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 nt mechanisms are obligatory for maintaining coronary blood flow.

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

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

9 ardiac efferent sympathetic signals modulate coronary blood flow.

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

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

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

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

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

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

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

17 room temperature saline was used to measure coronary blood flow.

18 in which arterial intimal thickening limits coronary blood flow.

19 coronary blood flow and preserved hyperemic coronary blood flow.

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

21 The alpha1-ARs regulate human coronary blood flow.

22 effects on coronary vascular resistance and coronary blood flow.

23 reperfusion injury following restoration of coronary blood flow.

24 Six waves predominantly drive human coronary blood flow.

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

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

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

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

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

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

31 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

32 8+/-1.2 versus 1.3+/-0.4s(-1)) and hyperemic coronary blood flow (4.8+/-1.5 versus 2.1+/-0.5s(-1)) co

33 0 minutes, the veratrine-induced increase in coronary blood flow (7+/-1 mL/min) was reduced by 66% an

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

35 Restoration of coronary blood flow after a heart attack can cause reper

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

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

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

39 Resting coronary blood flow and coronary functional hyperaemia a

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

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

42 Changes in coronary blood flow and epicardial diameter response to

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

44 Coronary blood flow and hemodynamics were continuously m

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

46 hological stress reflects similar changes in coronary blood flow and is a predictor of adverse cardio

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

48 s and lack the opportunity to determine true coronary blood flow and microvascular resistance.

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

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

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

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

53 choline are associated with elevated resting coronary blood flow and preserved hyperemic coronary blo

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

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

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

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

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

59 Coronary blood flow and vasodilatory responses of corona

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

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

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

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

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

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

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

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

68 Techniques to measure absolute coronary blood flow are promising but need validation.

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

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

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

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

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

74 Coronary blood flow at baseline for patients in group 1

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

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

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

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

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

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

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

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

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

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

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

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

87 7 days (n = 5) and 4 weeks (n = 4) to reduce coronary blood flow by a mean of 34% with severe regiona

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

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

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

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

92 ng a vicious cycle with deranging effects on coronary blood flow, cardiac metabolism and cardiac func

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

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

95 Resting coronary blood flow (CBF) (24.6 +/- 2.0 cm/s vs. 16.6 +/

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 serve were calculated as vasodilator/resting coronary blood flow (CFR and AchFR, respectively).

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

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

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

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

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

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

120 ysfunction was defined as a <50% increase in coronary blood flow, determined by Doppler flow, and/or

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

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

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

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

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

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

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

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

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

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

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

132 Adenosine increases coronary blood flow, exerts direct negative chronotropic

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

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

135 However, coronary blood flow immediately on reperfusion was signi

136 Reduced coronary blood flow impairs myocardial oxygen delivery a

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

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

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

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

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

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

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

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

145 iac output, peripheral tissue perfusion, and coronary blood flow in observational studies and some ra

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

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

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

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

150 Increases in coronary blood flow in response to sympathetic stimulati

151 Coronary blood flow in response to the endothelium-depen

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

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

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

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

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

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

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

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

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

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

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

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

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

165 d microvascular CED (%acetylcholine-mediated coronary blood flow increased from 7.2 [-18.0 to 32.4] t

166 d microvascular CED (%acetylcholine-mediated coronary blood flow increased from 7.2 [-18.0 to 32.4] t

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

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

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

170 2MI) related to a supply/demand imbalance of coronary blood flow is common and associated with poor p

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

172 Coronary blood flow is further compromised by other mech

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

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

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

176 Normal coronary blood flow is principally determined by a backw

177 Coronary blood flow is tightly regulated to ensure that

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

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

180 Second, to validate absolute coronary blood flow measured with continuous coronary th

181 Absolute coronary blood flow measured with saline infusion speeds

182 urteen closed-chest sheep underwent absolute coronary blood flow measurements with increasing saline

183 testing (n = 5), respectively: high resting coronary blood flow (n = 195, 19%); high resistance (n =

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

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

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

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

188 Increases in contractility (P < 0.05) and coronary blood flow (P < 0.05) were seen in vitro during

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

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

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

192 Coronary blood flow peaks in diastole when aortic blood

193 the lack of direct measurements of absolute coronary blood flow (Q) and microvascular resistance (R(

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 Vascular Kv1.5 channels connect coronary blood flow to myocardial metabolism and their d

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

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

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

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

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

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

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

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

217 LAD coronary blood flow velocity and free-breathing myocardi

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

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

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

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

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

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

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

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

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

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

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

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

230 [CI]: 1.01 to 1.12; p = 0.021), whereas low coronary blood flow was associated with increased risk o

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

232 Coronary blood flow was calculated from measurements of

233 Coronary blood flow was calculated from the diameter, as

234 Baseline coronary blood flow was determined using quantitative co

235 Baseline coronary blood flow was determined with quantitative cor

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

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

238 Coronary blood flow was measured by radiolabeled microsp

239 Coronary blood flow was measured in chronically instrume

240 Coronary blood flow was monitored and LAD segments excis

241 Coronary blood flow was monitored during and 120 min aft

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

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

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

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

246 Coronary flow reserve and coronary blood flow were obtained to test microvascular

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

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