ライフサイエンスコーパス: nitroglycerin

1 a nitric oxide synthase-independent agonist (nitroglycerin).

2 tal arithmetic, cold pressor, and sublingual nitroglycerin.

3 d by the endothelium-independent vasodilator nitroglycerin.

4 tal mortality was similar for nesiritide and nitroglycerin.

5 s of the initial dose of sublingual or spray nitroglycerin.

6 , 35% (49 of 141) had chest pain relief with nitroglycerin.

7 d administration of 200 microg intracoronary nitroglycerin.

8 g intracoronary adenosine, acetylcholine and nitroglycerin.

9 There were no differences in response to nitroglycerin.

10 -guanosine monophosphate (8-bromo-cGMP), and nitroglycerin.

11 tery relaxation to nitroprusside, but not to nitroglycerin.

12 intracoronary infusions of acetylcholine and nitroglycerin.

13 No therapy improved the dilator response to nitroglycerin.

14 intracoronary but not with intrapericardial nitroglycerin.

15 n of the endothelium-independent vasodilator nitroglycerin.

16 l segments, with trends toward reversal with nitroglycerin.

17 measured after administration of sublingual nitroglycerin.

18 dministration of 200 microg of intracoronary nitroglycerin.

19 s examined using intracoronary adenosine and nitroglycerin.

20 fter the administration of 0.4 mg sublingual nitroglycerin.

21 tanding of the clinical impact of angina and nitroglycerin.

22 ium-independent relaxation was studied using nitroglycerin.

23 in ointment, and intraarterial verapamil and nitroglycerin.

24 e to intracoronary (IC) acetylcholine and IC nitroglycerin.

25 amined by use of intracoronary adenosine and nitroglycerin.

26 nges in systemic hemodynamics were seen with nitroglycerin.

27 Topical application of nitroglycerin (0.1 and 1.0 microM) produced similar dose

28 at rest and during intracoronary infusion of nitroglycerin (0.3 to 0.6 microg.kg(-1).min(-1)).

29 bjects received repeated doses of sublingual nitroglycerin (0.4 mg) after the last dose of placebo or

30 0.3 or 0.5 microgram.kg-1.min-1 intravenous nitroglycerin; 0.0125, 0.025, or 0.1 mg clonidine orally

31 l-penicillamine (10(-4) mol/L, -34+/-5%) and nitroglycerin (10(-4) mol/L, -21+/-5%), also decreased t

32 5%], versus placebo, 224 [40.0%]; >1,000 ml: nitroglycerin, 119 [22.2%], versus placebo, 87 [15.5%];

33 nitroso-N-acetyl-penicillamine (-35+/-7%) or nitroglycerin (-16+/-5%) was not significantly affected

34 ersus placebo, 249 [44.5%]; 500 ml-1,000 ml: nitroglycerin, 180 [33.5%], versus placebo, 224 [40.0%];

35 Intrapericardial nitroglycerin (200 microg) was administered in five York

36 ylcholine (54 microgram over 2 minutes), and nitroglycerin (200 microgram) into the left anterior des

37 o BQ-123 with that elicited by intracoronary nitroglycerin (200 microgram).

38 ylcholine was -1% (range -33% to 28%) and to nitroglycerin 22% (range 0% to 54%).

39 98-1.04], p = 0.393) or blood loss (<500 ml: nitroglycerin, 238 [44.3%], versus placebo, 249 [44.5%];

40 ant difference in likelihood between groups (nitroglycerin, 27 [5.0%], versus placebo, 26 [4.6%]; OR

41 , p = 0.314) or satisfaction with treatment (nitroglycerin, 288 [75.4%], versus placebo, 303 [78.1%];

42 /-5% in both groups) and exogenous NO donor, nitroglycerin (-33+/-7% vs. -30+/-3%).

43 enosine (100 microgram. kg(-1). min(-1)) and nitroglycerin (40 microgram/min).

44 (29 g over 2 days) with background low-dose nitroglycerin (7.2 mg over 2 days) on early cardiac magn

45 was self-administered 2 puffs of sublingual nitroglycerin (800 mug; intervention, N = 543) or placeb

46 es from the CEE group dilated in response to nitroglycerin (9.1+/-2.1%, P<.05 versus control), wherea

47 activation as a fundamental requirement for nitroglycerin action at pharmacologically relevant conce

48 rasonography) were measured before and after nitroglycerin administration (400 mug s/l).

