ライフサイエンスコーパス: nitroprusside

1 of hemodynamic measurements before and after nitroprusside.

2 ndently to bradykinin, adenosine, and sodium nitroprusside.

3 ed dilation without altering the response to nitroprusside.

4 t to endothelium-independent NO donor sodium nitroprusside.

5 elaxation induced by either NS1619 or sodium nitroprusside.

6 micked by the nitric oxide (NO) donor sodium nitroprusside.

7 d to maximal vasodilatation via 28 mM sodium nitroprusside.

8 d to maximal vasodilatation via 28 mm sodium nitroprusside.

9 porine, the Ca(2+).P(i) ion pair, and sodium nitroprusside.

10 and 0.9-microg/kg boluses) of intracoronary nitroprusside.

11 nsfected with CCTeta and treated with sodium nitroprusside.

12 NG-nitro-l-arginine methyl ester and sodium nitroprusside.

13 flow to intra-arterial bradykinin and sodium nitroprusside.

14 relaxation in response to acetylcholine and nitroprusside.

15 in resting muscles with papaverine or sodium nitroprusside.

16 inhibitor, L-NAME, and the NO donor, sodium nitroprusside.

17 abrachial infusions of bradykinin and sodium nitroprusside.

18 (G)-nitro-L-arginine methyl ester and sodium nitroprusside.

19 d differences in the FBF responses to sodium nitroprusside.

20 ficantly influence responses to verapamil or nitroprusside.

21 n endothelium-independent dilation to sodium nitroprusside.

22 ht on how H2S is understood to interact with nitroprusside.

23 clearly show a therapeutic effect of sodium nitroprusside.

24 +/-5 to 29+/-6 mm Hg; P=0.02) increased with nitroprusside.

25 below normal levels by an infusion of sodium nitroprusside.

26 nding, and large intravenous doses of sodium nitroprusside.

27 formed with both intracoronary adenosine and nitroprusside (0.6 microg/kg).

28 of apelin-36, (Pyr(1))apelin-13, and sodium nitroprusside (0.6 nmol/min).

29 Intracoronary nitroprusside (0.9 microg/kg) decreased systolic blood p

30 The responses to sodium nitroprusside (1 microg (100 ml tissue)(-1) min(-1)) wer

31 +/- 0.8 vs. 5.4 +/- 0.8 nl s(1)) with sodium nitroprusside (10 microM) were attenuated >60% (P < 0.05

32 endothelium-independent vasodilator, sodium nitroprusside (10(-4) M), were unchanged pre- and post-C

33 Treatment with PE (10(-5) m) or sodium nitroprusside (10(-5) m) induced a significant increase

34 ereas treatment with PE (10(-5) m) or sodium nitroprusside (10(-5) m) induced a significant increase

35 nin (10(-10.5) to 10(-6.5) mol/L) and sodium nitroprusside (10(-9) to 10(-5) mol/L) was assessed by i

36 rdipine (15%), hydralazine (15%), and sodium nitroprusside (13%).

37 esuscitation-treated animals received sodium nitroprusside (2 mg) after 1 min of cardiopulmonary resu

38 , acetylcholine (5 to 20 microg/min), sodium nitroprusside (2 to 8 microg/min), and verapamil (10 to

39 etylcholine (5 to 20 microg/min), and sodium nitroprusside (2 to 8 microg/min).

40 adykinin (100 to 1,000 pmol/min), and sodium nitroprusside (2 to 8 mug/min).

41 Here we report that NO donors (sodium nitroprusside, 2',2'-(hydroxynitrosohydrazono)bis-ethani

42 st endothelium-dependent function and sodium nitroprusside (20 micro g/min) and adenosine (2.2 mg/min

43 conductance (CVC) at each site (28 mm sodium nitroprusside; 43 degrees C).

44 ized, blinded), with concomitant infusion of nitroprusside (50 microg/min, 6.4 minutes) to increase g

45 was altered by infusions of phenylephrine or nitroprusside (+/-60 mmHg over 60-90 s) in rats treated

46 us -34+/-4%; P=0.01), as was the response to nitroprusside (86+/-21% versus 171+/-22%; P=0.008).

