Perfusion-induced changes in cardiac contractility and oxygen consumption are not endothelium-dependent

Abstract

The results suggest that the arterial endothelium is not involved in the Gregg phenomenon.

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

“…The increase of F dev , which results from a change from low to high P perf (Gregg effect), has been reported several times in literature (1,14,15,17,18,39). 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.…”

“…From the literature, it is known that SACs could be located on the sarcolemma or t-tubular system of the cardiomyocytes (45); however, SACs have also been found on the vascular (33) or endocardial (24,27) endothelium. Dijkman et al (16)(17)(18) showed that perfusion-induced changes in contractility were related to Fig. 2.…”

“…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 coronary perfusion augments cardiac contractility in the rat through stretch-activated ion channels

“…The membrane deformation changes ion fluxes through SACs, resulting in increased cardiac contractility. This hypothesis is supported by the findings that the Gregg response was related to capillary perfusion (13,15) and changes in coronary vascular volume (3), but was not related to arterial endothelium or its released inotropic substances (12,14,32,33). The identity of the coronary perfusion-induced increased cation influx is not yet clear and needs further experiments.…”

“…An increase in coronary perfusion with a concomitant increased filling of the coronary vessels leads to an increase in cardiac contractility and cardiac oxygen consumption known as the Gregg effect (1,3,14,18,22,36). Filling of the coronary vessels will change hoop (circumferential) stress in the vessel wall, thereby mechanically deforming the membranes of myocardial cells.…”