49 MBF in the ischemic microcirculation during nitroglycerin administration occurs in tandem with incre

50 Patients continued to exercise after nitroglycerin administration with less ST-segment depres

51 es after either placebo or 0.8 mg sublingual nitroglycerin administration, followed by repeat SPECT i

52 enosine diphosphate (ADP)) and -independent (nitroglycerin) agonists before and during application of

53 pendent (NMDA and kainate) and -independent (nitroglycerin) agonists in nondiabetic and diabetic rats

54 e therapies improved the dilator response to nitroglycerin (all P>/=0.184).

55 Nitroglycerin also evoked greater mean maximal decreases

56 Vasodilation to nitroglycerin also increased, but this effect did not re

57 the presence of inducible ischemia or use of nitroglycerin, although they were younger and more likel

58 ion), and after sublingual administration of nitroglycerin (an endothelium-independent vasodilator).

59 ugh these vessels showed normal responses to nitroglycerin, an endothelium-independent vasodilator.

60 CAdiam) during a cold pressor test and after nitroglycerin and IMT were measured with ultrasound in 9

61 intracoronary acetylcholine, adenosine, and nitroglycerin and intracoronary ultrasound at the time o

62 poxic vasodilation and to the bioactivity of nitroglycerin and mediates the cardiovascular protective

63 nd endothelium-independent vasodilation with nitroglycerin and sodium nitroprusside were studied befo

64 perties that also potentiates the effects of nitroglycerin and thus represents a potentially benefici

65 HS was not triggered by nitroglycerin and was unaffected by sumatriptan, dihydro

66 inistration of acetylcholine, adenosine, and nitroglycerin and were then followed up for clinical out

67 ve carbon regions to the target contaminant (nitroglycerin) and degradation by sulfur-based intermedi

68 act readily with glycerin trinitrate (GTN ) (nitroglycerin) and propylene dinitrate, with rate consta

69 namics and symptoms at 3 hours compared with nitroglycerin, and has been added to the therapeutic arm

70 , wild-type controls stopped vasodilating to nitroglycerin, and the vascular sensitivity to nitroglyc

71 by the most commonly used antianginal drug, nitroglycerin, are incompletely understood.

72 The physiological effects of nitroglycerin as a potent vasodilator have long been doc

73 Nitroglycerin as needed and a beta- or calcium-channel b

74 ylcholine, the calcium ionophore A23187, and nitroglycerin, as well as superoxide production and NO s

75 In response to nitroglycerin at 4, 8, and 24 h, standing systolic BP fe

76 0.05), with no difference in the response to nitroglycerin at 48, 72, and 96 h (p > 0.2).

77 s mainly considered to be an alternative for nitroglycerin, because it has fewer side-effects, and it

78 in implants in response to acetylcholine and nitroglycerin before and following topical application o

79 lar effect, cardiomyocytes were treated with nitroglycerin before H-R.

80 a nitric oxide synthase-independent agonist (nitroglycerin) before and during application of superoxi

81 consisting of aspirin, intravenous heparin, nitroglycerin, beta-blockers, and analgesics.

82 eased by infusion of diethylamine/NONOate or nitroglycerin but was unaffected by Angeli's salt.

83 muscle cells or isolated blood vessels with nitroglycerin caused PKG1alpha disulfide dimerization.

