ライフサイエンスコーパス: coronary blood flow

1 c suction wave (the principal accelerator of coronary blood flow).

2 PPA had no significant effects on coronary blood flow.

3 e coronary artery stenoses via assessment of coronary blood flow.

4 it is an objective and quantitative index of coronary blood flow.

5 ame count, CTFC) were counted as an index of coronary blood flow.

6 f systole relative to diastole, and enhances coronary blood flow.

7 nt mechanisms are obligatory for maintaining coronary blood flow.

8 on measurements of mean and peak velocity of coronary blood flow.

9 stenosis, idazoxan and LNNA had no effect on coronary blood flow.

10 ardiac efferent sympathetic signals modulate coronary blood flow.

11 (P<.05) but not in coronary flow velocity or coronary blood flow.

12 locity, resulting in an increase in absolute coronary blood flow.

13 rest and during a pacing-induced increase in coronary blood flow.

14 nervous system is an important regulator of coronary blood flow.

15 ea, average coronary peak flow velocity, and coronary blood flow.

16 nal area, nor did it significantly influence coronary blood flow.

17 bly steep dose-response curve for increasing coronary blood flow.

18 The alpha1-ARs regulate human coronary blood flow.

19 effects on coronary vascular resistance and coronary blood flow.

20 Six waves predominantly drive human coronary blood flow.

21 ble distribution of systemic, pulmonary, and coronary blood flow.

22 was not induced in dogs with reduced resting coronary blood flow.

23 in ischemia and is an important regulator of coronary blood flow.

24 ventricular function at rest due to reduced coronary blood flows.

25 th the ACE DD compared with ACE II genotype (coronary blood flow -10 +/- 4% vs. 11 +/- 5%, p = 0.003,

26 mposing pacing tachycardia during global low coronary blood flow (32% of baseline).

27 rsus 3.0 [2.4-3.4] mL/min, P=0.24; change of coronary blood flow, 34.9% [-34.4% to 90.0%] versus 54.7

28 0 minutes, the veratrine-induced increase in coronary blood flow (7+/-1 mL/min) was reduced by 66% an

29 Changes in coronary blood flow (a measure of resistance vessel reac

30 The balance of systemic, pulmonary, and coronary blood flow after the Norwood operation for hypo

31 yperpolarization causing profound changes in coronary blood flow and cardiac function.

32 issues, including large increases in resting coronary blood flow and conductance.

33 Resting coronary blood flow and coronary functional hyperaemia a

34 s resulted in significant percent changes in coronary blood flow and coronary vascular resistance (-3

35 The percent changes in coronary blood flow and coronary vascular resistance in

36 Changes in coronary blood flow and epicardial diameter response to

37 study examined the effects of sildenafil on coronary blood flow and hemodynamics during exercise in

38 Coronary blood flow and hemodynamics were continuously m

39 ary infusion of ET-1 significantly decreased coronary blood flow and increased coronary vascular resi

40 opulsion) and distal (suction) influences on coronary blood flow and is purported to reflect myocardi

41 ew possibilities to measure maximal absolute coronary blood flow and minimal microcirculatory resista

42 Post-treatment maximal coronary blood flow and MPR in the lisinopril group incr

43 normal values, animals with CHF had reduced coronary blood flow and MVO2 at rest, with a blunted res

44 decrease myocardial oxygen demand, increase coronary blood flow and oxygen supply, and limit myocard

45 g endogenous bradykinin with HOE-140 reduced coronary blood flow and produced significant increases i

46 ling is a novel regulatory pathway governing coronary blood flow and protecting against I/R injury.

47 occurs as a result of an abrupt decrease in coronary blood flow and resultant imbalance in the myoca

48 Intracoronary bolus of apelin-36 increased coronary blood flow and the maximum rate of rise in left

49 ine if ticagrelor augments adenosine-induced coronary blood flow and the sensation of dyspnea in huma

50 Coronary blood flow and vasodilatory responses of corona

51 ortic valve leaflets without interference of coronary blood flow and with good acute valve function.

52 ained under basal conditions, during maximal coronary blood flow, and after inhibition of NO synthase

53 LV systolic function, left coronary blood flow, and AVO2 difference were measured i

54 Percent change in coronary artery diameter, coronary blood flow, and coronary vascular resistance we

55 te that NP12 reduces fibrosis, reestablishes coronary blood flow, and improves ventricular function f

56 Hemodynamics, segmental shortening, coronary blood flow, and in vitro coronary microvascular

57 in elucidating the spatial heterogeneity of coronary blood flow, and serve as a foundation for under

58 e was administered intravenously to increase coronary blood flow, and stenosis was achieved in the LC

59 to measure ventricular and aortic pressure, coronary blood flow, arterial-coronary sinus oxygen diff

60 as counted to objectively assess an index of coronary blood flow as a continuous variable.

