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1 BaCl2 (1 mM) and 4-aminopyridine (2 mM) did not alter th
2 BaCl2 (4 micromol/min, also used in subsequent experimen
3 BaCl2, alone or with ouabain, did not significantly infl
4 channel blocker (ranolazine to block NaV1.5, BaCl2 to block K2P channels) was applied to the solution
5 ither BaCl2 or Caff alone (CTL: 1.1 +/- 0.7, BaCl2: 1.0 +/- 0.7, Caff: 1.3 +/- 0.8 PVCs/injection, P
6 ive at large negative potentials by CsCl and BaCl2, respectively, did not affect DeltaVm, indicating
9 ition of KIR channels and Na(+)/K(+)-ATPase (BaCl2 and ouabain, respectively), and combined inhibitio
13 FBF (area under the curve) was attenuated by BaCl2 (-61+/-3%) and ouabain (-44+/-12%) alone, and this
14 ium equilibrium potential and was blocked by BaCl2 , characteristics of a G protein-coupled inwardly
15 fect of adenosine loading was not blocked by BaCl2 and therefore was not caused by an adenosine-activ
16 elicited recovery from arrhythmia induced by BaCl2, as would be expected from a blockade of NaV1.5.
19 nses to KCl (0.2 mmol/min) were inhibited by BaCl2, alone and plus ouabain, by 60+/-9% and 88+/-6%, r
23 cell AP duration (31.9-139.1 ms) by low-dose BaCl2 generated a wide range of host-donor repolarizatio
24 observed following pretreatment with either BaCl2 or Caff alone (CTL: 1.1 +/- 0.7, BaCl2: 1.0 +/- 0.
26 ed control (saline), KIR channel inhibition (BaCl2), combined inhibition of KIR channels and Na(+)/K(
29 ng the RT profile by perfusion of 50 mumol/L BaCl2 eliminated coupling-induced differences in vulnera
31 gues (60 microM nicotine, 55 mM KCl, or 2 mM BaCl2) resulted in co-release of t-PA in parallel with c
32 luxes were reduced by the addition of 1-5 mM BaCl2 or MgCl2 to the lumenal side, which contained 50 m
33 (CTL) and following pretreatment with 50 muM BaCl2 to reduce IK1, or 200 muM caffeine (Caff) to sensi
35 owever, pretreatment with the combination of BaCl2 + Caff resulted in a significant increase in PVCs
37 , Na(+)/K(+)-ATPase, NO, and prostaglandins (BaCl2, ouabain, L-NMMA [N(G)-monomethyl-L-arginine] and
39 studies are unraveling the reasons why urea, BaCl2, and low ionic strength are required to cleave von
40 response to acidosis was evaluated by using BaCl2 (100 mumol/L, nonspecific potassium channel inhibi
43 -0.7 mm) were produced by cross-linking with BaCl2 without additional poly-L-lysine coating and were
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