The Effect of External Constriction of a Blood Vessel on Blood Flow

Shipley, R. E.; Gregg, Donald E.

doi:10.1152/ajplegacy.1944.141.2.289

Cited by 99 publications

(26 citation statements)

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“…In the experimental animal the physiologic significance of artificially produced arterial stenoses has been extensively studied. 14 [18][19][20][21] al.20 produced varying degrees of coronary narrowing and showed that stenoses in excess of 30% to 45% diameter narrowing reduced coronary vasodilator responses in a predictable fashion. However, in human beings with CAD the relationship between the visually estimated percentage diameter stenosis and the consequent reduction in coronary flow reserve is poor.'…”

Section: Resultsmentioning

confidence: 99%

Does the quantitative assessment of coronary artery dimensions predict the physiologic significance of a coronary stenosis?

Zijlstra¹,

Ommeren²,

Reiber³

et al. 1987

Circulation

156

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Section: Resultsmentioning

confidence: 99%

Does the quantitative assessment of coronary artery dimensions predict the physiologic significance of a coronary stenosis?

Zijlstra¹,

Ommeren²,

Reiber³

et al. 1987

Circulation

156

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“…Other investigators have found that flow (or distal arterial pressure) begins to fall at lesser degrees of vessel narrowing when the distal vascular bed is dilated than when it is constricted (Shipley & Gregg, 1944;May et al 1963;Berguer & Hwang, 1974;Gould et al 1974;Young et al 1977). Most peripheral beds respond to stenosis by 'autoregulatory' peripheral vasodilatation which tends to accentuate the pressure gradient and the effective resistance of the stenosis.…”

Section: Factors Determining Stenosis Resistancementioning

confidence: 99%

“…The evaluation of the haemodynamic events after acute stenosis has been difficult, because in none of the above studies have there been simultaneous and continuous measurements of distal renal artery pressure and renal blood flow. This is particularly important in view of experimental and theoretical studies of the haemodynamic interrelationships in arterial stenosis (Shipley & Gregg, 1944;May, Van de Berg, De Weese & Rob, 1963;Thomas, Brockman & Foster, 1968;Berguer & Hwang, 1974;Gould, Lipscomb & Hamilton, 1974;Young, Cholvin, Kirkeeide & Roth, 1977). These indicate that in addition to the resistance offered by the arterial stenosis, the vascular resistance of the distal bed is an important determinant of both the pressure gradient across the stenosis and the blood flow.…”

Section: Introductionmentioning

confidence: 99%

Acute renal haemodynamic and renin‐angiotensin system responses to graded renal artery stenosis in the dog.

Anderson¹,

Johnston²,

Korner³

1979

The Journal of Physiology

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SUMMARY1. The acute renal haemodynamic and renin-angiotensin system responses to graded renal artery stenosis were studied in chronically instrumented, unanaesthetized dogs.2. Stenosis was induced over 30 sec by inflation of a cuff around the renal artery to lower distal pressure to 60, 40 or 20 mmHg, with stenosis maintained for 1 hr. This resulted in an immediate fall in renal vascular resistance, but over the next 5-30 min both resistance and renal artery pressure were restored back towards prestenosis values. Only transient increases in systemic arterial blood pressure and plasma renin and angiotensin levels were seen with the two milder stenoses. Despite restoration of renal artery pressure, renal blood flow remained reduced at all grades of stenosis.3. Pre-treatment with angiotensin I converting enzyme inhibitor or sarcosinel, isoleucine8 angiotensin II greatly attenuated or abolished the restoration of renal artery pressure and renal vascular resistance after stenosis, and plasma renin and angiotensin II levels remained high. Renal dilatation was indefinitely maintained, but the normal restoration of resistance and pressure could be simulated by infusing angiotensin II into the renal artery.4. The effective resistance to blood flow by the stenosis did not remain constant but varied with changes in the renal vascular resistance.

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“…Thus, a more meaningful index of the effect of a stenosis should be based on its effect on the vascular bed reserve."' l4i ' 5 The present study was undertaken to investigate (1) the pressure loss across arterial stenoses of varying severities at elevated flow rates, and (2) the corresponding effect of the stenosis on the vascular bed reserve.…”

mentioning

confidence: 99%

Hemodynamics of arterial stenoses at elevated flow rates.

Young¹,

Cholvin²,

Kirkeeide³

et al. 1977

Circulation Research

168

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HEMODYNAMICS OF ARTERIAL STENOSESTHE DEVELOPMENT of a stenosis in a major artery may significantly alter the blood supply to the peripheral vascular beds supplied by the artery. Since the early work of Mann et al., 1 much attention has been given to thisFrom the Department of Engineering Science and Mechanics, Biomedical Engineering Program, and the Department of Veterinary Anatomy, Physiology, and Pharmacology, Iowa State University, Ames, Iowa.Supported by the Engineering Research Institute, Iowa State Univerproblem, with special consideration given to the concept of the "critical stenosis," which generally has been defined as one for which a small, further increase in the severity of the stenosis will cause a significant reduction in blood VOL. 41, No. 1,JULY 1977 flow. This definition of a critical stenosis is not complete since the effect of a stenosis is influenced not only by the severity of the stenosis, but also by other geometric factors such as length, 2 "" 1 the peripheral resistance of the distal beds, 5 " 8 and collateral flow.9 "" The interaction between the flow through a stenosed artery, collateral flow, and peripheral resistance can be illustrated through the consideration of the simplified, but useful, hydraulic model shown in Figure 1. For this model it is assumed that the resistance of all peripheral beds distal to the stenosis can be considered as a lumped resistance R p . The time-averaged flow through the stenosis is Q s , net collateral flow is Q c , and the flow actually supplied to the distal beds is Q = Q s + Q c . The arterial pressure proximal to the stenosis is p a , and the venous pressure, p v , will be assumed to be zero. The bar over a symbol signifies its time-averaged value, i.e., the average value of the quantity taken over one cardiac cycle.In a normal vessel the commonly used relationship between pressure, flow, and peripheral resistance is 0 = Pa/Rp,which demonstrates that the flow is a function of the driving pressure p a and the resistance Rp. Furthermore, under normal flow conditions the collateral flow is expected to be negligible because the collateral resistance is large compared to the resistance of an unobstructed artery.As a stenosis develops, a pressure drop Ap = p a -pi is created across the stenosis, so that the driving pressure for flow to the peripheral beds is now p, rather than p a , and it is clear that the flow to the peripheral beds will be reduced unless the peripheral resistance can be reduced to compensate for the reduction in driving pressure or adequate collateral flow develops. In equation form Q = p,/R p = (p a -Ap~)/R P = ( Pa /R P )(l -Ap7p a ), (2) and this relationship shows how the pressure drop across the stenosis interacts with the peripheral resistance and arterial pressure to control the flow to the distal beds. A complicating feature of Equation 2 is the fact that the term Ap is a function of the flow through the stenosis. Thus, the effective resistance of the stenosis, as evidenced by Ap, changes the flow and, in fact, Ap increases...

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The Effect of External Constriction of a Blood Vessel on Blood Flow

Cited by 99 publications

References 0 publications

Does the quantitative assessment of coronary artery dimensions predict the physiologic significance of a coronary stenosis?

Does the quantitative assessment of coronary artery dimensions predict the physiologic significance of a coronary stenosis?

Acute renal haemodynamic and renin‐angiotensin system responses to graded renal artery stenosis in the dog.

Hemodynamics of arterial stenoses at elevated flow rates.

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