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 tor was a combination of norepinephrine plus dobutamine.

5 s performed using regadenoson, adenosine, or dobutamine.

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

7 c and lusitropic response to acute stress by dobutamine.

8 line and the partial agonists salbutamol and dobutamine.

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

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

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

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

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

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

15 restricted to norepinephrine, dopamine, and dobutamine.

16 ological concentrations of norepinephrine or dobutamine.

17 ion versus supply-demand ischemia induced by dobutamine.

18 ation of contractile function in response to dobutamine.

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

20 ing T709D-TRPV5 mutants were unresponsive to dobutamine.

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

22 -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).

23 -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).

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

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

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

27 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

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

29 6 564 (6.1%) heart failure hospitalizations: dobutamine 43%, dopamine 24%, milrinone 17%, or a combin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

47 Both groups received dopamine or dobutamine and intravenous immunoglobulin.

48 Digoxin, dobutamine and isoprenaline caused a significant increas

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

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

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

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

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

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

55 i.v. dopamine, (3) 10 ug kg(-1) min(-1) i.v. dobutamine, and (4) following creation of an intra-atria

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

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

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

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

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

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

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

63 20% +/- 5%) was of comparable effect size as dobutamine at a given temperature (hyperthermia: -28% +/

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

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

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

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

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

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

70 Personnel blinded to dobutamine cardiovascular magnetic resonance followed pa

71 Whereas dobutamine caused a significantly greater increase of PF

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

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

74 , and they maintained rate responsiveness to dobutamine challenge.

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

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

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

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

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

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

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

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

83 However, dobutamine did not alter either pulse pressure variation

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

85 15 min of a high cardiac workload induced by dobutamine (Dob).

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

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

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

89 Dobutamine echocardiography with hemodynamic measurement

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

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

92 single-photon-emission computed tomography, dobutamine echocardiography, or both.

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

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

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

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

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

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

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

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

101 lation and recovery from the sympathomimetic dobutamine HCl, one day after exposure.

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

103 (exercise in 692, dipyridamole in 4291, and dobutamine in 834).

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

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

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

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

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

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

110 sed rats compared to FA during recovery from dobutamine, indicating dysregulation of post-exertional

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

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

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

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

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

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

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

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

119 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

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

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

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

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

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

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

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

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

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

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

130 served chronotropic response to steady-state dobutamine infusion.

131 assessing MVO(2) and MBF at rest and during dobutamine infusion.

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

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

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

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

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

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

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

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

140 Dobutamine is recommended as the agent of choice to incr

141 Dobutamine is the currently recommended beta-adrenergic

142 Six known inotropes were tested: digoxin, dobutamine, isoprenaline, flecainide, verapamil and aten

143 With dobutamine, LV EW, MVO(2), and MBF increased in both HFp

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

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

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

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

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

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

150 exercise, n = 1,288; vasodilator, n = 1,860; dobutamine, n = 262) based on new or worsening RWMA in 2

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

152 upported a connection between the effects of dobutamine on relaxation rate and the expression of prot

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

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

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

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

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

158 cells under sustained application of either dobutamine or omecamtiv mecarbil.

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

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

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

162 gher doses of norepinephrine (p = 0.004) and dobutamine (p = 0.01) and reached higher MAPs (86 +/- 9

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

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

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

166 response to submaximal pharmacologic stress (dobutamine), patients with HFpEF have impairment in left

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

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

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

170 Levosimendan and dobutamine produced comparable increases in cardiac outp

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

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

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

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

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

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

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

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

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

180 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

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

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

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

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

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

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

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

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

189 Dobutamine stimulation did not increase cAMP in USP20-KO

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

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

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

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

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

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

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

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

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

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

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

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

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

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

204 One hundred eighty-three patients underwent dobutamine stress echocardiography before randomization.

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

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

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

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

209 Dobutamine stress echocardiography has been the cornerst

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

211 Dobutamine stress echocardiography is a useful tool for

212 Dobutamine stress echocardiography is a validated tool f

213 Dobutamine stress echocardiography is widely used to tes

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

215 Stress GLS measured during dobutamine stress echocardiography may provide increment

216 Data suggest that dobutamine stress echocardiography may underestimate via

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

218 The degree of ischemia assessed by dobutamine stress echocardiography predicts the placebo-

219 aortic stenosis used as controls) undergoing dobutamine stress echocardiography to assess FR and card

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

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

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

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

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

225 Dobutamine stress echocardiography with use of the wall-

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

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

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

229 n with left ventricular flow reserve (FR) on dobutamine stress echocardiography.

230 Patients underwent exercise treadmill or dobutamine stress echocardiography.

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

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

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

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

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

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

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

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

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

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

241 Dobutamine stress myocardial perfusion imaging has been

242 Dobutamine stress perfusion imaging is an important diag

243 Dobutamine stress revealed a near normal hemodynamic pro

244 Dobutamine stress RTCE appears to be a safe and feasible

245 MP imaging during dobutamine stress RTCE provides incremental prognostic i

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

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

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

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

250 acetate had a larger contractile response to dobutamine stress than non-treated animals.

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

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

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

254 In HFpEF during submaximal dobutamine stress, there is myocardial mechanical-, ener

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

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

257 ocardial infarction or death occurred during dobutamine stress.

258 sion, which is particularly important during dobutamine stress.

259 nges in regional myocardial perfusion during dobutamine stress.

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

261 ng postischemic from remote myocardium after dobutamine stress.

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

263 tine/ATP and CK kinetics, at rest and during dobutamine stress.

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

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

266 layed similar functional responses with both dobutamine tests.

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

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

269 Surprisingly, some dobutamine-treated cardiomyocytes augmented Ca(2+) relea

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

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

272 Dobutamine use was uncommon.

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

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

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

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

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

278 Dobutamine was infused into the right atrium in an amoun

279 Dobutamine was more frequently used in patients with str

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

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

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

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

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

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

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

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

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

289 Variable doses of adenosine combined with dobutamine were administered to induce a wide range of M

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

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

292 n hour, but responses of individual cells to dobutamine were significantly more variable.

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