47 ], coinfused with nitric oxide donor, sodium nitroprusside [90 to 900 ng/min]), or a single oral dose

48 Further, humans treated with nitroprusside, a drug that releases nitric oxide and cya

49 c activity of Tanshinone IIA, because sodium nitroprusside, a GSK3beta activator, largely offset its

50 BDL-CSA transport was also reduced by sodium nitroprusside, a NO donor, and by phorbol ester, a prote

51 After the infusion of sodium nitroprusside, a rapid (within 4 hours) improvement of s

52 ation of l-arginine transport whereas sodium nitroprusside activated an outward potassium current.

53 pulmonary resuscitation that includes sodium nitroprusside, active compression-decompression cardiopu

54 matosensory stimulation, the NO donor sodium nitroprusside, added within the range of physiological c

55 measurements compared with adenosine, sodium nitroprusside also appears to be a suitable hyperemic st

56 During hypoxia, nebulized nitroprusside also reduced pulmonary artery pressure fro

57 Neither inhaled nitric oxide nor nebulized nitroprusside altered pH, Pao2, or Paco2.

58 low concentrations of 8-bromo-cGMP or sodium nitroprusside (an NO donor).

59 sumption and vasodilator responses to sodium nitroprusside, an endothelium-independent vasodilator.

60 Sodium nitroprusside, an NO donor as well, also increases iNOS

61 In m Lepr(db) control mice, sodium nitroprusside and acetylcholine induced dose-dependent v

62 endothelium-independent function with sodium nitroprusside and adenosine.

63 The NO donors sodium nitroprusside and dipropylenetriamine NONOate were able

64 inhibited by the NO-liberating agent sodium nitroprusside and dipropylenetriamine NONOate, whereas t

65 During therapy (7.3 +/- 6 days) with sodium nitroprusside and diuresis, hemodynamics improved, eNO c

66 Responses to nitroprusside and L-NMMA were not significantly differen

67 s in Bacillus subtilis was induced by sodium nitroprusside and nitric oxide.

68 es were assessed using sequential boluses of nitroprusside and phenylephrine (modified Oxford techniq

69 Sequential nitroprusside and phenylephrine (modified Oxford test) w

70 two trials of sequential bolus injections of nitroprusside and phenylephrine in 14 young healthy subj

71 during sequential bolus injections of sodium nitroprusside and phenylephrine in 22 young, 21 older se

72 was assessed after administration of sodium nitroprusside and phenylephrine.

73 performed for an AHB-based buffer, and both nitroprusside and Raman tests confirmed the formation of

74 e mimicked by the nitric oxide donors sodium nitroprusside and spermine NONOate, suggesting a role fo

75 aggregation by the nitric oxide donor sodium nitroprusside and the phosphodiesterase 5 inhibitor sild

76 response both to acetylcholine and to sodium nitroprusside and the responses were similar in vessels

77 otected against cell death induced by sodium nitroprusside and TNFalpha plus actinomycin D and preven

78 Nitroprusside and verapamil are more potent than adenosi

79 intravenous vasodilators (ie, nitroglycerin, nitroprusside), and intravenous inotropes (ie, dobutamin

80 er exposure to the nitric oxide donor sodium nitroprusside, and betaine was able to rescue H3K4me3 le

81 a-arterial infusion of acetylcholine, sodium nitroprusside, and N(G)-monomethyl-L-arginine (L-NMMA).

82 r intra-arterial infusions of acetylcholine, nitroprusside, and the NO synthase inhibitor NG-monometh

83 s to selective receptor blockade, adenosine, nitroprusside, and verapamil against the aspirate-induce

84 nfusion of acetylcholine, bradykinin, sodium nitroprusside, and verapamil.

