ライフサイエンスコーパス: hyperkalemic

1 K(+)), AS(-/-) mice decompensated and became hyperkalemic.

2 hemic tissue atrial segment exposed to cold, hyperkalemic blood cardioplegia (mean, 60 minutes) and a

3 cyte contractile function when compared with hyperkalemic cardioplegia (58+/-4 microm/s, P<.05).

4 l channel blockade, myocytes were exposed to hyperkalemic cardioplegia (stress) with and without a K(

5 Hyperkalemic cardioplegia and rewarming caused a signifi

6 Hyperkalemic cardioplegia has been the gold standard for

7 free Ca2+ increased from normothermia during hyperkalemic cardioplegia in control (81+/-4 to 145+/-7

8 Hypothermic hyperkalemic cardioplegia results in significant myocyte

9 tress, similar to that previously noted with hyperkalemic cardioplegia, but did not alter volume chan

10 re media for 2 hours at 37 degrees C (n=60); hyperkalemic cardioplegia, incubation for 2 hours in hyp

11 Stress (exposure to hyperkalemic cardioplegia, metabolic inhibition, or osmo

12 kade (5-hydroxydecanoate) during exposure to hyperkalemic cardioplegia.

13 otassium (sK(ATP)) channel after exposure to hyperkalemic cardioplegia.

14 Endothelin-1 (ET-1) is released after hyperkalemic cardioplegic arrest (CA) and reperfusion an

15 ocytes (32+/-1 versus 22+/-1 microm/s) after hyperkalemic cardioplegic arrest (P<.05).

16 ventricular (LV) dysfunction can occur after hyperkalemic cardioplegic arrest and subsequent reperfus

17 ocyte intracellular calcium increased during hyperkalemic cardioplegic arrest compared with baseline

18 determine whether PCO supplementation during hyperkalemic cardioplegic arrest would provide protectiv

19 er risk for decreased LV contractility after hyperkalemic cardioplegic arrest.

20 legia, incubation for 2 hours in hypothermic hyperkalemic cardioplegic solution (n=60); or PCO/cardio

21 Hypothermic hyperkalemic cardioplegic solutions are currently used f

22 sterone levels detected under hypovolemic or hyperkalemic challenge can lead to increased or decrease

23 d after CP from an atrial segment exposed to hyperkalemic cold blood CP (mean CP time, 58 minutes) fo

24 B and hearts were arrested for 1 hour with a hyperkalemic, cold blood cardioplegic solution.

25 ed by 60 minutes of intermittent 4 degrees C hyperkalemic crystalloid (Plegisol) or BCP with (+) or w

26 g global ischemia compared with traditional, hyperkalemic depolarized arrest, which is known to be as

27 A potentially beneficial alternative to hyperkalemic (depolarizing) cardioplegia is arrest in a

28 (FHHt), an autosomal dominant, hypertensive, hyperkalemic disorder, implicating this novel WNK pathwa

29 wisdom of its use in the management of acute hyperkalemic episodes.

30 Familial hyperkalemic hypertension (FHHt) is a monogenic disease

31 Recently, familial hyperkalemic hypertension (FHHt) was shown to result fro

32 ) 1 (WNK1) gene are responsible for Familial Hyperkalemic Hypertension (FHHt), a rare form of human h

33 in these WNK kinase genes can cause familial hyperkalemic hypertension (FHHt), an autosomal dominant,

34 ations in either WNK1 or WNK4 cause familial hyperkalemic hypertension (FHHt), suggesting that the pr

35 with no lysine (WNK) kinases causes familial hyperkalemic hypertension (FHHt).

36 ly recognized that the phenotype of familial hyperkalemic hypertension is mainly a consequence of inc

37 from rare mutations in WNKs causing familial hyperkalemic hypertension to acquired forms of hypertens

38 These side effects resemble familial hyperkalemic hypertension, a genetic disease characteriz

39 pseudohypoaldosteronism type II, or familial hyperkalemic hypertension, which features arterial hyper

40 nases or kelch-like 3 protein cause familial hyperkalemic hypertension.

41 ulation may be most useful in distinguishing hyperkalemic patients who have mineralocorticoid deficie

42 normoKPP families actually have a variant of hyperkalemic periodic paralysis (hyperKPP) due to a muta

43 Hyperkalemic periodic paralysis (HyperKPP) is an autosom

44 Hyperkalemic periodic paralysis (HyperKPP) produces myot

45 Hyperkalemic periodic paralysis (HyperPP) is a disorder

46 1) underlie a variety of diseases, including hyperkalemic periodic paralysis (HyperPP), paramyotonia

47 (periodic ataxia with myokymia and hypo- and hyperkalemic periodic paralysis) are due to mutation in

48 disorders such as paramyotonia congenita and hyperkalemic periodic paralysis, our study exemplifies h

49 letal muscle sodium channel in families with hyperkalemic periodic paralysis, paramyotonia congenita,

50 gain-of-function defects causing myotonia or hyperkalemic periodic paralysis.

51 ned in two patients with lupus nephritis and hyperkalemic (presumed voltage defect) dRTA.

52 microvessels isolated from hypo-, normo- and hyperkalemic rats (2.3+/-0.1, 3.9+/-0.1 and 7.2+/-0.6 mM

53 In normo- and hyperkalemic rats, the sum of the ouabain- and bumetanid

54 st, RRP estimates from strongly depolarizing hyperkalemic solutions closely matched those obtained wi

55 (K-H), pinacidil (50 micromol/L in K-H), or hyperkalemic St.