ライフサイエンスコーパス: BaCl2

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 Using a BaCl2-induced damage model, we find that RNA toxicity le

7 ive at large negative potentials by CsCl and BaCl2, respectively, did not affect DeltaVm, indicating

8 ning tetraethylammonium chloride (10 mM) and BaCl2, (1 mM).

9 ium (KIR ) channels and Na(+) /K(+) -ATPase (BaCl2 + ouabain).

10 ition of KIR channels and Na(+)/K(+)-ATPase (BaCl2 and ouabain, respectively), and combined inhibitio

11 ons were blocked by the K(+) channel blocker BaCl2 (100 muM, n = 7).

12 elay in AV nodal conduction was abolished by BaCl2 (100 micromol/L).

13 116, a selective m2 mAChR antagonist, and by BaCl2, an antagonist of K(ir) channels.

14 FBF (area under the curve) was attenuated by BaCl2 (-61+/-3%) and ouabain (-44+/-12%) alone, and this

15 ium equilibrium potential and was blocked by BaCl2 , characteristics of a G protein-coupled inwardly

16 fect of adenosine loading was not blocked by BaCl2 and therefore was not caused by an adenosine-activ

17 elicited recovery from arrhythmia induced by BaCl2, as would be expected from a blockade of NaV1.5.

18 At pHo 7.3, ISO was inhibited by BaCl2 (IC50 465 microM), but unaffected by ZnCl2 (100 mi

19 dosis-induced dilation was also inhibited by BaCl2 but not by iberiotoxin.

20 nses to KCl (0.2 mmol/min) were inhibited by BaCl2, alone and plus ouabain, by 60+/-9% and 88+/-6%, r

21 Addition of barium chloride (BaCl2) to the culture further increased Ptx yield.

22 Compared with control, BaCl2 significantly reduced peak FBF (-50+/-6%; P<0.05),

23 .3 +/- 2.8 PVCs/injection, P < 0.05 vs. CTL, BaCl2, Caff).

24 cell AP duration (31.9-139.1 ms) by low-dose BaCl2 generated a wide range of host-donor repolarizatio

25 observed following pretreatment with either BaCl2 or Caff alone (CTL: 1.1 +/- 0.7, BaCl2: 1.0 +/- 0.

26 The permeability of the electrolyte BaCl2 decreased by 54% after G1-NH2 modification using E

27 ed control (saline), KIR channel inhibition (BaCl2), combined inhibition of KIR channels and Na(+)/K(

28 KA channel was blocked by 5 mM intracellular BaCl2 or by 10 nM extracellular iberiotoxin.

29 nd Na(+) /K(+) -ATPase (l-NMMA + ketorolac + BaCl2 + ouabain).

30 ng the RT profile by perfusion of 50 mumol/L BaCl2 eliminated coupling-induced differences in vulnera

31 depolarization with 140 mM [K+]o, or by 1 mM BaCl2.

32 gues (60 microM nicotine, 55 mM KCl, or 2 mM BaCl2) resulted in co-release of t-PA in parallel with c

33 luxes were reduced by the addition of 1-5 mM BaCl2 or MgCl2 to the lumenal side, which contained 50 m

34 (CTL) and following pretreatment with 50 muM BaCl2 to reduce IK1, or 200 muM caffeine (Caff) to sensi

35 tal RH FBF before or after administration of BaCl2 plus ouabain.

36 owever, pretreatment with the combination of BaCl2 + Caff resulted in a significant increase in PVCs

37 us ketorolac; and L-NMMA plus ketorolac plus BaCl2 plus ouabain.

38 , Na(+)/K(+)-ATPase, NO, and prostaglandins (BaCl2, ouabain, L-NMMA [N(G)-monomethyl-L-arginine] and

39 Group 2 received ouabain rather than BaCl2 in the second trial.

40 studies are unraveling the reasons why urea, BaCl2, and low ionic strength are required to cleave von

41 response to acidosis was evaluated by using BaCl2 (100 mumol/L, nonspecific potassium channel inhibi

42 Ouabain (2.7 nmol/min), alone and with BaCl2, reduced flow by 10+/-2% and 28+/-3%, respectively

43 luence on current density when examined with BaCl2 as the charge carrier.

44 -0.7 mm) were produced by cross-linking with BaCl2 without additional poly-L-lysine coating and were

45 Additionally, pretreatment with BaCl2 + Caff led to sustained monomorphic VT arising fro