85 110 bpm; (3) during intravenous infusion of nitroprusside; and (4) during intravenous dobutamine inf

86 Sodium nitroprusside, another NO donor also inhibited AIIt-medi

87 utious extrapolation of the use of nebulized nitroprusside as a convenient bridge to inhaled nitric o

88 ce plus abdominal binding and 2 mg of sodium nitroprusside at 1, 4, and 8 minutes of cardiopulmonary

89 After six hours of therapy with nitroprusside (at which time the dose had been increased

90 Importantly, sodium nitroprusside attenuated C. jejuni-induced colitis in Il

91 duced to a similar extent in each group with nitroprusside, but the drop in systemic arterial pressur

92 idence interval, 5 to 48; P=0.01), to sodium nitroprusside by 20% (95% confidence interval, 3 to 40;

93 synaptosomes with H2O2, diamide, and sodium nitroprusside caused aggregation of CaMKII through forma

94 (Pyr(1))apelin-13, acetylcholine, and sodium nitroprusside caused forearm vasodilatation in patients

95 Although bradykinin and sodium nitroprusside caused similar vasodilation, SFLLRN-induce

96 Although sodium nitroprusside caused venodilation (p < 0.0001), apelin-3

97 The effects of rotenone and sodium nitroprusside (complex inhibitors of the respiratory cha

98 (P<0.01), and 5- hydroxytrytamine and sodium nitroprusside did not evoke an increase in coronary flow

99 lation by measuring acetylcholine and sodium nitroprusside dose responses.

100 othelial t-PA release, bradykinin and sodium nitroprusside dose-response curves were repeated in the

101 alf-maximal vasodilation were comparable for nitroprusside (+E, 3.3x10(-8); -E, 1.9x10(-8) mol/L) and

102 Endothelium-independent dilatation to sodium nitroprusside (EID), was not altered by age or sirtinol

103 from fasting blood, skin responses to sodium nitroprusside (endothelium independent) and acetylcholin

104 diopulmonary resuscitation (n = 8) or sodium nitroprusside-enhanced cardiopulmonary resuscitation (n

105 mpedance threshold device (n = 6), or sodium nitroprusside-enhanced cardiopulmonary resuscitation (n

106 domized to three different protocols: sodium nitroprusside-enhanced cardiopulmonary resuscitation (n=

107 Sodium nitroprusside-enhanced cardiopulmonary resuscitation con

108 d untreated ventricular fibrillation, sodium nitroprusside-enhanced cardiopulmonary resuscitation dem

109 The addition of epinephrine to sodium nitroprusside-enhanced cardiopulmonary resuscitation dur

110 This study demonstrates that sodium nitroprusside-enhanced cardiopulmonary resuscitation fac

111 cardiopulmonary resuscitation in the sodium nitroprusside-enhanced cardiopulmonary resuscitation gro

112 cardiopulmonary resuscitation in the sodium nitroprusside-enhanced cardiopulmonary resuscitation gro

113 Sodium nitroprusside-enhanced cardiopulmonary resuscitation inc

114 s with pulseless electrical activity, sodium nitroprusside-enhanced cardiopulmonary resuscitation inc

115 his study was to assess the effect of sodium nitroprusside-enhanced cardiopulmonary resuscitation on

116 and 35+/-5 mL/min in the control and sodium nitroprusside-enhanced cardiopulmonary resuscitation plu

117 cardiopulmonary resuscitation (n=8), sodium nitroprusside-enhanced cardiopulmonary resuscitation plu

118 Control and sodium nitroprusside-enhanced cardiopulmonary resuscitation plu

119 onary resuscitation versus control or sodium nitroprusside-enhanced cardiopulmonary resuscitation plu

120 In pigs, sodium nitroprusside-enhanced cardiopulmonary resuscitation sig

121 re of 35 degrees C was decreased with sodium nitroprusside-enhanced cardiopulmonary resuscitation ver

122 We hypothesize that sodium nitroprusside-enhanced cardiopulmonary resuscitation wil

123 We hypothesized that sodium nitroprusside-enhanced cardiopulmonary resuscitation wou

124 at the addition of epinephrine during sodium nitroprusside-enhanced cardiopulmonary resuscitation wou

125 shold device, and abdominal pressure (sodium nitroprusside-enhanced cardiopulmonary resuscitation) ha

126 hanced cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation+ade

127 tion+adenosine, and controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitation+ade

128 hanced cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation+ade

129 ation+adenosine, or controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitation+ade

130 hanced cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation+ade

131 ation+adenosine, or controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitation+ade

132 ectively (p<.01 for controlled pauses-sodium nitroprusside-enhanced cardiopulmonary resuscitation+ade

133 After 1 min of sodium nitroprusside-enhanced cardiopulmonary resuscitation, ad

134 Sodium nitroprusside-enhanced cardiopulmonary resuscitation, so

135 andard cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation, so

136 andard cardiopulmonary resuscitation, sodium nitroprusside-enhanced cardiopulmonary resuscitation, so

137 ther reduce reperfusion injury during sodium nitroprusside-enhanced cardiopulmonary resuscitation, we

138 Sodium nitroprusside-enhanced cardiopulmonary resuscitation-tre

139 and end-tidal CO2 were increased with sodium nitroprusside-enhanced cardiopulmonary resuscitation.