84 Administration of nitroglycerin causes changes in the systemic and coronar

85 ntively deficient in hypotensive response to nitroglycerin compared with wild-type littermates as mea

86 vs. 3.31 +/- 0.22 on placebo; p = 0.028) and nitroglycerin consumption (2.03 +/- 0.20 on ranolazine v

87 versus 3.5+/-1.2 episodes/week) and reduced nitroglycerin consumption (33.8+/-2.3 versus 4.1+/-1.5 t

88 cy averaged 5.63 +/- 0.18 episodes/week, and nitroglycerin consumption averaged 4.72 +/- 0.21 tablets

89 ignificantly reduced frequency of angina and nitroglycerin consumption compared with placebo and was

90 Efficacy was also assessed by nitroglycerin consumption per week and the Seattle Angin

91 gesics, adrenergics, proton-pump inhibitors, nitroglycerin, diazepam, metoclopramide, acetylcysteine

92 ercept or attenuation of liver ischemia with nitroglycerin did not decrease this hepatic stellate cel

93 Responses to adenosine and nitroglycerin did not differ significantly.

94 dothelium-independent dilatation (sublingual nitroglycerin) did not differ among the groups at baseli

95 lium-independent dilatation (EID; sublingual nitroglycerin) did not differ between groups.

96 ere was no association between epicardial IC-nitroglycerin dilation and outcomes.

97 S, 100 U/mL of heparin, and 250 microg/mL of nitroglycerin eliminated infusion-related infarction.

98 ium-dependent dilation) and after sublingual nitroglycerin (endothelium-independent dilation).

99 um-dependent vasodilation) and to sublingual nitroglycerin (endothelium-independent vasodilation).

100 Nitroglycerin-enhanced coronary MRA can noninvasively me

101 bute to the powerful antiischemic effects of nitroglycerin, especially during low-flow states.

102 Compared with the dilation from nitroglycerin, ET-1 contributed to 39% of the coronary t

103 However, the molecular mechanisms by which nitroglycerin exerts its biological functions are still

104 Sublingual nitroglycerin, given to five subjects with angina while

105 n of 1,2-glyceryl dinitrate and nitrite from nitroglycerin (glyceryl trinitrate [GTN]) within mitocho

106 ity of the cellular mechanisms through which nitroglycerin (glyceryl trinitrate, GTN) elicits nitric

107 ase-2 (ALDH2) catalyzes the bioactivation of nitroglycerin (glyceryl trinitrate, GTN) in blood vessel

108 Nitroglycerin (glyceryl trinitrate, GTN), originally man

109 e headache 4-6 h after infusing the NO donor nitroglycerin [glyceryl trinitrate (GTN)] to migraineurs

110 ministration were reported more often in the nitroglycerin group (36 [9.8%] versus 15 [4.0%], OR 2.60

111 sGC was only activated 67-fold by nitroglycerin (GTN) and Cys; and in the absence of Cys,

112 Nitrates such as nitroglycerin (GTN) and nitric oxide donors such as S-ni

113 ltured porcine aortic endothelial cells with nitroglycerin (GTN) or 1H-[1,2,4]-oxadiazolo[4,3-a]quino

114 scular bioactivation of the antianginal drug nitroglycerin (GTN) to yield nitric oxide (NO) or a rela

115 scular bioactivation of the antianginal drug nitroglycerin (GTN), resulting in activation of soluble

116 iethylamine/NONOate nor the nitrovasodilator nitroglycerin had an appreciable effect on basal levels.

117 Although nitroglycerin has remained in clinical use since 1879, t

118 interval [CI], 1.25-2.38), particularly oral nitroglycerin (HR, 1.81; 95% CI, 1.14-2.90), was associa

119 We hypothesized that nitroglycerin improves O2 delivery to ischemic tissue by

120 not alter responses of the basilar artery to nitroglycerin in alcohol-fed rats, and did not alter res

121 point was the rate of increase (>=3%) after nitroglycerin in mean lumen diameter of the in-stent/sca

122 ge in the E/A' ratio after administration of nitroglycerin in patients with a high versus a normal pr

123 The use of nitroglycerin in the treatment of angina pectoris began

124 he release of NO from nitroprusside, but not nitroglycerin, in calf pulmonary artery.

125 Nitroglycerin, in the absence of supplemental ascorbate,

126 Clonidine and nitroglycerin increased gastric compliance, but normal p

127 The belief that chest pain relief with nitroglycerin indicates the presence of active coronary

128 BF, as an index of synaptic activity, during nitroglycerin-induced cluster headache attacks in nine p

129 iated dilatation (endothelium dependent) and nitroglycerin-induced dilatation (endothelium independen

130 steine were measured at each time point, and nitroglycerin-induced dilatation at was assessed at 0, 1

131 Nitroglycerin-induced dilatation was unchanged after bot

132 Nitroglycerin-induced dilatation was unchanged by oral h

133 ed dilation (FMD; endothelium dependent) and nitroglycerin-induced dilation (NID; endothelium indepen

134 ion had no effect on endothelium-independent nitroglycerin-induced dilation.