61 ce was determined in the adults by recording coronary blood flow as driving pressure was altered by i

62 he univariate and multivariate correlates of coronary blood flow at 90 min after thrombolytic adminis

63 umen geometry is not the sole determinant of coronary blood flow at 90 min following thrombolytic adm

64 Coronary blood flow at baseline for patients in group 1

65 YSED, P < 0.05) was accompanied by impaired coronary blood flow at rest and during exercise.

66 eak flow velocity, and calculated volumetric coronary blood flow at the 0.1 and 1 mumol/L concentrati

67 ACE inhibition enhances coronary blood flow at the time of reperfusion and can p

68 Intracoronary infusions increased coronary blood flow (baseline, 64.6 +/- 5.1 ml/min; CNP-

69 Volumetric coronary blood flow (BF) can be a valuable aid in the an

70 teries during adenosine-induced increases in coronary blood flow, but arterioles showed minimal regul

71 hrombolysis have been associated with slower coronary blood flow, but the independent contribution of

72 nondiabetics, insulin consistently increased coronary blood flow, but this effect was absent in NIDDM

73 ) synthesis results in very little change in coronary blood flow, but this is thought to be because c

74 rgic nitric oxide (NO)-dependent increase in coronary blood flow by 23+/-3 mL/min (Bezold-Jarisch ref

75 n of SMTC (0.625 micromol/min) reduced basal coronary blood flow by 34.1+/-5.2% (n=10; P<0.01) and ep

76 oronary artery stenosis (CAS), which reduced coronary blood flow by 40% for 90 minutes, and subsequen

77 7 days (n = 5) and 4 weeks (n = 4) to reduce coronary blood flow by a mean of 34% with severe regiona

78 ronary vasodilator and causes an increase of coronary blood flow by activation of A2A-adenosine recep

79 Measurements of mean velocity of coronary blood flow by Doppler catheters have significan

80 r endothelial K(ATP) channels to control the coronary blood flow by modulating the release of the vas

81 coronary intervention (PCI) aims to increase coronary blood flow by relieving epicardial obstruction.

82 cient functioning of the heart by regulating coronary blood flow, cardiac pacemaking, and contractili

83 ch is related to the augmentation in resting coronary blood flow caused by hypertension.

84 ET-1 resulted in an accentuated decrease in coronary blood flow (CBF) and coronary artery diameter (

85 with intracoronary Doppler ultrasound-based coronary blood flow (CBF) as a method for detecting and

86 ned by quantitative coronary angiography and coronary blood flow (CBF) by the product of coronary CSA

87 One month later, there was an increase in coronary blood flow (CBF) distal to the stenotic artery,

88 O production does not impair the increase in coronary blood flow (CBF) during exercise, suggesting th

89 we investigated the relationship between the coronary blood flow (CBF) effects of A2 stimulation and

90 ere compared with flow probe measurements of coronary blood flow (CBF) in the left anterior descendin

91 We hypothesized that coronary blood flow (CBF) reserve could be quantified no

92 We, therefore, hypothesized that abnormal coronary blood flow (CBF) reserve observed during hyperl

93 here were no significant differences in peak coronary blood flow (CBF) response to intracoronary aden

94 annels are important metabolic regulators of coronary blood flow (CBF) that are activated in the sett

95 V) by intravascular Doppler velocimetry, and coronary blood flow (CBF) was calculated.

96 chronically instrumented for measurements of coronary blood flow (CBF), ventricular and aortic pressu

97 uantify waves that accelerate and decelerate coronary blood flow (CBF).

98 essures, wall thickness, and left circumflex coronary blood flow (CBF).

99 of systemic hemodynamics and left circumflex coronary blood flow (CBF).

100 ary stenosis (CS) (30% reduction in baseline coronary blood flow [CBF]) followed by full reperfusion

101 , resulting in repeated cyclic variations in coronary blood flow (CFVs) caused by the formation/dislo

102 Coronary blood flow, coronary artery diameter, and the e

103 There was no significant effect on coronary blood flow, coronary vascular resistance, or co

104 tion and distal embolization, improvement in coronary blood flow could be attenuated despite luminal

105 Intracoronary injections increased coronary blood flow (delta baseline coronary flow, 30 +/

106 coronary angiography, and percent change in coronary blood flow (%deltaCBF) was calculated using int

107 e-dimensional (3D) computed tomography (CT), coronary blood flow distribution determined with microsp

108 ning, ie, the repeated brief interruption of coronary blood flow during early reperfusion.

