Reactive dilation and late-hyperemic constriction of epicardial coronary artery after short coronary occlusion

Yamamoto, Hirotaka; Tomoike, H.; Hisano, Kyoko; Inoue, Takeshi; Mohri, Masahiro; Nakamura, Motoomi

doi:10.1152/ajpheart.1986.251.3.h554

Cited by 3 publications

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“…The flow difference between 3 and 10 minutes of occlusion was not significant although the difference between 1 and 3 minutes (and 1 and 10 minutes) of occlusion was statistically different. The velocity response was similar in nature to the Forearm volume, 1,261 ±45; n=8forall observations; Blood flow, forearm blood flow, ml/min • 100 ml; Velocity, brachial artery blood flow velocity, cm/sec; Area, brachial artery area, cm 2 ; Diameter, brachial artery diameter, cm; 1,3, 10 minutes, respective response following release of arterial occlusion.…”

Section: Discussionsupporting

confidence: 56%

“…In an effort to determine whether arterial conductance vessels dilate in response to increased blood flow stimuli, brachial artery area (cm 2 ) and diameter (cm) were derived by simultaneous measurement of forearm blood flow (ml/min-100 ml) and brachial artery blood flow velocity (cm/sec) following the release of arterial occlusion. Measurements were made at rest and at the time of maximal flow after the release of graded periods of forearm arterial occlusion (20 seconds to 10 minutes).…”

Section: Characteristics Of Flow-mediated Brachial Artery Vasodilatiomentioning

confidence: 99%

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Characteristics of flow-mediated brachial artery vasodilation in human subjects.

Sinoway

Hendrickson

Davidson

et al. 1989

Circulation Research

121

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In an effort to determine whether arterial conductance vessels dilate in response to increased blood flow stimuli, brachial artery area (cm 2 ) and diameter (cm) were derived by simultaneous measurement of forearm blood flow (ml/min-100 ml) and brachial artery blood flow velocity (cm/sec) following the release of arterial occlusion. Measurements were made at rest and at the time of maximal flow after the release of graded periods of forearm arterial occlusion (20 seconds to 10 minutes). These studies showed a graded large vessel dilation following occlusions of up to 1 minute (baseline diameter, 0.33±0.01; after 1 minute occlusion, 0.45±0.02 cm; /?<0.05) after which time diameter plateaued (after 10 minutes of occlusion, 0.48±0.02 cm). In addition, the time course of diameter and flow changes after 3 minutes of arterial occlusion were examined. Flow was maximal at 5 seconds but diameter was maximal at 15-30 seconds after release. Furthermore, the half time for the return of diameter to baseline was longer than that for blood flow. We also measured the diameter after forearm heating (42° C) and noted a substantial increase in diameter (before heating, 0.32±0.01; after heating, 0.39±0.02 cm; p<0.05). Finally, we applied pressure to the venous side of arteriovenous fistulae in five hemodialysis patients. This maneuver was associated with large reductions in forearm blood flow (baseline flow, 63.3±10.6; venous compression flow, 36.0±4.4 ml/minl00 ml;/?<0.05) and a decrease in brachial artery size (baseline diameter, 0.63±0.07; venous compression diameter, 0.58±0.06 cm; p<0.05). We conclude that 1) the human brachial artery size changes in response to changes in blood flow, and 2) the maximal dilation occurs after maximal flow is noted. This process has been termed reactive dilation, 1 and it has been suggested that the process is truly localized to the large vessel and may require endothelial integrity.5 A relation between increased blood flow and large vessel dilation in human subjects has not been previously described.Recently, we have developed a noninvasive technique that allows us to calculate brachial artery diameter at frequent intervals (10-15 seconds) from simultaneously measured forearm blood flow (straingauge plethysmography) and brachial artery blood velocity (a transcutaneous Doppler probe). With this technique, we make use of the equation, vessel area=flow (ml/min)-^ velocity (cm/min). In this paper, we hypothesized that acute alterations in forearm blood flow would be associated with directionally similar changes in brachial artery size. Our results would suggest that the process of reactive dilation does indeed exist in human subjects. Subjects and Methods DesignAfter signing an informed consent, 11 young healthy subjects (mean age of 23 years) had simultaneous measurements of forearm blood flow and brachial artery blood velocity in order to calculate brachial artery diameter. The study was divided into five major parts: Part A (n=8) consisted of measurement of blood flow and blood velocity and calcu...