140 spread throughout the first 3 mins of sodium nitroprusside-enhanced cardiopulmonary resuscitation.

141 In contrast, focal delivery of sodium nitroprusside evoked similar local dilations without Ca(

142 tion of cytosolic guanylyl cyclase by sodium nitroprusside had no effect on Ca2+ efflux, Ca2+ influx,

143 ystemic hemodynamic effects of intracoronary nitroprusside have yet to be determined in humans.

144 did not alter relaxation responses to sodium nitroprusside, iloprost, or the K(+) channel activators

145 to phenylephrine, acetylcholine, and sodium nitroprusside improved after Aza in HHcy mice.

146 We determined the response to intravenous nitroprusside in 25 patients with severe aortic stenosis

147 abrachial infusions of bradykinin and sodium nitroprusside in 33 sedentary adults: 10 normal-weight (

148 h is becoming a viable alternative to sodium nitroprusside in children.

149 ontrary, in 16 hypertensive patients, sodium nitroprusside in equidepressor doses induced a significa

150 ine the acute hemodynamic response to sodium nitroprusside in LGSAS with preserved EF.

151 junction potentials and responses to sodium nitroprusside in murine colonic muscles.

152 nses to vasodilation with intravenous sodium nitroprusside in patients with HFrEF (n = 174) and HFpEF

153 sing bolus doses of phenylephrine and sodium nitroprusside, in anaesthetized male Wistar rats at a co

154 Intracoronary nitroprusside, in doses commonly used for the treatment

155 itroso-N-acetyl-dl-penacillamine, and sodium nitroprusside, inactivated both isoforms in a dose-depen

156 Nitroprusside increased sympathetic outflow significantl

157 In contrast, sodium nitroprusside induced similar relaxations in the two exp

158 Acetylcholine-induced and sodium nitroprusside-induced dilation in resistance arteries wa

159 blunted compared with lean rats, but sodium nitroprusside-induced dilation was comparable.

160 athetic nerve activity response to transient nitroprusside-induced hypotension (53.3 +/- 3.7 vs. 40.1

161 before, during and after a 10 min period of nitroprusside-induced hypotension.

162 and 9 control subjects at rest and during a nitroprusside-induced hypotensive stimulus.

163 After 24 hours of nitroprusside infusion (dose, 128+/-96 microg per minute

164 hange during baseline measurements or during nitroprusside infusion but decreased during pacing (from

165 Under nitroprusside infusion, a neurovascular-coupling inhibit

166 mal vasodilatation achieved via 28 mm sodium nitroprusside infusion.

167 r after bradykinin, acetylcholine and sodium nitroprusside infusions (p < 0.001), but this was unaffe

168 Cs into neurons, whereas the NO donor sodium nitroprusside inhibited NPC proliferation and increased

169 tion, but the nitric oxide (NO) donor sodium nitroprusside initiated biphasic rises.

170 Sodium nitroprusside is one of several agents considered effect

171 Treatment with sodium nitroprusside led to increases in the phosphorylation of

172 lized to maximal CVC (CVCmax, 28.0 mM sodium nitroprusside + local heating to 43 degrees C).

173 zed to maximal CVC (%CVC(max)) (28 mm sodium nitroprusside + local heating to 43 degrees C).

