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1 onium) or a drop in arterial blood pressure (nitroglycerine).
2  phenylephrine, phentolamine, labetalol, and nitroglycerine.
3                               Preclinically, nitroglycerine activates the underlying neural mechanism
4 ial pacing induced vasoconstriction, whereas nitroglycerine administration resulted in significant va
5 e injected into the portal circulation after nitroglycerine administration, they penetrated more dist
6  explosives including PETN, tetryl, RDX, and nitroglycerine along with various compositions containin
7 al nailfold capillaries after application of nitroglycerine and brimonidine.
8 r (nifedipine), and splanchnic vasodilators (nitroglycerine, calcitonin gene-related peptide [CGRP],
9                      These data suggest that nitroglycerine can be used as an effective and reliable
10                               Preclinically, nitroglycerine caused an increase in ongoing firing and
11                                              Nitroglycerine did not meaningfully increase intrapulmon
12 y cranial-evoked sensitivity, in response to nitroglycerine followed by triptan treatment.
13 herapy using a calcium channel antagonist or nitroglycerine, followed by botulinum toxin and, less fr
14                                              Nitroglycerine increased both hepatic and splenic blood
15           Pretreatment with phentolamine and nitroglycerine increased transplanted cell entry in live
16  that mice lacking TRESK develop exaggerated nitroglycerine-induced mechanical and thermal hyperalges
17                                              Nitroglycerine-induced relaxation was associated with a
18                                              Nitroglycerine-induced relaxation was associated with a
19  versus old) with no apparent differences in nitroglycerine-induced relaxation.
20  phosphorylation and Ca2+, partially mediate nitroglycerine-induced relaxation.
21 f TNT without false positives from traces of nitroglycerine is possible.
22  hemodynamic instability, shock, intravenous nitroglycerine, left-ventricular hypertrophy, sustained
23 n blood flow before and after application of nitroglycerine (mean difference, 0.035; 95% CI, 0.008-0.
24 that disappeared after the administration of nitroglycerine (NTG).
25                   By contrast, direct-acting nitroglycerine or prostacyclin improved cell engraftment
26 reased, whereas treatment with L-arginine or nitroglycerine patches decreased AR activity and sorbito
27 tment with L-arginine (a precursor of NO) or nitroglycerine patches prevented sorbitol accumulation.
28 ministration of phentolamine, labetalol, and nitroglycerine prevented the phenylephrine-induced chang
29                      Vascular drugs, such as nitroglycerine, prostacyclin, and bosentan, offer opport
30                          When homogenates of nitroglycerine-relaxed tissues were centrifuged at 6000
31 itance is regulated by alpha-adrenergic- and nitroglycerine-responsive elements.
32                            Using the chronic nitroglycerine rodent migraine model, we demonstrate tha
33 f TNT is sufficiently different from that of nitroglycerine so that unambiguous detection of TNT with
34                                        Using nitroglycerine to trigger migraine attacks, we investiga
35                                  However, in nitroglycerine-treated animals, sinusoidal blood flow wa
36 icacy parameters including angina frequency, nitroglycerine usage, exercise time, and Canadian Cardio
37                    Nitrovasodilators such as nitroglycerine, via production of nitric oxide and an in
38  impairment in response to acetylcholine and nitroglycerine was prevented by AG treatment (P < 0.005)