Contribution of myocardial contractility to myocardial perfusion

Trimble, Jason L; Downey, James M.

doi:10.1152/ajpheart.1979.236.1.h121

Cited by 6 publications

(3 citation statements)

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“…Our finding that contractility is not important in determining the flow impediment in the dog heart, especially for physiological levels of systolic LVP, is consistent with the reports of Klassen & Zborowska-Sluis (1979) and of Trimble & Downey (1979). The former authors, both in the presence and in the absence of autoregulation, reported no alteration in transmural gradient of flow (endo/epi ratio) when the force of contraction of segments of myocardium was increased, while the coronary and ventricular pressure were maintained stable in the physiological range.…”

Section: Implication Of the Findingssupporting

confidence: 92%

Systolic coronary flow impediment in the dog: role of ventricular pressure and contractility

Pagliaro

Gattullo

et al. 1998

Experimental Physiology

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SUMMARYThe present study was planned to investigate the effect of left ventricular pressure and inotropic state on coronary arterial inflow in systole in the anaesthetized dog. A wide range of left ventricular systolic pressures, including the physiological range, were studied. Experiments were done under conditions of maximal vasodilatation and low perfusion pressure in order to avoid vascular autoregulative interference and to keep the microvascular pressure within the normal range. In five anaesthetized dogs, perfused with extracorporeal circulation system, ventricular volume was changed from 20 to 50 ml in steps of 10 ml by filling an intraventricular latex balloon, and the related changes in left ventricular pressure and coronary flow were measured. The volume was then extended to 70 ml to obtain an overstretch which induced a transient decrease in cardiac contractility. During the period of low cardiac contractility the volume was brought back to 20 ml in steps of 10 ml. Systolic ventricular pressure changed with volume but was lower during the period of low contractility. For systolic pressures below 100 mmHg there was no significant relationship between pressure and coronary systolic flow, but the relationship shifted to higher flows during low contractility. For systolic pressures above 100 mmHg systolic coronary flow decreased significantly when systolic pressure increased. In this case the slopes of the relationships were not significantly different before and after the reduction in contractility. These findings suggest that for systolic pressures less than 100 mmHg (i.e. below the physiological range) the shielding effect of the contracting ventricle prevents the ventricular pressure from being transmitted in the myocardial wall. When systolic pressure exceeds 100 mmHg the shielding effect is overcome and the amplitude of the systolic flow reduction varies with ventricular pressure.

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Section: Implication Of the Findingssupporting

confidence: 92%

Systolic coronary flow impediment in the dog: role of ventricular pressure and contractility

Pagliaro

Gattullo

et al. 1998

Experimental Physiology

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“…Considering the facts that in various animal experimental models other factors, such as perfusion pressure (7), heart rate (9), extravascular compression forces (8,28), vascular remodeling due to medial thickening (2) or perivascular fibrosis (11), and coronary capillary resistance (12), have been implicated in the alterations of maximal myocardial perfusion, their contribution to the difference in the level of maximal perfusion in our two groups of infarcted rats cannot be excluded. However, since our data indicate that perfusion pressure, heart rate, and the size of capillary bed were similar in MI ϩ IVA and MI rats, neither of these factors could affect the level of maximal myocardial perfusion.…”

Section: Discussionmentioning

confidence: 99%

Preservation of coronary reserve by ivabradine-induced reduction in heart rate in infarcted rats is associated with decrease in perivascular collagen