174 However, vasodilators such as nitroprusside may improve myocardial performance if peri

175 d metal-nitrosyl linkage isomerism in sodium nitroprusside (Na(2)[Fe(II)(CN)(5)NO].2H(2)O, SNP) disso

176 ca have recommended consideration for use of nitroprusside, nitroglycerin, or nesiritide in addition

177 Neither injection of the vasodilator sodium nitroprusside nor blood withdrawal from the superior ven

178 oline) and -independent vasodilation (sodium nitroprusside) of isolated, pressurized coronary small a

179 O when adding gas or the (*)NO donor, sodium nitroprusside, on injection into plant leaves, was demon

180 ation of 10(-4) M adenosine, 10(-4) M sodium nitroprusside or 10(-5) M pinacidil directly to capillar

181 CH (P=0.009) but not the responses to sodium nitroprusside or adenosine.

182 +/-5%, P<0.01) but was not altered to sodium nitroprusside or bradykinin.

183 human corneal cells was induced with sodium nitroprusside or camptothecin and activation of prothrom

184 lase-cyclic GMP-protein-kinase-G system with nitroprusside or membrane-permeant cyclic GMP analogs mi

185 Injection of sodium nitroprusside or selective PKG activators into the later

186 n response to stimulation with either sodium nitroprusside or sphingosine 1-phosphate.

187 y treatment with the nitric oxide (NO) donor nitroprusside or the ATP-sensitive potassium (K(ATP)) ch

188 nalyzed in response to phenylephrine, sodium nitroprusside, or acetylcholine with or without inhibito

189 experience a reduction in stroke volume with nitroprusside (p < 0.0001), suggesting greater vulnerabi

190 All measures of afterload were reduced with nitroprusside (P<0.001 for all).

191 (P<0.05), acetylcholine (P<0.05), and sodium nitroprusside (P<0.001) infusions 2 hours after exposure

192 esponse to acetylcholine (P=0.01) and sodium nitroprusside (P=0.004).

193 01) without affecting the response to sodium nitroprusside (P=0.31).

194 ne (P=0.01) but not apelin (P=0.3) or sodium nitroprusside (P=0.9) was attenuated in patients with he

195 ne, combined fetal treatment with L-NAME and nitroprusside prevents generalized vasoconstriction and

196 blunted compared with m Lepr(db), but sodium nitroprusside produced comparable dilation.

197 Intracoronary nitroprusside produced equivalent coronary hyperemia wit

198 bradykinin (BK) were similar, whereas sodium nitroprusside produced maximal dilation locally without

199 Both inhaled nitric oxide and nebulized nitroprusside produced prompt, significant, selective re

200 Compared with adenosine, intracoronary nitroprusside produces an equivalent but more prolonged

201 ule-1 and blood flow responses to L-NMMA and nitroprusside (r=0.53, P=0.004 and r=-0.66, P<0.001, res

202 Nitroprusside rapidly and markedly improves cardiac func

203 In all patients, nitroprusside reduced elastance, left ventricular fillin

204 Treatment with the NO donor sodium nitroprusside reduced levels of HIF-1alpha, whereas NO d

205 Nitroprusside reduced mean pulmonary artery pressure (25

206 Nitroprusside reduces afterload and left ventricular fil

207 extracts showed capacity to scavenge sodium nitroprusside-released nitric oxide (NO), RM being more

208 ent vasodilation to acetylcholine and sodium nitroprusside, respectively.

209 Sodium nitroprusside response was unchanged by all treatments.

210 Conversely, injection of sodium nitroprusside resulted in a positive chronotropic effect

211 onors dipropylenetriamine NONOate and sodium nitroprusside showed opposite effects.

212 upon exposure to H(2)O(2), but not to sodium nitroprusside, SIN-1, and DETA-NO.

213 (20 mM; to inhibit NOS activity) and sodium nitroprusside (SNP 10 microM) were infused by microdialy

214 ction relative to adenosine (ADO) and sodium nitroprusside (SNP) (PE-mediated DeltaFVC: ATP: -16 +/-

215 ects observed upon the application of sodium nitroprusside (SNP) and H2S can be ascribed to the gener

216 ood pressure (BP) induced by stepwise sodium nitroprusside (SNP) and phenylephrine (PhE) infusion.