109 amide (10-50 microgram/kg per min) decreased coronary blood flow during exercise at coronary pressure

110 nitric oxide (NO) production in maintaining coronary blood flow during exercise in hearts with colla

111 of CHF on myocardial oxygen consumption and coronary blood flow during exercise.

112 ocked, both adenosine and NO act to increase coronary blood flow during exercise.

113 The increase in coronary blood flow during infusion of the peak dose of

114 subset of 6 patients, enalaprilat increased coronary blood flow during infusion, but this effect dis

115 play an important role in the regulation of coronary blood flow during metabolic stress.

116 t increase in left anterior descending (LAD) coronary blood flow during resting conditions, with a no

117 In 26 patients, we measured coronary blood flow, epicardial diameter and coronary si

118 Adenosine increases coronary blood flow, exerts direct negative chronotropic

119 This study evaluated the determinants of coronary blood flow following thrombolytic administratio

120 s by coronary stenosis, ie, 40% reduction of coronary blood flow for 90 minutes, followed by full rep

121 However, coronary blood flow immediately on reperfusion was signi

122 hown to improve epicardial and microvascular coronary blood flow in acute myocardial infarction (AMI)

123 Despite the lower values for coronary blood flow in animals with CHF, there was no ev

124 primarily due to an improvement in regional coronary blood flow in areas of myocardial ischemia.

125 Despite an appreciable increase in basal coronary blood flow in cyanotic congenital heart disease

126 (Study to Assess the Effect of Ticagrelor on Coronary Blood Flow in Healthy Male Subjects; NCT0122660

127 ressure over time (dP/dtmax), -dP/dtmax, and coronary blood flow in isolated hearts perfused on a Lan

128 ces coronary artery dilatation and increases coronary blood flow in men with established coronary art

129 and antagonists suggests that ATP regulates coronary blood flow in mice through activation of P2Y (m

130 receptor antagonism significantly increased coronary blood flow in response to acetylcholine at 12 w

131 significant improvement in percent change of coronary blood flow in response to acetylcholine at 6 mo

132 After 6 months, the coronary blood flow in response to acetylcholine in the

133 ED was defined as <50% change in coronary blood flow in response to intracoronary infusio

134 Increases in coronary blood flow in response to sympathetic stimulati

135 Coronary blood flow in response to the endothelium-depen

136 myocardial ischemia, despite restoration of coronary blood flow in the absence of tissue necrosis.

137 In 10 dogs, low coronary blood flow in the circumflex artery was deliver

138 While attention has focused on coronary blood flow in the culprit artery in acute myoca

139 groups in clinical characteristics or in the coronary blood flow in the response to acetylcholine at

140 othelial function and augmented postischemic coronary blood flow in this model of ischemia-reperfusio

141 This catheter was placed in a model of coronary blood flow in which the fluid velocity was accu

142 with transient relaxations, which increases coronary blood flow, in part, by release of nitric oxide

143 ovascular and epicardial responses with SNP (coronary blood flow increase 196 +/- 26% vs. 121 +/- 11%

144 ivities of mtALDH in situ and attenuated the coronary blood flow increase and declines in blood press

145 Coronary blood flow increased 35% (P=0.007), whereas cor

146 Coronary blood flow increased 45% (P=0.02), whereas coro

147 mption increased approximately 3.7-fold, and coronary blood flow increased approximately 3.2-fold fro

148 In the normal dogs, coronary blood flow increased during exercise in proport

149 and epicardial responses with acetylcholine; coronary blood flow increased from 82+/-7 to 90+/-8 mL/m

150 by 58 +/- 5.2% (P < 0.05) of the increase in coronary blood flow induced at 3-4 min of pacing from 31

151 There were no treatment effects on coronary blood flow, infarct size, or the rate of ECG ST

152 of cardiac sympathetic nerves in regulating coronary blood flow is controversial.

153 Coronary blood flow is further compromised by other mech

154 e a decrease in coronary perfusion pressure, coronary blood flow is increased.

155 In the working heart, coronary blood flow is linked to the production of metab

156 t artery patency occurs more rapidly, normal coronary blood flow is more often restored, and reperfus

157 Normal coronary blood flow is principally determined by a backw

158 nificant role in the regulation of the basal coronary blood flow, it can play a major role in the cor

159 Measurements of forearm blood flow, coronary blood flow, left ventricular pressure, and card

160 not cause a significant change in the basal coronary blood flow nor in the immediate increase (withi

161 A significant increase in coronary blood flow occurred at all concentrations of te

162 he treatment of myocardial ischemia increase coronary blood flow or reduce myocardial demand.

163 locity, coronary-artery diameter, volumetric coronary blood flow, or coronary vascular resistance.