Dedkov¹,

Zheng²,

Christensen³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Dedkov EI, Zheng W, Christensen LP, Weiss RM, MahlbergGaudin F, Tomanek RJ. Preservation of coronary reserve by ivabradine-induced reduction in heart rate in infarcted rats is associated with decrease in perivascular collagen. Am J Physiol Heart Circ Physiol 293: H590-H598, 2007. First published March 23, 2007; doi:10.1152/ajpheart.00047.2007.-We tested the hypothesis that chronically reducing the heart rate in infarcted middle-aged rats using ivabradine (IVA) would induce arteriolar growth and attenuate perivascular collagen and, thereby, improve maximal perfusion and coronary reserve in the surviving myocardium. Myocardial infarction (MI) was induced in 12-mo-old male Sprague-Dawley rats, which were then treated with either IVA (10.5 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ; MI ϩ IVA) or placebo (MI) via intraperitoneal osmotic pumps for 4 wk. Four weeks of IVA treatment limited the increase in left ventricular end-diastolic pressure and the decrease in ejection fraction but did not affect the size of the infarct, the magnitude of myocyte hypertrophy, or the degree of arteriolar and capillary growth. However, treatment reduced interstitial and periarteriolar collagen in the surviving myocardium of MI ϩ IVA rats. The reduced periarteriolar collagen content was associated with improvement in maximal myocardial perfusion and coronary reserve. Although the rates of proliferation of periarteriolar fibroblasts were similar in the MI and MI ϩ IVA groups, the expression levels of the AT 1 receptor and transforming growth factor (TGF)-␤1 in the myocardium, as well as the plasma level of the ANG II peptide, were lower in treated rats 14 days after MI. Therefore, our data reveal that improved maximal myocardial perfusion and coronary reserve in MI ϩ IVA rats are most likely the result of reduced periarteriolar collagen rather than enhanced arteriolar growth. myocardial infarction; coronary circulation; coronary vessels; reninangiotensin system A MYOCARDIAL INFARCTION (MI) initiates progressive structural remodeling within the surviving left ventricular (LV) myocardium. Features of such remodeling include cardiac myocyte hypertrophy, fibroblast proliferation, and interstitial/perivascular fibrosis (4, 26). These alterations compromise maximal coronary blood perfusion and coronary reserve in the remaining LV myocardium (5,6,15,16,18,20).Since adequate tissue perfusion is key for survival and effective function of hypertrophied myocytes in the remaining overloaded LV myocardium, the recovery of normal tissue perfusion in this region has become a major focus of several studies (14, 15), including those from our laboratory (5, 20). Because the major cause of limited myocardial perfusion and coronary reserve in post-MI hearts was long thought to be a failure to match the adaptive growth of the intramyocardial vasculature to the degree of myocyte hypertrophy, earlier studies, which were conducted on young and young-adult rats, were designed either to reduce myocyte hypertrophy (14,24) or to promote the growth of the coronary vasculature (20).MI i...

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“…First, the increase in heart rate decreases maximum coronary blood flow rates by increasing the total time spent in systole (23). Second, the increased contractility increases systolic compression of the intramural coronary vessels (325,385,533,563). However, the increased contractility simul-taneously augments myocardial relaxation which increases the diastolic perfusion time (142,465,625).…”

Section: Effective Perfusion Pressure: Extravascular Compressive Forcesmentioning

confidence: 99%

Regulation of Coronary Blood Flow During Exercise

Duncker

Bache

2008

Physiological Reviews

783

684

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Exercise is the most important physiological stimulus for increased myocardial oxygen demand. The requirement of exercising muscle for increased blood flow necessitates an increase in cardiac output that results in increases in the three main determinants of myocardial oxygen demand: heart rate, myocardial contractility, and ventricular work. The approximately sixfold increase in oxygen demands of the left ventricle during heavy exercise is met principally by augmenting coronary blood flow (~5-fold), as hemoglobin concentration and oxygen extraction (which is already 70-80% at rest) increase only modestly in most species. In contrast, in the right ventricle, oxygen extraction is lower at rest and increases substantially during exercise, similar to skeletal muscle, suggesting fundamental differences in blood flow regulation between these two cardiac chambers. The increase in heart rate also increases the relative time spent in systole, thereby increasing the net extravascular compressive forces acting on the microvasculature within the wall of the left ventricle, in particular in its subendocardial layers. Hence, appropriate adjustment of coronary vascular resistance is critical for the cardiac response to exercise. Coronary resistance vessel tone results from the culmination of myriad vasodilator and vasoconstrictors influences, including neurohormones and endothelial and myocardial factors. Unraveling of the integrative mechanisms controlling coronary vasodilation in response to exercise has been difficult, in part due to the redundancies in coronary vasomotor control and differences between animal species. Exercise training is associated with adaptations in the coronary microvasculature including increased arteriolar densities and/or diameters, which provide a morphometric basis for the observed increase in peak coronary blood flow rates in exercise-trained animals. In larger animals trained by treadmill exercise, the formation of new capillaries maintains capillary density at a level commensurate with the degree of exercise-induced physiological myocardial hypertrophy. Nevertheless, training alters the distribution of coronary vascular resistance so that more capillaries are recruited, resulting in an increase in the permeability-surface area product without a change in capillary numerical density. Maintenance of alpha- and ss-adrenergic tone in the presence of lower circulating catecholamine levels appears to be due to increased receptor responsiveness to adrenergic stimulation. Exercise training also alters local control of coronary resistance vessels. Thus arterioles exhibit increased myogenic tone, likely due to a calcium-dependent protein kinase C signaling-mediated alteration in voltage-gated calcium channel activity in response to stretch. Conversely, training augments endothelium-dependent vasodilation throughout the coronary microcirculation. This enhanced responsiveness appears to result principally from an increased expression of nitric oxide (NO) synthase. Finally, physical conditioning decreases e...

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Contribution of myocardial contractility to myocardial perfusion

Cited by 6 publications

References 0 publications

Systolic coronary flow impediment in the dog: role of ventricular pressure and contractility

Systolic coronary flow impediment in the dog: role of ventricular pressure and contractility

Preservation of coronary reserve by ivabradine-induced reduction in heart rate in infarcted rats is associated with decrease in perivascular collagen

Regulation of Coronary Blood Flow During Exercise

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