217 P) induced by intravenous infusion of sodium nitroprusside (SNP) and phenylephrine.

218 Apoptosis was induced by addition of sodium nitroprusside (SNP) at 1-2 mM to >80% confluent primary

219 sulin alone (Control) or insulin plus sodium nitroprusside (SNP) at variable rate to double leg blood

220 a-arterial infusions of ACh, ATP, and sodium nitroprusside (SNP) before and during ascorbic acid (AA)

221 h study day, 3 acetylcholine (ACh) or sodium nitroprusside (SNP) dose-response studies were performed

222 tment blocked, whereas L-arginine and sodium nitroprusside (SNP) each enhanced, EC uptake of fluoresc

223 to examine the safety and efficacy of sodium nitroprusside (SNP) for patients with acute decompensate

224 ical stressor [hemodynamic stress via sodium nitroprusside (SNP) i.v.] on stimulus evoked responses o

225 The NO donor sodium nitroprusside (SNP) increased intracellular Ca(2+) wave

226 ted whether activation of GSK3beta by sodium nitroprusside (SNP) mitigates kidney injury in diabetes.

227 the effects of nitric oxide (NO) and sodium nitroprusside (SNP) on Bacillus subtilis physiology and

228 with control subjects (P=0.002), but sodium nitroprusside (SNP) responses were not (P=0.3).

229 3-morpholinosydnonimine (SIN-1), and sodium nitroprusside (SNP) resulted in apoptotic cell death at

230 Exposure to the NO donor sodium nitroprusside (SNP) showed that high NO levels suppresse

231 ells perished via apoptosis following sodium nitroprusside (SNP) treatment.

232 e endothelium-independent vasodilator sodium nitroprusside (SNP) were examined.

233 ries exposed to authentic ONOO- or to sodium nitroprusside (SNP)+xanthine (XA)+xanthine oxidase (XO).

234 cells and is suppressed by NO donors [sodium nitroprusside (SNP), 3-morpholinosydnonimine-1, and S-ni

235 ) inhibited purified sGC activated by sodium nitroprusside (SNP), a precursor of nitric oxide (NO), e

236 ) recovery was partially inhibited by sodium nitroprusside (SNP), an NO donor, and l-arginine, the en

237 ro-N-acetyl-d,l-penicillamine (SNAP), sodium nitroprusside (SNP), and hydrogen peroxide than were MS

238 dministration of another vasodilator, sodium nitroprusside (SNP), may equally improve CBF and cerebra

239 given a 1-mL bolus injection of GTN, sodium nitroprusside (SNP), or adenosine through a catheter in

240 Here we show that the NO donor, sodium nitroprusside (SNP), rapidly represses c-myc gene transc

241 ulation, but infusion of the NO donor sodium nitroprusside (SNP), so as to similarly reduce baseline

242 tophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP), were negatively correlated with per

243 olus doses of the nitric oxide donor, sodium nitroprusside (SNP), were studied.

244 usion of exogenous NO, in the form of sodium nitroprusside (SNP), would fully restore vasodilatation

245 695, Thr696 and Thr853 in response to sodium nitroprusside (SNP)-induced relaxation in denuded rabbit

246 in human brain endothelial cells with sodium nitroprusside (SNP).

247 ere sensitized by GSK3beta activator, sodium nitroprusside (SNP).

248 ion caused by the nitric oxide donor, sodium nitroprusside (SNP).

249 pplication of acetylcholine (ACh) and sodium nitroprusside (SNP).

250 , 3-morpholinosydnonimine (SIN-1), or sodium nitroprusside (SNP).

251 Microinjection of the NO donor sodium nitroprusside (SNP, 1 mM, 50 nl) at a cardioinhibitory s

252 The NO donor sodium nitroprusside (SNP, 10 mM) stimulates additional cGMP pr

253 trus roots with NaHS (a H2S donor) or sodium nitroprusside (SNP, a NO donor) for 2 days (d) could eli

254 (ACh; 7.5, 15, and 30 microg/min) and sodium nitroprusside (SNP; 0.8,1.6, and 3.2 microg/min) were as

255 oline (ACh; 1 x 10(9)-1 x 10(5)m) and sodium nitroprusside (SNP; 1 x 10(9)-1 x 10(4)m), constrictor r

256 ylpenicillamine (SNAP; 50 microM) and sodium nitroprusside (SNP; 100 microM) did not change the gener

257 In eight subjects increasing doses of sodium nitroprusside (SNP; 8.4 x 10(-6)-8.4 x 10(-3)m) were adm

258 (ACh; endothelium dependent) but not sodium nitroprusside (SNP; endothelium independent).

