, treprostinil and MRE-269, improved RV function. The effect was, however, absent in hearts with RV hypertrophy and failure. Treprostinil and MRE-269 even impaired RV function in hearts with manifest RV failure.Copyright Ó 2016 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited. A C C E P T E D 3 Conclusion:Iloprost, treprostinil and MRE-269 improved RV function in the healthy rat heart. RV hypertrophy abolished the positive inotropic effect and in the failing right ventricle, MRE-269 and treprostinil impaired RV function. This may be related to changes in prostanoid receptor expression and reduced coronary flow reserve in the hypertrophic and failing right ventricle.

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Section: A C C E P T E Dmentioning

confidence: 64%

Inotropic Effects of Prostacyclins on the Right Ventricle Are Abolished in Isolated Rat Hearts With Right-Ventricular Hypertrophy and Failure

Holmboe

Andersen

Johnsen

et al. 2017

Journal of Cardiovascular Pharmacology

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“…Recently, we showed in perfused rat papillary muscle that the Gregg effect, which is accompanied by an increase in muscle diameter (transversal stretch), was initiated by activation of Gd 3ϩ -sensitive SACs (31) -sensitive positive inotropic mechanism is active. The Gregg effect has been suggested to be related to the "garden hose" effect, a better overlap of the actin and myosin filaments of the cardiomyocytes, resulting via the Frank-Starling mechanism in increased force development (5,28). However, the present study shows that the initial perfusion-induced increase in force is related to a Gd 3ϩ -sensitive increase in [Ca 2ϩ ] i via SACs and is not related to an initial higher sensitivity of the myofilaments for calcium.…”

Section: Discussionmentioning

confidence: 99%

Coronary perfusion and muscle lengthening increase cardiac contraction: different stretch-triggered mechanisms

Lamberts

Rijen

Sipkema

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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Westerhof. Coronary perfusion and muscle lengthening increase cardiac contraction: different stretch-triggered mechanisms. Am J Physiol Heart Circ Physiol 283: H1515-H1522, 2002. First published May 23, 2002 10.1152/ajpheart. 00113.2002.-An increase in coronary perfusion, transversal stretch of the myocardium, increases developed force (Fdev) (Gregg effect) through activation of stretch-activated ion channels (SACs). Lengthening of the muscle, longitudinal stretch of the myocardium, causes an immediate increase in Fdev followed by a slow Fdev increase (Anrep effect). In isometrically contracting perfused papillary muscles of Wistar rats, we investigated whether both effects were based on similar stretch-induced mechanisms by measuring Fdev and intracellular Ca 2ϩ concentration ([Ca 2ϩ ]i) after a muscle length increase from 85% to 95% Lmax (length at which maximal isometric force develops) at low and high coronary perfusion before and after inhibition of SACs with gadolinium (10 mol/l Gd 3ϩ ). The increase of F dev and peak [Ca 2ϩ ]i by the Gregg effect was of similar magnitude as the Anrep effect (from 3.5 Ϯ 0.8 to 3.9 Ϯ 1.2 mN/mm 2 and from 3.0 Ϯ 0.7% to 3.8 Ϯ 0.9% normalized [Ca 2ϩ ]i, means Ϯ SE). SAC blockade completely blunted the increase of Fdev and peak [Ca 2ϩ ]i by the Gregg effect; however, it did not affect the Anrep effect. The slow force response, but not the calcium response, was augmented by an increase in coronary perfusion. Therefore, increased coronary perfusion, transversal stretch of the myocardium, and muscle lengthening, longitudinal stretch of the myocardium, increase myocardial contraction in the rat through different stretch-triggered mechanisms. myocardial stretch; papillary muscles; gadolinium; streptomycin; stretch-activated ion channels INCREASED CORONARY PERFUSION induces a slow increase of myocardial contraction, which is known as the Gregg effect (1,7,14,15,17,19,22,39). Recently, we showed in perfused rat papillary muscle that the increase in coronary perfusion, which is accompanied by an increase in muscle diameter, was initiated by activation of Gd 3ϩ -sensitive stretch-activated ion channels (SACs) (31), suggesting that transversal stretch (deformation) of the myocardium is fundamental for the Gregg effect.Increased diastolic filling of the heart results via the Frank-Starling mechanism in an immediate increase in myocardial contraction to elevate cardiac output and eventually match venous return (38). Subsequently, myocardial contraction increases slowly, which is known as the Anrep effect (44). In vitro, this biphasic response to longitudinal stretch of the myocardium was first shown by Parmley and Chuck (34). The first, rapid increase in force is related to an increase of responsiveness of the myofilaments for internal calcium (2). The second, slower force response has been attributed to a slow rise of intracellular Ca 2ϩ concentration ([Ca 2ϩ ] i ) (3). In rat and cat papillary muscles, the Anrep effect was triggered by stretch-sensitive but endothelium-independ...

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“…However, as discussed above, there is no evidence for such a fall and the available studies actually suggest that the size of the transient may increase. A final possibility is that ischaemia leads to the reversal of the so-called 'garden hose effect' whereby increased pressure in the coronary circulation leads to an increase in developed pressure (Arnold, Kosche, Miessner, Neitzert & Lochner, 1968). However, recent work by Kitakaze & Marban (1989) suggest that the 'garden hose effect' may result in large part from an effect of coronary artery pressure on [Ca2+]i in ventricular tissue, and not, as previously assumed (Arnold et al 1968), from an effect on muscle length.…”

Section: Metabolic Changes During Brief Periods Of Ischaemiamentioning

confidence: 96%

“…A final possibility is that ischaemia leads to the reversal of the so-called 'garden hose effect' whereby increased pressure in the coronary circulation leads to an increase in developed pressure (Arnold, Kosche, Miessner, Neitzert & Lochner, 1968). However, recent work by Kitakaze & Marban (1989) suggest that the 'garden hose effect' may result in large part from an effect of coronary artery pressure on [Ca2+]i in ventricular tissue, and not, as previously assumed (Arnold et al 1968), from an effect on muscle length. If this is correct, a significant 'reversed garden hose effect' in early ischaemic contractile failure should manifest itself as a decrease in [Ca21]i, and direct measurements of [Caa2+]i during this period suggest that no such decrease occurs (see above).…”

Section: Metabolic Changes During Brief Periods Of Ischaemiamentioning

confidence: 96%

Metabolic changes during ischaemia and their role in contractile failure in isolated ferret hearts.

Elliott

Smith

Eisner

et al. 1992

The Journal of Physiology

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SUMMARY1. The effects of global ischaemia on phosphorus metabolites, intracellular pH (pHi) and developed pressure were measured in isolated whole ferret hearts using 31P nuclear magnetic resonance (NMR) spectroscopy.2. Brief (10 min) periods of global ischaemia reduced left ventricular developed pressure (LVDP) to undetectable levels. This fall in LVDP was accompanied by a fall in the intracellular concentration of phosphocreatine (PCr) [ATP]i reaches sub-millimolar levels, to a rise in resting pressure (rigor contracture).

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The importance of the perfusion pressure in the coronary arteries for the contractility and the oxygen consumption of the heart

Cited by 215 publications

References 31 publications

Inotropic Effects of Prostacyclins on the Right Ventricle Are Abolished in Isolated Rat Hearts With Right-Ventricular Hypertrophy and Failure

Inotropic Effects of Prostacyclins on the Right Ventricle Are Abolished in Isolated Rat Hearts With Right-Ventricular Hypertrophy and Failure

Coronary perfusion and muscle lengthening increase cardiac contraction: different stretch-triggered mechanisms

Metabolic changes during ischaemia and their role in contractile failure in isolated ferret hearts.

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