Pressure measurements in the terminal vascular bed of the epimyocardium of rats and cats.

Tillmanns, Harald; Steinhausen, M.; Leinberger, H.; Thederan, H.; Kübler, W.

doi:10.1161/01.res.49.5.1202

Cited by 81 publications

(30 citation statements)

References 27 publications

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“…4), the profile showed a flat region followed by a large drop in pressure for vessels Ͻ100 m in diameter. This is in agreement with experimental epicardial and subendocardial pressure measurements (5,11,31). Furthermore, a very steep drop in pressures was observed at the smallest arteriolar diameters.…”

Section: Analysis Of Coronary Arterial Flowsupporting

confidence: 91%

Analysis of blood flow in the entire coronary arterial tree

Mittal¹,

Zhou²,

Linares³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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A hemodynamic analysis of coronary blood flow must be based on the measured branching pattern and vascular geometry of the coronary vasculature. We recently developed a computer reconstruction of the entire coronary arterial tree of the porcine heart based on previously measured morphometric data. In the present study, we carried out an analysis of blood flow distribution through a network of millions of vessels that includes the entire coronary arterial tree down to the first capillary branch. The pressure and flow are computed throughout the coronary arterial tree based on conservation of mass and momentum and appropriate pressure boundary conditions. We found a power law relationship between the diameter and flow of each vessel branch. The exponent is ϳ2.2, which deviates from Murray's prediction of 3.0. Furthermore, we found the total arterial equivalent resistance to be 0.93, 0.77, and 1.28 mmHg ⅐ ml Ϫ1 ⅐ s Ϫ1 ⅐ g Ϫ1 for the right coronary artery, left anterior descending coronary artery, and left circumflex artery, respectively. The significance of the present study is that it yields a predictive model that incorporates some of the factors controlling coronary blood flow. The model of normal hearts will serve as a physiological reference state. Pathological states can then be studied in relation to changes in model parameters that alter coronary perfusion. vascular reconstruction; coronary morphometry; flow simulation; flow resistance; transit time THE CORONARY VASCULAR SYSTEM constitutes the specialized channels that conduct oxygenated blood throughout the myocardium. The function of this network is to continuously supply blood to meet the requirements of the beating heart. Numerous attempts have been made at simulation of blood flow through these specialized channels to understand the spatial and temporal distribution of blood flow. Much of the modeling of the coronary circulation, however, has centered around lumped-parameter models in which the coronary vasculature or subgroup of vessels are treated as single entities whose whole behavior is characterized by a limited number of parameters. Despite the usefulness of such models, they are generally limited to global aspects of coronary blood flow (10, 21). For example, lumped models cannot be used to predict the significant spatial distribution of coronary blood flow.Over a decade ago, a program was initiated to provide the necessary details of the coronary vascular anatomy (vascular geometry and branching pattern) to enable anatomically based modeling of coronary circulation. In this approach, the vascular system comprised of millions of distensible vessel branches, strategically distributed and mostly embedded within the myocardium, must be modeled in as much detail as possible rather than "lumped." Although we are still several years away from accomplishing this goal, some important strides have been made. As a first step, Kassab and colleagues (13,(15)(16)(17)(18) reconstructed the entire vascular anatomy of the porcine heart in the framework of a ma...

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Section: Analysis Of Coronary Arterial Flowsupporting

confidence: 91%

Analysis of blood flow in the entire coronary arterial tree

Mittal¹,

Zhou²,

Linares³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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“…However, studies in normotensive animals suggest that nearly 50% of coronary resistance resides in the large and middlesized arterioles. 34 - 35 Whether a similar resistance pattern is present in hypertensive animals remains to be determined, but the finding of a decreased ratio of lumen diameter to wall thickness involving predominantly the arterioles >50 ^m in SHR (Reference 34 and the present study) is consistent with the conclusion that the increase in systemic blood pressure may be transmitted only to this segment of the coronary circulation. It is well acknowledged, however, that numerous factors determine the functional and structural response of the peripheral vasculature to hypertension. '…”

Section: Vascular Remodeling In Hypertension and Agingsupporting

confidence: 86%

Effects of hypertension and aging on coronary arteriolar density.

