ライフサイエンスコーパス: dobutamine

1 se or pharmacological stress (typically with dobutamine).

2 60 +/- 13 years, 47% men) undergoing SE (56% dobutamine).

3 hy (34% with treadmill exercise and 66% with dobutamine).

4 line and the partial agonists salbutamol and dobutamine.

5 d with supply of the beta-adrenergic agonist dobutamine.

6 se of heart rate to different dose levels of dobutamine.

7 e computed for all subjects at rest and with dobutamine.

8 during infusion of 10 (microg . kg(-1))/min dobutamine.

9 of the heart rate-blood pressure product by dobutamine.

10 ation of contractile function in response to dobutamine.

11 efore and after infusion of the beta-agonist dobutamine.

12 e patient (7%) received neither dopamine nor dobutamine.

13 restricted to norepinephrine, dopamine, and dobutamine.

14 ological concentrations of norepinephrine or dobutamine.

15 ion versus supply-demand ischemia induced by dobutamine.

16 er min) with a subgroup of SC patients given dobutamine.

17 ons with abnormal function at lower doses of dobutamine.

18 ac efficiency in contrast to epinephrine and dobutamine.

19 ing T709D-TRPV5 mutants were unresponsive to dobutamine.

20 s performed using regadenoson, adenosine, or dobutamine.

21 aseline during VS only at the lowest dose of dobutamine.

22 c and lusitropic response to acute stress by dobutamine.

23 nd in response to sympathomimetic challenge (dobutamine 0.3-10 mug/kg/min) using a left ventricular p

24 -0.06 versus -0.17+/-0.10; P<0.001) and with dobutamine (-0.07+/-0.06 versus -0.21+/-0.11; P<0.001).

25 -0.06 versus -0.27+/-0.03; P<0.001) and with dobutamine (-0.17+/-0.08 versus -0.37+/-0.10; P<0.001).

26 ncreased Ecc at rest (-0.27+/-0.07) and with dobutamine (-0.37+/-0.15) compared with both viable and

27 also observed lower ICU cumulative dosage of dobutamine (12 vs 19 mg/kg; p = 0.003) and a shorter ICU

28 red-cell transfusions (13.6% vs. 7.0%), and dobutamine (15.4% vs. 2.6%) (P<0.001 for all comparisons

29 1.7 +/- 0.7 s(-1); blood: 2.0 +/- 1.1 s(-1); dobutamine: 3.4 +/- 2.3 s(-1); metoprolol: 1.0 +/- 0.4 s

30 ns, whereas two additional groups were given dobutamine (30-60 microg x kg(-1) x min(-1)intravenously

31 circumflex flow was decreased by 30% before dobutamine (40 micro g/kg/min intravenously).

32 6 564 (6.1%) heart failure hospitalizations: dobutamine 43%, dopamine 24%, milrinone 17%, or a combin

33 ns causing alterations in regional function: dobutamine, 5-min coronary occlusion with reperfusion up

34 infusions of apelin-13 (0.25 mug/kg/min) or dobutamine (7.5 mug/kg/min).

35 maintained a positive inotropic response to dobutamine 8 weeks after MI.

36 patients who underwent pharmacological (752 dobutamine, 800 dipyridamole) stress echo for the evalua

37 Increasing doses of dobutamine, a beta1-adrenergic agonist, were administere

38 dministered antibiotic and EC-SERS to detect dobutamine, a drug commonly administered after heart sur

39 sine also increased sprouting and concurrent dobutamine administration reduced it, confirming that lo

40 istensibility at rest and during intravenous dobutamine administration using cardiovascular magnetic

41 ionship (i.e., contractility) increased with dobutamine after liraglutide (P < 0.001) but not saline

42 sion, repetitive supply-demand ischemia with dobutamine alters glucose uptake within the remote myoca

43 proterenol, epinephrine), a partial agonist (dobutamine), an antagonist (alprenolol), and an inverse

44 ring contractility modulation by esmolol and dobutamine and assessed during preload reduction and aft

45 The average dobutamine and atropine doses were 48 microg/kg/min and

46 ant (25%), milrinone-predominant (1%), mixed dobutamine and dopamine pattern (32%), and mixed pattern

47 clusion, and lusitropic state was changed by dobutamine and esmolol infusion.

48 ion, whereas lusitropic state was changed by dobutamine and esmolol infusion.

49 sion with reperfusion up to 1 h, followed by dobutamine and esmolol infusions.

