Increasing coronary perfusion pressure on diastolic and systolic performance is less pronounced in right ventricle than in left ventricle

Fukui, Akio; Yamaguchi, Seiji; Tamada, Yoshiaki; Mikami, Hiroshi; Shirakabe, Masanori; Baniya, Gajendra; Tomoike, Hitonobu

doi:10.1016/s0008-6363(96)00044-2

Cited by 9 publications

(3 citation statements)

References 28 publications

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“…28 and 30). These data indicate that a "garden hose effect," i.e., a change in muscle length with an increase in perfusion pressure (16,130,322), plays a minor role. This has been confirmed by many experimental studies (8,27,43,104,183,229,262,353) and was well reviewed by Downey et al (109).…”

Section: The Gregg Effectmentioning

confidence: 84%

“…This phenomenon was attributed to an "erectile effect" of the coronary vasculature. Although some investigators could not reproduce this effect (1,398), it is generally agreed that an increase in coronary perfusion shifts the diastolic ventricular pressure-volume relationship upward and leftward, leading to increased ventricular stiffness (89,121,130,131,287,289,304,313,334,431,449). However, there is discussion whether flow is related to shear force or to pressure in the vasculature, or both (212).…”

Section: A Coronary Flow and Cardiac Muscle In Diastolementioning

confidence: 99%

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Cross-Talk Between Cardiac Muscle and Coronary Vasculature

Westerhof¹,

Boer²,

Lamberts³

et al. 2006

Physiological Reviews

235

209

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The cardiac muscle and the coronary vasculature are in close proximity to each other, and a two-way interaction, called cross-talk, exists. Here we focus on the mechanical aspects of cross-talk including the role of the extracellular matrix. Cardiac muscle affects the coronary vasculature. In diastole, the effect of the cardiac muscle on the coronary vasculature depends on the (changes in) muscle length but appears to be small. In systole, coronary artery inflow is impeded, or even reversed, and venous outflow is augmented. These systolic effects are explained by two mechanisms. The waterfall model and the intramyocardial pump model are based on an intramyocardial pressure, assumed to be proportional to ventricular pressure. They explain the global effects of contraction on coronary flow and the effects of contraction in the layers of the heart wall. The varying elastance model, the muscle shortening and thickening model, and the vascular deformation model are based on direct contact between muscles and vessels. They predict global effects as well as differences on flow in layers and flow heterogeneity due to contraction. The relative contributions of these two mechanisms depend on the wall layer (epi- or endocardial) and type of contraction (isovolumic or shortening). Intramyocardial pressure results from (local) muscle contraction and to what extent the interstitial cavity contracts isovolumically. This explains why small arterioles and venules do not collapse in systole. Coronary vasculature affects the cardiac muscle. In diastole, at physiological ventricular volumes, an increase in coronary perfusion pressure increases ventricular stiffness, but the effect is small. In systole, there are two mechanisms by which coronary perfusion affects cardiac contractility. Increased perfusion pressure increases microvascular volume, thereby opening stretch-activated ion channels, resulting in an increased intracellular Ca2+ transient, which is followed by an increase in Ca2+ sensitivity and higher muscle contractility (Gregg effect). Thickening of the shortening cardiac muscle takes place at the expense of the vascular volume, which causes build-up of intracellular pressure. The intracellular pressure counteracts the tension generated by the contractile apparatus, leading to lower net force. Therefore, cardiac muscle contraction is augmented when vascular emptying is facilitated. During autoregulation, the microvasculature is protected against volume changes, and the Gregg effect is negligible. However, the effect is present in the right ventricle, as well as in pathological conditions with ineffective autoregulation. The beneficial effect of vascular emptying may be reduced in the presence of a stenosis. Thus cardiac contraction affects vascular diameters thereby reducing coronary inflow and enhancing venous outflow. Emptying of the vasculature, however, enhances muscle contraction. The extracellular matrix exerts its effect mainly on cardiac properties rather than on the cross-talk between cardiac muscle and coronary c...