164 duced increase in flow velocity (P<.025) and coronary blood flow (P<.05) but not epicardial coronary

165 Brief interruptions of coronary blood flow paradoxically protect the heart from

166 t spontaneous beating frequency, heart rate, coronary blood flow, peak LV pressure, end-diastolic LV

167 Coronary blood flow peaks in diastole when aortic blood

168 reas of investigation include myocardial and coronary blood flow quantification, and intracoronary im

169 tosis correlated significantly with regional coronary blood flow reduction (r = 0.75, p < 0.01).

170 portant implications regarding postoperative coronary blood flow regulation, increases in myocardial

171 (mean stenosis = 7%) underwent assessment of coronary blood flow reserve and coronary flow velocity r

172 dial coronary vasculature and measurement of coronary blood flow reserve are possible using second ha

173 Endothelium-dependent coronary blood flow reserve to acetylcholine (10(-6) to

174 However, the peak coronary blood flow response in baboons (+8 +/- 3 from 4

175 rtic stiffness, and eliminated impairment of coronary blood flow responses and endothelium-dependent

176 tive coronary angiography and distal Doppler coronary blood flow studies (basal and after adenosine-i

177 results from the attenuation or cessation of coronary blood flow such that oxygen delivery to the myo

178 might be expected to impair the increase in coronary blood flow that occurs during exercise.

179 reserve (FFR), which is the ratio of maximal coronary blood flow through a stenotic artery to the blo

180 The percent change of coronary blood flow to acetylcholine (%delta CBF Ach) wa

181 blunted but did not abolish the response of coronary blood flow to exercise.

182 glucose uptake during moderate reductions in coronary blood flow under insulin-stimulated conditions.

183 In 21 patients, coronary blood flow velocity (0.014-inch Doppler flow wi

184 ted with a substantially larger increment in coronary blood flow velocity (0.51 versus 0.14 m/s, P <0

185 nia] vs 14% +/- 24 [adenosine]; P = .80) and coronary blood flow velocity (21% +/- 16 [hypercapnia] v

186 nance dose of ticagrelor versus prasugrel on coronary blood flow velocity (CBFV) during increasing do

187 Coronary blood flow velocity (CBFV) was measured by usin

188 Coronary blood flow velocity (CBV; Duplex Ultrasound), h

189 adjunctive PTCA significantly improve distal coronary blood flow velocity and DSVR but not CFR.

190 LAD coronary blood flow velocity and free-breathing myocardi

191 f this study was to assess serial changes in coronary blood flow velocity before and after Rotablator

192 ulated as the ratio of hyperemic to baseline coronary blood flow velocity in the left anterior descen

193 e receptor-mediated, whereas the increase in coronary blood flow velocity is due to activation of A2

194 er and wall thickness, and a left circumflex coronary blood flow velocity transducer.

195 luses of adenosine; however, the increase in coronary blood flow velocity was not significantly affec

196 His (A-H) interval, chest pain severity, and coronary blood flow velocity were made before and after

197 FR has traditionally required measurement of coronary blood flow velocity with the Doppler wire and,

198 LV contraction and relaxation, it increases coronary blood flow velocity, predominantly by increasin

199 sed both epicardial cross-sectional area and coronary blood flow velocity, resulting in an increase i

200 entiated ACH-mediated coronary vasodilation; coronary blood flow was 36 +/- 11% higher (p < 0.02), an

201 During control conditions, coronary blood flow was 49 +/- 3 mL/min at rest and incr

202 Percent baseline of coronary blood flow was also significantly increased in

203 of intracoronary infusion at 20% of measured coronary blood flow was begun using 20 mmol/L [2-(13)C]g

204 Coronary blood flow was calculated from measurements of

205 Coronary blood flow was calculated from the diameter, as

206 Baseline coronary blood flow was determined using quantitative co

207 Baseline coronary blood flow was determined with quantitative cor

208 In addition, canine coronary blood flow was greater during infusion of renit

209 Coronary blood flow was higher in Groups II, III, and IV

210 Coronary blood flow was measured by radiolabeled microsp

211 Coronary blood flow was measured in chronically instrume

212 Coronary blood flow was monitored and LAD segments excis

213 Coronary blood flow was monitored during and 120 min aft

214 However, coronary blood flow was significantly reduced (p < 0.05)

215 hermodilution-based assessment of volumetric coronary blood flow, we observed that intracoronary infu

216 ane coronary angiography, and measurement of coronary blood flow, we represented the artery in accura

217 Isovolumic left ventricular function and coronary blood flow were measured.

218 Thus, myocardial ischemia is lack of coronary blood flow with electric, functional, metabolic

219 This study compared angiographically graded coronary blood flow with intracoronary Doppler flow velo