50 Both groups received dopamine or dobutamine and intravenous immunoglobulin.

51 Currently available inotropes, such as dobutamine and milrinone, act (directly or indirectly) b

52 ias and a lower mortality rate compared with dobutamine and milrinone.

53 In two patients receiving dobutamine and one receiving dopamine, tapering or disco

54 est the hypothesis that addition of low-dose dobutamine and quantification of inotropic reserve in se

55 on and fractional area changes compared with dobutamine and saline placebo.

56 e the significance of heart rate response to dobutamine and the assessment of left ventricular (LV) f

57 T abnormality was seen only at high doses of dobutamine and was influenced by the stenosis severity.

58 Nineteen studies (14 vasodilator, 4 dobutamine, and 1 that used both) involved a total of 11

59 thmias, neuropsychiatric symptoms, dosing of dobutamine, and intravenous contrast.

60 conditions (created after baseline by blood, dobutamine, and metoprolol infusion), we compared differ

61 atus of each animal by blood administration, dobutamine, and metoprolol infusion.

62 during intravenous infusion of adenosine and dobutamine, and MP and PI were calculated.

63 s]) by using three stress agents (adenosine, dobutamine, and regadenoson) in three different institut

64 Both dipyridamole and dobutamine are used clinically as pharmacologic stress a

65 It is likely to serve as an alternative to dobutamine as an inotropic agent for management of postr

66 sed maximum systolic pressure in response to dobutamine as measured using implantable telemetry devic

67 jected to beta-adrenergic stress by infusing dobutamine at 5, 10 and 15 mug kg(-1) min(-1) before and

68 20% +/- 5%) was of comparable effect size as dobutamine at a given temperature (hyperthermia: -28% +/

69 ial visualization with echocardiography) for dobutamine/atropine MRI for the detection of inducible i

70 dose, and after peak intravenous infusion of dobutamine/atropine.

71 Reduced dobutamine augmentation of systolic function in cMyBP-C(

72 cardiac function was assessed in response to dobutamine before and after oral sildenafil (100 mg, n=1

73 rong, endothelium-independent relaxations to dobutamine (beta(1)-receptor agonist; 78 +/- 6%; P < 0.0

74 Compared to dobutamine, both nesiritide doses were administered for

75 of LGE or contractile reserve in response to dobutamine can assess the likelihood of recovery of func

76 e of this study was to assess the utility of dobutamine cardiovascular magnetic resonance (DCMR) resu

77 Personnel blinded to dobutamine cardiovascular magnetic resonance followed pa

78 Whereas dobutamine caused a significantly greater increase of PF

79 om contractile reserve was identified during dobutamine challenge (increase in stroke volume >20%), 1

80 ed the HR response of WKY and SH rats during dobutamine challenge and prevented HR recovery at rest.

81 s with a low output and a low mean gradient, dobutamine challenge may aid in selecting those who woul

82 and myocardial ischemia in rats undergoing a dobutamine challenge test, which can be used to mimic ex

83 , and they maintained rate responsiveness to dobutamine challenge.

84 ow established cardiovascular MRI (including dobutamine cine MRI and vasodilator perfusion MRI techni

85 d delayed contrast-enhanced MRI and low-dose dobutamine cine MRI for evaluation of viability.

86 ificantly alter diastolic changes induced by dobutamine compared with results with placebo.

87 ft ventricular dysfunction underwent EMM and dobutamine (D) cardiac magnetic resonance imaging (CMR)

88 Dobutamine decreased the rate of [1-(13)C]acetylcarnitin

89 However, in Scn5a+/DeltaKPQ mice, dobutamine delayed the changes in ventricular repolarisa

90 In particular, dobutamine detection with EC-SERS was found to have a li

91 Surface biotinylation showed that dobutamine did not affect plasma membrane abundance of T

92 However, dobutamine did not alter either pulse pressure variation

93 sine stress, but little data exist regarding dobutamine (Dob) stress or the long-term reproducibility

94 15 min of a high cardiac workload induced by dobutamine (Dob).

95 otropes increased by 193 a year, whereas the dobutamine, dopamine, and milrinone doses used decreased

96 hat of WT abnormality at all but the highest dobutamine dose.

97 ed for bypass surgery underwent preoperative dobutamine echocardiography (DE) and intraoperative myoc

98 ation in man and its comparative accuracy to dobutamine echocardiography (DE) or thallium 201 (Tl(201

99 contrast echocardiography (MCE) and low-dose dobutamine echocardiography (LDDE) in predicting recover

100 Contractile reserve was assessed by dobutamine echocardiography at four weeks in patients wi

101 tenosis as well as the higher sensitivity of dobutamine echocardiography for MVS compared with SVS.