135 7 +/- 1.6%, p < 0.02), with no difference in nitroglycerin-induced endothelium-independent vasodilata

136 kedly blunted in TG mice in response to both nitroglycerin-induced hypotension and phenylephrine-indu

137 The nitroglycerin-induced increase in tissue Po2 was disprop

138 In contrast, no significant difference in nitroglycerin-induced vascular relaxation as well as nor

139 om knock-ins were markedly less sensitive to nitroglycerin-induced vasodilation (EC(50)=39.2 +/- 10.7

140 establish whether kinase oxidation underlies nitroglycerin-induced vasodilation in vivo, we used a Cy

141 We hypothesized that nitroglycerin-induced vasodilation is mediated by disulf

142 Clinical Dementia Rating scores) and FMD and nitroglycerin-induced vasodilation of the brachial arter

143 lfide formation is a significant mediator of nitroglycerin-induced vasodilation, and tolerance to nit

144 rce of NO responsible for low-dose (1-10 nM) nitroglycerin-induced vasorelaxation.

145 Flow-mediated, endothelium-dependent and nitroglycerin-induced, endothelium-independent vasodilat

146 With background nitroglycerin infusion administered to all patients, tho

147 oline infusion) and endothelium-independent (nitroglycerin infusion) vasodilation of the radial arter

148 nistration of milrinone, norepinephrine, and nitroglycerin infusions.

149 ary diameter measurement after intracoronary nitroglycerin injection 5, 20, and 35 mm distal to the s

150 dothelium-dependent cases; and intracoronary nitroglycerin injection for endothelium-independent case

151 Bypass time, intravenous nitroglycerin injections, or myocardial infarction in th

152 Nitroglycerin is a nitric oxide donor that exerts potent

153 cerin-induced vasodilation, and tolerance to nitroglycerin is associated with loss of kinase oxidatio

154 s NAC administered with low-dose intravenous nitroglycerin is associated with reduced infarct size in

155 gastrointestinal tract, and the skin; thus, nitroglycerin is available in a number of preparations f

156 In this study, we found that nitroglycerin is neither clinically effective nor cost-e

157 interaction between tadalafil and sublingual nitroglycerin lasted 24 h, but was not seen at 48 h and

158 Isosorbide dinitrate and nitroglycerin markedly inhibited KCl contractions (47 +/

159 brachial artery diameter (flow mediated and nitroglycerin mediated), with the particulate pollutant

160 mediated (-10.7%; 95% CI, -17.3 to -3.5) and nitroglycerin-mediated (-5.4%; 95% CI, -10.5 to -0.1) va

161 dilatation (FMD) and endothelial-independent nitroglycerin-mediated dilatation (NMD).

162 ial stiffness, flow-mediated dilation (FMD), nitroglycerin-mediated dilation (GMD), urinary nitric ox

163 tests (VFTs): flow-mediated dilation (FMD), nitroglycerin-mediated dilation (NMD), carotid-femoral p

164 ediated dilation (FMD)] and before and after nitroglycerin-mediated dilation (NMD).

165 vity, we examined flow-mediated dilation and nitroglycerin-mediated dilation in 73 healthy subjects (

166 e no differences in median flow-mediated and nitroglycerin-mediated dilation or CPT of the brachial a

167 Nitroglycerin-mediated dilation was also significantly l

168 d brachial artery flow-mediated dilation and nitroglycerin-mediated dilation were determined by ultra

169 hial artery flow-mediated dilation (FMD) and nitroglycerin-mediated dilation were determined in women

170 21.7 to -2.4), and PM2.5 was associated with nitroglycerin-mediated reactivity (-7.6%; 95% CI, -12.8