et al. 1993

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Coronary reserve has been shown repeatedly to be depressed in hypertension and aging. The underlying mechanisms remain elusive, but structural alterations of the coronary vasculature have been implicated. In this study, we measured maximal coronary dilator capacity and structural characteristics relevant to coronary resistance in aging normotensive (Wistar-Kyoto, n=22) and spontaneously hypertensive rat (SHR) strains (R=25) at 1-5, 4, 11, 16, and 22 months of age. Coronary flow measurements, using radiolabeled microspheres, demonstrated a significant (p<0.01) hypertension-and age-related decline in maximal coronary dilator capacity. After flow measurements, vascular dimensions and arteriolar density were obtained from 1-fj.m sections prepared from perfusion-fixed hearts. A total of 10,012 arterioles were analyzed, 4,820 in hypertensive and 5,192 in normotensive rats. There was an 18-28% reduction in arteriolar density in hypertensive rats that specifically affected the terminal arteriolar bed at 1.5-11 months. However, the decrement in arteriolar density stabilized at 10% and 6% in 16-and 22-month-old hypertensive rats, respectively. Arteriolar density was not affected by aging. In both strains, there was a significant (p<0.01) age-related decrease in the ratio of lumen diameter to wall thickness in arterioles >50 fim. In addition, there was an overall 30% decrease (p<0.01) in the ratio of lumen diameter to wall thickness in hypertensive compared with normotensive rats. These data indicate that both hypertension and aging are accompanied by structural alterations of the coronary resistance vasculature. These structural alterations may contribute to the depression in coronary reserve that complicates hypertension and aging. here is increasing evidence that the cardiovascular consequences of aging and hypertension are similar in many respects, 1 -2 an observation that may account for the greater severity of hypertension in the elderly population.3 As a result, a precise delineation of the biological changes that occur during the aging and hypertensive processes or an improved understanding of the mechanisms underlying these alterations may have important clinical implications and offer new therapeutic perspectives. Various studies have reported that coronary reserve, which reflects the ability of the coronary circulation to dilate in response to a stimulus, was depressed in aging and hypertension. 4 -7 The mechanisms responsible for this limitation of myocardial perfusion remain elusive, although alterations in the functional or structural characteristics of the coronary resistance vessels have been postulated. Smooth musle cell abnormalities or an altered endothelial modulation of vascular tone have been described during hypertension and aging, resulting in a diminished response to vasodilators.2 -8 Several studies have also reported the presence of structural alterations, including vascular hypertrophy, luminal narrowing, or both, in hypertensive hearts both in humans 9 -10 and in animals. 11-12 However, ther...

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“…Comparably sized arteries of the rat, however, showed only minimal and inconsistent pressure differences from the ascending aorta. 22 The lumen diameter of the arteries used in the present study averaged about 200 \x.m, which is 15-20 times smaller than the porcine conductance vessels. 23 However, arteries of 100-200 \im, which are recognized as …”

Section: Reactivity To Transmural Pressure Changesmentioning

confidence: 63%

Reactivity of isolated porcine coronary resistance arteries to cholinergic and adrenergic drugs and transmural pressure changes.

Nakayama

Osol

Halpern

1988

Circulation Research

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The reactivity of porcine intramyocardial resistance arteries (223 ± 7 (xtn i.d., n = 30) was investigated with a pressurized in vitro preparation. Diameter changes in response to acetylcholine and to adrenergic drugs and dynamic changes in transmural pressure changes were investigated. Acetylcholine produced concentration-dependent constrictions, causing maximal reductions of 71 ± 3 % in lumen diameter, with EC,, values averaging 1.9 x 10~7 M (u = 7). These responses were inhibited by atropine (10~7 M) and therefore were mediated by muscarinic receptors. In addition, acetylcholine did not elicit relaxation in nine out of 10 vessels precontracted with U46619 (10~7 M). Norepinephrine and epinephrine never produced constrictions (n = 6) even in the presence of propranolol (10"' M). Both norepinephrine and isoproterenol caused dose-dependent relaxations in acetylcholine-precontracted vessels, with IC M values of 8.2x 10"' M (n = 5) and 6.6x 10"' M (n = 6), respectively. These relaxations were suppressed by propranolol. Between transmural pressures of 10 and 90 mm Hg, there was no intrinsic myogenic tone (n = 7). In addition, the vessels responded only passively to sudden pressure changes of 40 mm Hg. In all vessels, the functional integrity of the endothelium was verified by relaxations to substance P (10"' M) and/or bradykinin (10"' M). This is the first in vitro study of coronary resistance arteries that demonstrates that 1) acetylcholine is a potent constrictor of these arteries, suggesting that parasympathetic mechanisms may play an important role in coronary blood flow regulation; 2) a-adrenoreceptor influence is minimal or entirely absent; and 3) these arteries do not possess an intrinsic myogenic tone and respond passively to transmural pressure change. Hence, myogenic mechanisms do not appear to be of primary importance in the autoregulation of coronary blood flow. (Circulation Research 1988;62:741-748)

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Pressure measurements in the terminal vascular bed of the epimyocardium of rats and cats.

Cited by 81 publications

References 27 publications

Analysis of blood flow in the entire coronary arterial tree

Analysis of blood flow in the entire coronary arterial tree

Effects of hypertension and aging on coronary arteriolar density.

Reactivity of isolated porcine coronary resistance arteries to cholinergic and adrenergic drugs and transmural pressure changes.

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