102 Dobutamine echocardiography with hemodynamic measurement

103 Noninvasive tests, such as dobutamine echocardiography, are gaining in favor.

104 photon-emission computed tomography (SPECT), dobutamine echocardiography, or both to assess myocardia

105 when performed in conjunction with low-dose dobutamine echocardiography.

106 raphy, 25% by angiography) were studied with dobutamine echocardiography.

107 he wall-motion index as assessed by means of dobutamine echocardiography.

108 te dehydrogenase flux, and (3) rats in which dobutamine elevated cardiac workload.

109 lusion at all experimental stages (baseline, dobutamine, esmolol) led to a significant decrease (P <

110 taline = zinterol = albuterol > salmeterol > dobutamine > or = ephedrine.

111 The response of systolic strain to low-dose dobutamine has significant promise in discriminating bet

112 The stress ECG and heart rate response to dobutamine have prognostic value and should be incorpora

113 Milrinone was used in 84.8% and dobutamine in 15.2%.

114 th with (99m)Tc-sestamibi SPECT and low-dose dobutamine in canine stunning and subendocardial infarct

115 increased in response to either adenosine or dobutamine in N and HC+S animals.

116 f LV function and the heart rate response to dobutamine in risk stratification of these patients is u

117 to a similar degree as a significant dose of dobutamine in the normal porcine heart.

118 = 6), and during 40 microg x kg x min(-1) of dobutamine in the presence of either one-vessel (Group 2

119 ine and nitrite infusions, Vs and SR at peak dobutamine increased in regions exhibiting ischemia (Vs

120 Dobutamine increased ventricular rate (p < 0.001) and re

121 Phenylephrine, but not dobutamine, increased secretin-stimulated choleresis in

122 rpose of this study was to determine whether dobutamine-induced abnormal stress changes in left ventr

123 del, we tested whether sSR and T(RL) tracked dobutamine-induced changes in regional myocardial perfus

124 gated by examining the drug's suppression of dobutamine-induced increase in myocardial contractility.

125 In those with an LVEF <40%, a dobutamine-induced increase in WMSI does not predict MI

126 to moderate reductions in LVEF (40% to 55%), dobutamine-induced increases in WMSI forecast MI and car

127 on, risk factors for PE, and the presence of dobutamine-induced ischemia, LVSV reserve and the stress

128 S did not change with dobutamine infusion (-17.7 +/- 3.4% versus -18.4 +/- 3.9

129 V hemodynamics and the inotropic response to dobutamine infusion (4 and 16 ng.g(-1).min(-1)) were als

130 2.3+/-1.2 during pacing, P<0.05) and during dobutamine infusion (from 3.0+/-1.0 to 1.7+/-0.6 with do

131 ork) but an attenuated inotropic response to dobutamine infusion (P<0.01 versus WT).

132 espectively), both of which increased during dobutamine infusion (P<0.02 and <0.03, respectively).

133 xcept in highly selected circumstances (2C); dobutamine infusion administered or added to vasopressor

134 inal aortic valve area < or =1.2 cm2 at peak dobutamine infusion and a mean gradient of >30 mm Hg wer

135 increase in cardiac workload for 5 min with dobutamine infusion and aortic constriction.

136 denced by a significantly greater Emax after dobutamine infusion and percentage of contraction in iso

137 rdia, or supraventricular tachycardia during dobutamine infusion between RTCE and DSE.

138 fferent autonomic responses to the stress of dobutamine infusion compared to non-ischaemic (normal) r

139 studied at baseline and at three progressive dobutamine infusion dosages (5, 10, and 20 mug/kg/min).

140 that basal LV +dP/dt was similar, but graded dobutamine infusion was associated with a more robust LV

141 of nitroprusside; and (4) during intravenous dobutamine infusion.

142 served chronotropic response to steady-state dobutamine infusion.

143 ction in healthy pigs and compared them with dobutamine infusion.

144 pressure-volume relations at rest and under dobutamine infusion.

145 ected at rest but was impaired during graded dobutamine infusion.

146 ent states of preload at baseline and during dobutamine infusion.

147 ry time) under baseline, esmolol (2 mg/min), dobutamine infusions (5 microg/kg/min) and following vol

148 fect of age on the responses to steady-state dobutamine infusions is unclear.