171 Flow- and nitroglycerin-mediated reactivity of the brachial artery

172 At baseline, nitroglycerin-mediated vasodilation also was impaired (1

173 No differences were found in nitroglycerin-mediated vasodilation and in vitro ET-1 pr

174 y, flow-mediated, endothelium-dependent, and nitroglycerin-mediated, endothelium-independent vasodila

175 nd chronic cephalic allodynia in the chronic nitroglycerin model, an effect that was lost in Dlx-DOR

176 d efficacy of a novel formulation of topical nitroglycerin, MQX-503, in the treatment of RP in an amb

177 reinjection in 80% of patients who received nitroglycerin (n = 20) compared with 40% of the patients

178 Cases in which patients received nitroglycerin, nesiritide, milrinone, or dobutamine were

179 Nitroglycerin (NG) and nitrocellulose (NC) are constitue

180 1,3,5-trimethylene-2,4,6-trinitramine (RDX), nitroglycerin (NG) and pentaerythritol tetranitrate (PET

181 species of Pseudomonas capable of utilizing nitroglycerin (NG) as a sole nitrogen source were isolat

182 P. fluorescens I-C that removed nitrite from nitroglycerin (NG) by cleavage of the nitroester bond we

183 An IMS spectrum of nitroglycerin (NG) was obtained utilizing RIIN for trand

184 uene (2,6-DNT), 2,4,6-trinitrotoluene (TNT), nitroglycerin (NG), 1,3,5-trinitroperhydro-1,3,5-triazin

185 ith diuretics, intravenous vasodilators (ie, nitroglycerin, nitroprusside), and intravenous inotropes

186 ol) or treated by direct LAD infusion of (i) nitroglycerin (NTG) (0.5 microg.kg(-1).min(-1)); (ii) 8-

187 of continuous transdermal administration of nitroglycerin (NTG) (10 mg/24 hours) on platelet free ra

188 1.3 vs. 2.4%, p = 0.014) and vasodilation to nitroglycerin (NTG) (13.0 vs. 17.8%, p < 0.05) were sign

189 This study was conducted to compare nitroglycerin (NTG) 0.4% ointment with placebo for pain

190 Intracoronary nitroglycerin (NTG) administered to five dogs revealed a

191 ects of high-dose (50 to 100 mg) transdermal nitroglycerin (NTG) and placebo given daily for 12 hours

192 nd endothelium-independent vasodilation with nitroglycerin (NTG) and sodium nitroprusside (SNP) befor

193 Sildenafil and nitroglycerin (NTG) are vasodilator agents that may affe

194 The efficacy of nitroglycerin (NTG) as a vasodilator is limited by toler

195 e antiarrhythmic effects of intrapericardial nitroglycerin (NTG) during acute myocardial ischemia in

196 A 60-minute intravenous (IV) infusion of nitroglycerin (NTG) ending 1 hour before occlusion reduc

197 Nitroglycerin (NTG) improves myocardial perfusion, reduc

198 Nitroglycerin (NTG) induces delayed preconditioning (PC)

199 dralazine (HYD) alone or in combination with nitroglycerin (NTG) or isosorbide dinitrate restores Ca(

200 to receive a 4-hour intravenous infusion of nitroglycerin (NTG) or normal saline; on the following d

201 -month) efficacy of intermittent transdermal nitroglycerin (NTG) patches on LV remodeling in 291 surv

202 We have previously shown that nitroglycerin (NTG) therapy increases vascular expressio

203 d the hypothesis that chronic treatment with nitroglycerin (NTG) to induce nitrate tolerance, which i

204 Ten healthy male subjects received nitroglycerin (NTG) transdermally at a dosage of 0.4 mg/

205 esponse to sublingual (SL) administration of nitroglycerin (NTG) was evaluated at baseline and at 2 a

206 he brachial artery to flow and to sublingual nitroglycerin (NTG) was recorded (conduit vessel respons

207 Nitroglycerin (NTG), a nitric oxide (NO) donor, has been

208 ediated dilation (FMD), and flow-independent nitroglycerin (NTG)-mediated dilation and vasoreactivity

209 Nitroglycerin (NTG)-triggered central sensitization (CS)

210 m) was performed before and after sublingual nitroglycerin (NTG).

211 nduced by an NO donor diethylamine(DEA)NO or nitroglycerin (NTG).