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Section: Discussionsupporting

confidence: 56%

Section: Characteristics Of Flow-mediated Brachial Artery Vasodilatiomentioning

confidence: 99%

Characteristics of flow-mediated brachial artery vasodilation in human subjects.

Sinoway

Hendrickson

Davidson

et al. 1989

Circulation Research

121

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“…Nineteen mongrel dogs (30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43)(44)(45) branch of the LAD below the site of constriction, enabling the pressure gradient across the stenosis to be measured ( Figure 1). …”

Section: Materials and Methods Surgical Preparationmentioning

confidence: 99%

Local platelet activation causes vasoconstriction of large epicardial canine coronary arteries in vivo. Thromboxane A2 and serotonin are possible mediators.

et al. 1989

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The goal of the present study was to demonstrate that intracoronary platelet deposition may trigger intense vasoconstriction of large epicardial coronary arteries in vivo and that this is largely mediated by thromboxane A2 and serotonin released by activated platelets. Cyclic flow variations (progressive declines in blood flow followed by sudden restorations of flow) due to recurrent intracoronary platelet activation and thrombus formation were induced by damaging the endothelium and placing a cylindrical constrictor on the left anterior descending coronary artery (LAD) in open-chest, anesthetized dogs. Coronary diameters were measured in vivo by means of ultrasonic crystals sutured on the LAD immediately distal to the constrictor (LADI) and 1 cm below (LAD2) and on the circumflex coronary artery (Cx). Coronary artery diastolic diameters were measured continuously before and during cyclic flow variations and after they were abolished by administration of LY53857, a serotonin-receptor antagonist (group 1, n =7), or SQ29548, a thromboxane-receptor antagonist (group 2, n = 7). During cyclic flow variations, at the nadir of coronary flow, LADI (a site of maximal platelet accumulation) cross-sectional area decreased by 52±10% and 38±6% in group 1 and 2 animals, respectively (p <0.001 compared with values recorded during a brief LAD occlusion obtained by a suture snare), whereas LAD2 (a site of minimal or no platelet accumulation) cross-sectional area did not differ from that recorded during the brief LAD occlusion. SQ29548 abolished cyclic flow variations in seven of seven dogs and LY53857 in six of seven, but they affected the increased coronary vasoconstriction differently: LADI cross-sectional area increased by 32±N6% of the control value in SQ29548-treated animals, whereas it returned to baseline dimension values in the LY53857-treated group as these interventions also abolished the cyclic flow variations. We conclude that a marked coronary vasoconstriction may be triggered by local platelet deposition and that thromboxane A2 and serotonin are mediators of this vasoconstriction. (Circulation 1989;79:154-166) It is currently believed that the pathophysiology of unstable angina is a primary reduction in coronary blood flow.

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Effects of ionic and nonionic contrast media on coronary diameter and blood flow in chronically instrumented dogs

Egashira¹,

Tomoike²,

Nishijima³

et al. 1989

American Heart Journal

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Reactive dilation and late-hyperemic constriction of epicardial coronary artery after short coronary occlusion

Cited by 3 publications

References 0 publications

Characteristics of flow-mediated brachial artery vasodilation in human subjects.

Characteristics of flow-mediated brachial artery vasodilation in human subjects.

Local platelet activation causes vasoconstriction of large epicardial canine coronary arteries in vivo. Thromboxane A2 and serotonin are possible mediators.

Effects of ionic and nonionic contrast media on coronary diameter and blood flow in chronically instrumented dogs

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