149 n patterns were recorded during baseline and dobutamine infusions simultaneous with ventricular press

150 mean arterial pressure > or = 65 mm Hg (1C); dobutamine inotropic therapy when cardiac output remains

151 eplenishment) was seen at the lowest dose of dobutamine irrespective of the stenosis severity, wherea

152 Dobutamine is a commonly used inotropic treatment for CH

153 etheless mandatory because responsiveness to dobutamine is limited with numerous side effects.

154 isease (CAD), but the basis for doing so for dobutamine is not clear.

155 Dobutamine is recommended as the agent of choice to incr

156 Dobutamine is the currently recommended beta-adrenergic

157 effect of supply-demand ischemia induced by dobutamine may increase glucose metabolism within remote

158 tween stress agents (adenosine median, 0.34; dobutamine median, 1.34; regadenoson median, 1.13; P < .

159 evelopment of acute cardiac failure during a dobutamine-mediated stress protocol.

160 troprusside), and intravenous inotropes (ie, dobutamine, milrinone).

161 sodilators in these patients, but the use of dobutamine, milrinone, inhaled nitric oxide, and intrave

162 ous administration of epinephrine (n = 6) or dobutamine (n = 3).

163 of this research was to study the effect of dobutamine on left ventricular (LV) filling in ischemic

164 We also suggest dobutamine or epinephrine in the presence of cardiogenic

165 ocities, at rest and after administration of dobutamine or esmolol.

166 te to high pre-test probability referred for dobutamine or exercise stress echocardiography were pros

167 n-hospital mortality than those treated with dobutamine or milrinone.

168 Randomized Evaluation of Cardiac Ectopy with Dobutamine or Nesiritide Therapy) trial were analyzed.

169 ed in 90% of adenosine studies, but never in dobutamine or regadenoson studies.

170 ion was not changed by prolonged infusion of dobutamine or treatment with a beta-adrenergic antagonis

171 e randomized to treatment with levosimendan, dobutamine, or saline placebo.

172 volume area (i.e., cardiac efficiency) with dobutamine (P = 0.017).

173 ments increased significantly in response to dobutamine (P=0.04), whereas Ecc did not change in nonvi

174 e infusion (from 3.0+/-1.0 to 1.7+/-0.6 with dobutamine, P<0.0001).

175 acyclin, nitric oxide, sildenafil, dopamine, dobutamine, phenylephrine, isoproterenol, and vasopressi

176 spital patterns based on the type of agents: dobutamine-predominant (29% of hospitals), dopamine-pred

177 However, during inotropic stimulation with dobutamine, preload-recruitable stroke work failed to re

178 Levosimendan and dobutamine produced comparable increases in cardiac outp

179 and ex vivo studies, apelin-13 compared with dobutamine provoked distinctive effects on cardiac funct

180 ropic support in RVH is best accomplished by dobutamine, reflecting its better coupling to adenylyl c

181 st, clenbuterol, but not the beta-1 agonist, dobutamine, reinstated cocaine seeking, suggesting that

182 energic receptor agonists (phenylephrine and dobutamine, respectively) on bile and bicarbonate secret

183 p < or = 0.005) compared with milrinone and dobutamine, respectively.

184 In 1%-50% IT, a normal dobutamine response helps differentiate segments with gr

185 ransmurality of late gadolinium enhancement, dobutamine response improves the predictive power of car

186 s who then received sildenafil, their second dobutamine response was significantly blunted, with peak

187 Infusion of the beta-agonist dobutamine resulted in accelerated rates of pressure dev

188 o (risk ratio 0.82 [0.69; 0.97], p = .02) or dobutamine (risk ratio 0.68 [0.52-0.88]; p = .003) as co

189 pressure targets, packed red blood cells or dobutamine should be considered.

190 mary cell cultures with the beta1-AR agonist dobutamine showed enhanced apical-to-basolateral transep

191 c studies show deficits in both baseline and dobutamine-stimulated cardiac function in all of the dys

192 e therefore tested whether sildenafil blunts dobutamine-stimulated cardiac function in humans.

193 Moreover, basal and dobutamine-stimulated cardiac function, measured by tran

194 axation (dP/dt; Tau (1)/2; Tau (1)/e) during dobutamine stimulation (P < 0.01) despite having no infl

195 arameters were measured at baseline and peak dobutamine stimulation before and during the coronary st

196 In the absence of coronary stenosis, dobutamine stimulation caused a significant increase in

197 report on the clinical utility of diagnostic dobutamine stimulation during cardiac catheterization in

198 MBF versus those with preserved RMBF at peak dobutamine stimulation.

199 c resonance spectroscopy) at rest and during dobutamine stress (heart rate increase, 65+/-22% and 69+

200 improvement in myocardial performance during dobutamine stress and a reduction in postischemic stunni

201 systolic and diastolic function, response to dobutamine stress and myocardial fibrosis were assessed.