212 in a canine model of CHF and compared it to nitroglycerin (NTG).

213 and following smooth muscle relaxation with nitroglycerin (NTG).

214 on (FMD) and the dilatation after sublingual nitroglycerin (NTG, 25 microgram) were measured by using

215 atients had significant reduction in angina (nitroglycerin [NTG] use=53.9+/-10.0/wk pre-GTx versus 9.

216 and endothelium-independent vasodilation to nitroglycerin of both axillary arteries were measured.

217 pressors: intraosseous phentolamine, topical nitroglycerin ointment, and intraarterial verapamil and

218 ffects of intrapericardial and intracoronary nitroglycerin on coronary cross-sectional area as assess

219 The effects of intracoronary nitroglycerin on coronary luminal area were used for com

220 Occlusion failed to respond to nitroglycerin or balloon dilation, and stenting was requ

221 Patients who received intravenous nitroglycerin or nesiritide had lower in-hospital mortal

222 omenon resulting from continuous exposure to nitroglycerin or other nitrovasodilators.

223 images were similar in patients who received nitroglycerin or placebo.

224 for blood exposed in vitro to 0.1 micromol/L nitroglycerin or the NO donor SNAP, as compared with con

225 nded consideration for use of nitroprusside, nitroglycerin, or nesiritide in addition to diuretics to

226 s (Valsalva maneuver, abdominal compression, nitroglycerin, or vena caval obstruction).

227 ients with or without chest pain relief with nitroglycerin (P > 0.2).

228 ) to the endothelium-independent vasodilator nitroglycerin (p=0.003).

229 in response to acetylcholine (P=0.0006) and nitroglycerin (P=0.04).

230 t further augmented by the administration of nitroglycerin (P=0.648).

231 Application of transdermal nitroglycerin patches or treatment with L-arginine did n

232 025, or 0.1 mg clonidine orally; or combined nitroglycerin plus clonidine.

233 .50+/-4.1%, respectively; P<0.0001), whereas nitroglycerin produced similar vasodilation (14.2+/-5.7%

234 Clonidine but not nitroglycerin reduced aggregate and pain perception aver

235 Nitroglycerin reduced cPP by 10.0 +/- 6.0 mm Hg (p < 0.0

236 -dependent increase in esterase activity and nitroglycerin reductase activity upon addition of coenzy

237 Whereas nitroglycerin reduction occurred in an electrochemical c

238 Nitroglycerin relaxes the stomach without altering perce

239 Nitroglycerin relieved chest pain in 39% of patients (18

240 and -independent agonists (acetylcholine and nitroglycerin, respectively) into the ipsilateral femora

241 ameter in response to reactive hyperemia and nitroglycerin, respectively.

242 holine response (r=0.49, P<0.05) but not the nitroglycerin response (r=0.13, P>0.05).

243 3.2+/-0.8%, P=0.03) but had no effect on the nitroglycerin response.

244 Nitroglycerin responses are not enhanced, but SNP-mediat

245 Infusion of nitroglycerin resulted in a 1.8-fold increase in flow be

246 edistribution images, 58% of those receiving nitroglycerin showed improved reversibility after reinje

247 y records of angina frequency and sublingual nitroglycerin (SL NTG) use.

248 at 10 PM and to note symptoms and sublingual nitroglycerin (SL-NTG) use in a diary.

249 HF-HP patients received nitric oxide donors (nitroglycerin/sodium nitroprusside).

250 he trial was to determine whether sublingual nitroglycerin spray was clinically effective and cost-ef

251 OTC had no effect on arterial dilation to nitroglycerin, systemic blood pressure, heart rate, or r

252 uate the effects of intermittent transdermal nitroglycerin (TD-NTG) on the occurrence of ischemia dur

253 Vasodilation to nitroglycerin tended to be lower in the OSAS group (78.6

254 termining nitro compounds of interest (e.g., nitroglycerin) that have poor UV chromophores.