259 endothelium-independent vasodilator (sodium nitroprusside, SNP), or potassium chloride (KCl) at rest

260 ME); low-dose NO infusion (1.0 microM sodium nitroprusside, SNP); adrenergic blockade (10 mM bretyliu

261 city of vascular smooth muscle cells (sodium nitroprusside; SNP).

262 ore, CCTeta had no effect on basal or sodium nitroprusside-stimulated alphabeta(Cys-105) sGC, a const

263 Sodium nitroprusside stimulation of the cGMP-generating cyclase

264 taneous vasodilatation in response to sodium nitroprusside, suggesting that ET-1 diminishes the dilat

265 fore therapy (A), after initial diuretic and nitroprusside therapy to optimize hemodynamics (B, mean

266 The effect of nitroprusside to antagonize UK 14,304 responses was prev

267 by i.v. injection of phenylephrine or sodium nitroprusside to increase or decrease arterial blood pre

268 c and hemodynamic responses of intracoronary nitroprusside to intracoronary adenosine in patients dur

269 eart received infusion of intravenous sodium nitroprusside to reduce blood pressure and arterial afte

270 t that 1) the ability of the NO donor sodium nitroprusside to reduce blood pressure is impaired in RG

271 ide toxicity and prophylactic measure during nitroprusside treatment, inosine may serve as a biomarke

272 Change in SVI with nitroprusside varied inversely to baseline SVI and demon

273 ne and substance P) and -independent (sodium nitroprusside) vasodilators were measured in eight healt

274 blood pressure (baroreflex activation) with nitroprusside, venous NE concentration increased to the

275 ters was increased to 43 degrees C and 28 mm nitroprusside was infused to achieve maximal vasodilatat

276 The nitric oxide (NO) donor sodium nitroprusside was injected intraperitoneally (2 mg/kg da

277 rt rate to transient hypotension with sodium nitroprusside was normalized by 66% compared with CHF co

278 ls to endothelium-independent agonist sodium nitroprusside was not altered, the endothelium-dependent

279 At the end of each protocol, 56 mm sodium nitroprusside was perfused at microdialysis sites to rai

280 re locally heated to 43 degrees C and sodium nitroprusside was perfused to elicit maximal vasodilatat

281 Maximal relaxation to sodium nitroprusside was similar in aorta from normal and LPS-t

282 ry action of both carbamylcholine and sodium nitroprusside was ultimately dependent on muscarinic rec

283 n to endothelium-independent NO donor sodium nitroprusside was unaffected after all time periods of i

284 e endothelium-independent vasodilator sodium nitroprusside was unaffected by AGE-Glu.

285 dothelium-independent vasodilation to sodium nitroprusside was unaffected.

286 hereas direct vessel relaxation using sodium nitroprusside was unaltered.

287 bitor NG-monomethyl-L-arginine (L-NMMA); and nitroprusside was used to assess sensitivity to nitric o

288 Nitroprusside was well tolerated and had minimal side ef

289 ine or the fall in pressure evoked by sodium nitroprusside, was significantly attenuated in depleted

290 sion of acetylcholine, substance P or sodium nitroprusside were 25 +/- 4, 30 +/- 7 and 29 +/- 5 ml mi

291 elaxation responses to bradykinin and sodium nitroprusside were assessed at days 5 and 10 postinfecti

292 es to intrabrachial acetylcholine and sodium nitroprusside were assessed using venous occlusion pleth

293 FFR measurements with intracoronary nitroprusside were identical to those obtained with intr

294 Acetylcholine and sodium nitroprusside were iontophoresed into the forearm skin.

295 e P, isoproterenol (isoprenaline) and sodium nitroprusside were measured by strain-gauge plethysmogra

296 (P < 0.05) to the nitric oxide donor sodium nitroprusside were reduced in protein-restricted group f

297 ose-response curves to bradykinin and sodium nitroprusside were repeated with a coinfusion of the ant

298 asoactive challenge (acetylcholine or sodium nitroprusside) were quantified in vivo in pigs by electr

299 Responses to acetylcholine, but not sodium nitroprusside, were impaired in patients with diabetes (

300 very strongly induced in response to sodium nitroprusside, which indicates its involvement in stress