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Section: The Gregg Effectmentioning

confidence: 84%

Section: A Coronary Flow and Cardiac Muscle In Diastolementioning

confidence: 99%

Cross-Talk Between Cardiac Muscle and Coronary Vasculature

Westerhof¹,

Boer²,

Lamberts³

et al. 2006

Physiological Reviews

235

209

View full text Add to dashboard Cite

show abstract

“…According to known mechanisms of cardiac autoregulation, the behavior could be explained by the Gregg phenomenon, the Gardenhose effect or a SDA. Since the right ventricular afterload increase is likely to lead to decreased rather than increased coronary perfusion and increased coronary perfusion has less effect on right ventricular performance than is the case in the left ventricle 30 , 31 , we consider the influence of both the Gregg phenomenon and the Gardenhose effect in the RV to be insufficient to explain the above results. In view of a stable heart rate during the preload and pulmonary artery occlusion interventions, a sympathetic or parasympathetic activation seems unlikely as well (AN: 87.8 ± 11 bpm, AE_PAearly: 88.4 ± 10.9 bpm, AE_Palate: 88.81 ± 12.88 bpm).…”

Section: Discussionmentioning

confidence: 99%

Intrinsic mechanisms of right ventricular autoregulation

Meinert-Krause,

Mechelinck,

Hein

et al. 2024

Sci Rep

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To elucidate the adaptation of the right ventricle to acute and intermittently sustained afterload elevation, targeted preload reductions and afterload increases were implemented in a porcine model involving 12 pigs. Preload reduction was achieved via balloon occlusion of the inferior vena cava before, immediately and 5 min after acute afterload elevation induced by pulmonary artery occlusion or thromboxane A2 analog (U46619) infusion. Ventricular response was monitored by registration of pressure–volume (PV) loops using a conductance catheter. The end-systolic pressure–volume relationship (ESPVR) during pure preload reduction was adequately described by linear regression (mean and SEM slope of ESPVR (Ees) 0.414 ± 0.064 mmHg/ml), reflecting the classical Frank-Starling mechanism (FSM). The ESPVR during acute afterload elevation exhibited a biphasic trajectory with significantly distinct slopes (mean and SEM Ees bilin1: 1.256 ± 0.066 mmHg ml; Ees bilin2: 0.733 ± 0.063 mmHg ml, p < 0.001). The higher slope during the first phase in the absence of ventricular dilation could be explained by a reduced amount of shortening deactivation (SDA). The changes in PV-loops during the second phase were similar to those observed with a preload intervention. The persistent increase in afterload resulted in an increase in the slopes of ESPVR and preload recruitable stroke work (PRSW) with a slight decrease in filling state, indicating a relevant Anrep effect. This effect became more pronounced after 5 min or TXA infusion. This study demonstrates, for the first time, the relevance of intrinsic mechanisms of cardiac autoregulation in the right ventricle during the adaptation to load. The SDA, FSM, and Anrep effect could be differentiated and occurred successively, potentially with some overlap. Notably, the Anrep effect serves to prevent ventricular dilation.

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Different Responses in Adult and Neonatal Hearts to Changes in Coronary Perfusion Pressure

et al. 2006

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The influence of coronary perfusion pressure on neonatal heart function has not been evaluated. We compared the coronary perfusion pressure-cardiac function relationship between neonatal and adult hearts. Neonatal and adult rabbit hearts were examined. The coronary perfusion pressure was changed in increments of 10 mmHg. Coronary blood flow and left ventricular functions were measured at each coronary perfusion pressure. Autoregulatory capacity for coronary blood flow was quantified by calculating the autoregulation index. In neonatal hearts, left ventricular developed pressure was decreased at high perfusion pressure, whereas in adult hearts left ventricular developed pressure increased at high perfusion pressure. In neonatal hearts, left ventricular enddiastolic pressure was elevated at both low and high perfusion pressure, whereas in adult hearts left ventricular enddiastolic pressure remained constant at all perfusion pressures. Adult hearts exhibited coronary blood flow autoregulation in the perfusion pressure range between 40 and 90 mmHg. In contrast, neonatal hearts did not show autoregulation in any perfusion pressure range. In neonatal hearts, both low and high perfusion pressure caused deterioration in ventricular function attributable to the immaturity of coronary autoregulatory capacity. We conclude that coronary perfusion pressure should be controlled within a narrow range for neonates.

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Increasing coronary perfusion pressure on diastolic and systolic performance is less pronounced in right ventricle than in left ventricle

Abstract: Accordingly, increases in coronary perfusion pressure and/or flow decreased the RV distensibility and enhanced the RV contractile function, the extent of which, however, was less than that in the LV.

Cited by 9 publications

References 28 publications

Cross-Talk Between Cardiac Muscle and Coronary Vasculature

Cross-Talk Between Cardiac Muscle and Coronary Vasculature

Intrinsic mechanisms of right ventricular autoregulation

Different Responses in Adult and Neonatal Hearts to Changes in Coronary Perfusion Pressure

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