255 tely 7.5 orders of magnitude from 0.05 h for nitroglycerin to 2 x 10(6) h for 2,3,4,5,2',3',5',6'-oct

256 atients more frequently required intravenous nitroglycerin to control the index episode of chest pain

257 Enzymatic pathways converting nitroglycerin to vasoactive compounds have been identifi

258 We used glyceryl trinitrate (nitroglycerin) to trigger premonitory symptoms and migra

259 dmitted for chest pain, relief of pain after nitroglycerin treatment does not predict active coronary

260 creased in wild-type mouse aortas by in vivo nitroglycerin treatment, but this oxidation was lost as

261 With nitroglycerin treatment, similar to SIN-1 treatment, myo

262 ethanol metabolism and decreased efficacy of nitroglycerin treatment.

263 Here, we demonstrate that nitroglycerin triggers constitutive nitric oxide synthas

264 Nitroglycerin undergoes metabolism that generates severa

265 Nitroglycerin usage decreased in active CP but did not c

266 sion, average daily anginal attack count and nitroglycerin usage.

267 es, p = 0.008), as was the weekly sublingual nitroglycerin use (1.7 [95% CI: 1.6 to 1.9] doses vs. 2.

268 ts, ranolazine reduced angina and sublingual nitroglycerin use and was well tolerated.

269 Ranolazine reduced angina attacks and nitroglycerin use by about 1 per week vs placebo (P<.02)

270 bo on weekly angina frequency and sublingual nitroglycerin use in subjects with type 2 diabetes melli

271 s, time to angina, or frequency of angina or nitroglycerin use were noted between groups.

272 Anginal episodes and nitroglycerin use were recorded with daily entry into a

273 significant reductions of angina frequency, nitroglycerin use, and SAQ angina frequency for patients

274 wal due to adverse events, angina frequency, nitroglycerin use, or exercise duration.

275 ia flow-mediated dilation) and -independent (nitroglycerin) vascular responses of the brachial artery

276 s (primary clinical outcome, 505 [93.3%] for nitroglycerin versus 518 [92.0%] for placebo, odds ratio

277 The adjusted OR for nesiritide compared with nitroglycerin was 0.94 (95% CI 0.77 to 1.16, p = 0.58).

278 s they developed limiting angina, sublingual nitroglycerin was administered to half the patients, and

279 Intrapericardial nitroglycerin was associated with a mean 31.7% increase

280 In contrast, intracoronary nitroglycerin was associated with a smaller mean increas

281 troglycerin, and the vascular sensitivity to nitroglycerin was decreased, whereas this tolerance phen

282 Nitroglycerin was detected in soil and water samples fro

283 although the sensitivity of radial artery to nitroglycerin was greater (EC(50)=33+/-7 nmol/L) than th

284 an established contraction (KCl 40 mmol/L); nitroglycerin was most effective in reversing RA contrac

285 Vascular cGMP in response to 0.1 micromol/L nitroglycerin was significantly higher in the radial art

286 reas endothelium-independent vasodilation to nitroglycerin was similar in both groups.

287 reas endothelium-independent vasodilation to nitroglycerin was similar in both groups.

288 atation of the basilar artery in response to nitroglycerin was similar in insulin treated diabetic ra

289 atation of the basilar artery in response to nitroglycerin was similar in non-alcohol-fed and alcohol

290 Maximum relaxation of all vessels to nitroglycerin was similar, although the sensitivity of r

291 tic nitrate ester, glycerol trinitrate (GTN, nitroglycerin), was examined using cultured plant cells

292 x vivo in response to acetylcholine, but not nitroglycerin, was inhibited by transduction of dn-Akt t

293 iated pain using the human migraine trigger, nitroglycerin, we observed increased expression of DOR i

294 factor and propensity score-adjusted ORs for nitroglycerin were 0.69 (95% confidence interval [CI] 0.

295 Nifedipine, isosorbide, and nitroglycerin were further evaluated for the ability to

296 uctions in MVO2 in response to diltiazem and nitroglycerin were not altered by inhibiting NO.

297 Dose-response curves to bradykinin and nitroglycerin were obtained from 12 subjects with OSAS a

298 to phenylephrine, acetylcholine, A23187 and nitroglycerin were studied in organ baths.

299 and an endothelium-independent vasodilator, nitroglycerin, were determined.

300 e achieved with intrapericardial delivery of nitroglycerin without systemic hypotension.