202 s assessed by exercise stress testing and by dobutamine stress cardiac magnetic resonance imaging.

203 derwent a radionuclide (RN) stress test or a dobutamine stress echocardiogram (DSE).

204 re elevated immediately after a standardized dobutamine stress echocardiogram and decreased after 1 h

205 bnormal blood pressure (BP) responses during dobutamine stress echocardiography (DSE) are associated

206 sought to determine the prognostic value of dobutamine stress echocardiography (DSE) for predicting

207 on analysis (WMA) during submaximal and peak dobutamine stress echocardiography (DSE) for the diagnos

208 ative predictive value (NPV) of preoperative dobutamine stress echocardiography (DSE) in patients who

209 mal myocardial perfusion scintigraphy (MPS), dobutamine stress echocardiography (DSE) or coronary ang

210 eline positron emission tomography (PET) and dobutamine stress echocardiography (DSE) were performed

211 th 1,012 patients who underwent conventional dobutamine stress echocardiography (DSE) without contras

212 ave been performed during low- and high-dose dobutamine stress echocardiography and have been applied

213 armacological radionucleotide stress test or dobutamine stress echocardiography before transplant.

214 ine patients with class III/IV CHF underwent dobutamine stress echocardiography before treatment with

215 diography (RTCE) improves the sensitivity of dobutamine stress echocardiography for detecting coronar

216 s; 53% men) underwent outpatient exercise or dobutamine stress echocardiography for known or suspecte

217 Dobutamine stress echocardiography has been the cornerst

218 e of MP and wall motion (WM) analysis during dobutamine stress echocardiography in predicting the out

219 Dobutamine stress echocardiography is a useful tool for

220 Dobutamine stress echocardiography is a validated tool f

221 Hence, measurement of GLS at rest and during dobutamine stress echocardiography may be helpful to enh

222 Stress GLS measured during dobutamine stress echocardiography may provide increment

223 Data suggest that dobutamine stress echocardiography may underestimate via

224 tudinal strain (GLS) measured at rest and at dobutamine stress echocardiography on the outcome of pat

225 In total, 314 individuals underwent dobutamine stress echocardiography to detect or exclude

226 sured by speckle tracking at rest and during dobutamine stress echocardiography to document the exten

227 tively studied 788 patients with RTCE during dobutamine stress echocardiography using intravenous com

228 GLS <|10|% measured during dobutamine stress echocardiography was also independentl

229 ents with type 2 diabetes mellitus underwent dobutamine stress echocardiography with tissue Doppler i

230 Dobutamine stress echocardiography with use of the wall-

231 dministered in a double-blind fashion during dobutamine stress echocardiography, at separate visits a

232 ardial contractile reserve, as determined by dobutamine stress echocardiography, predicts improvement

233 her non-invasive imaging techniques, such as dobutamine stress echocardiography, radionuclide scintig

234 ons with more established techniques such as dobutamine stress echocardiography, single photon emissi

235 xercise testing, symptom questionnaires, and dobutamine stress echocardiography.

236 Patients underwent exercise treadmill or dobutamine stress echocardiography.

237 a major determinant of cardiac output during dobutamine stress in DCM, and is itself determined by th

238 ase (CAD) on peak cardiac output (CO) during dobutamine stress in patients with dilated cardiomyopath

239 ischemic left ventricular dysfunction during dobutamine stress in patients with type 2 diabetes melli

240 s changes in autonomic modulation induced by dobutamine stress in the presence and absence of myocard

241 and prevents cardiac pump failure induced by dobutamine stress in vivo.

242 In the absence of myocardial ischaemia, dobutamine stress is associated with a residual predomin

243 The sympathetic response to dobutamine stress is augmented as the burden of myocardi

244 g risk stratification of patients undergoing dobutamine stress myocardial perfusion imaging (DSMPI).

245 of this study was to determine the safety of dobutamine stress myocardial perfusion imaging (MPI) obt

246 Dobutamine stress myocardial perfusion imaging has been

247 Dobutamine stress perfusion imaging is an important diag

248 Dobutamine stress revealed a near normal hemodynamic pro

249 Dobutamine stress RTCE appears to be a safe and feasible

250 MP imaging during dobutamine stress RTCE provides incremental prognostic i

251 a four-year period, 1,486 patients underwent dobutamine stress RTCE with low mechanical index pulse s

252 oglycan have reduced survival during in vivo dobutamine stress testing compared to controls.

253 n patients without inducible ischemia during dobutamine stress testing in whom one might otherwise as

254 ement, cardiac magnetic resonance (including dobutamine stress testing), and the Short Form-36 questi

255 An abnormal response to dobutamine stress was identified in the RV of mdx mice a

256 At eight weeks, LV angiograms (rest and dobutamine stress) and histologic analysis were performe

257 During dobutamine stress, heart rate increased from 423 +/- 50

258 Under dobutamine stress, treated animals had smaller LV end-di

259 However, at peak dobutamine stress, VS attenuated the increase in left ve

260 ocardial infarction or death occurred during dobutamine stress.

261 sion, which is particularly important during dobutamine stress.

262 nges in regional myocardial perfusion during dobutamine stress.

263 s are able to predict changes in RMBF during dobutamine stress.

264 ng postischemic from remote myocardium after dobutamine stress.

265 , and WMSI were assessed at rest and at peak dobutamine stress.

266 omparable with those previously reported for dobutamine stress.

267 toperative protocol (fluid, with and without dobutamine) targeted to achieve their individual preoper

268 In the initial dobutamine test, systolic and diastolic function improve

269 layed similar functional responses with both dobutamine tests.

270 Noninvasive dobutamine tissue-tagged MRI with calculation of 3D stra

271 the same segments, those that improved with dobutamine to normal range demonstrated greater improvem

272 We studied 170 patients who underwent dobutamine (up to 50 microg/kg/min)-atropine stress test

273 h a nonstatistically significant increase in dobutamine use (14% vs. 4%, p = .06) and red blood cell

274 Dobutamine use was uncommon.

275 TDI indices increased with administration of dobutamine (v(endo) from 2.2+/-0.3 to 3.8+/-0.2 cm/s [P<

276 The functional response to dobutamine was assessed in vivo by echocardiography.

277 e derivative of left ventricular pressure by dobutamine was blunted by intrapericardial NTG (from 3,9

278 Contractile reserve to dobutamine was depressed (62.3 +/- 0.9 FA versus 49.2 +/

279 In 4 mice, the hemodynamic response to dobutamine was examined by measuring heart rate, cardiac

280 Dobutamine was infused into the right atrium in an amoun

281 Dobutamine was more frequently used in patients with str

282 ncy tissue-tagging at rest and with low-dose dobutamine was performed in 16 normal volunteers and 14

283 In human embryonic kidney (HEK293) cells, dobutamine was shown to stimulate cAMP production, signi

284 expected increase in myosin head transfer by dobutamine was significantly blunted in diabetic animals

285 Dobutamine was superior to dopamine as an RV inotrope, b

286 At each temperature step, IV dobutamine was titrated to double maximum left ventricul

287 Dobutamine was used in 12 (86%) and dopamine in seven (5

288 iac events with normal SE (both exercise and dobutamine) was 127% higher in patients who achieved sub

289 ard events with normal SE (both exercise and dobutamine) was 70% higher in patients who achieved subm

290 s for nesiritide compared with milrinone and dobutamine were 0.59 (95% CI 0.48 to 0.73, p < or = 0.00

291 xation responses to beta-AR stimulation with dobutamine were compromised in externally paced diabetic

292 ved nitroglycerin, nesiritide, milrinone, or dobutamine were identified and reviewed (n = 15,230).

293 Norepinephrine may be combined with dobutamine when cardiac output is being measured.

294 Inotropic effects of AS were additive to dobutamine, whereas DEA/NO blunted beta-stimulation and

295 re development and relaxation in response to dobutamine, whereas expression of phosphor-ablated TnI a

296 d increased activity of TRPV5 in response to dobutamine, which could be prevented by the PKA inhibito

297 trast, infarcted nNOS(-/-) mice responded to dobutamine with a dramatic fall in LV contractility (P<0

298 prognosis animals had a blunted response to dobutamine with respect to stroke volume and kinetic ene

299 rain determination at rest and with low-dose dobutamine would discriminate between viable and nonviab

300 Vasopressor score ([dopamine x 1] + [dobutamine x 1] + [epinephrine x 100] + [norepinephrine