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

13 kade (5-hydroxydecanoate) during 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 xplored the safety and feasibility of PBD in hyperkalemic CKD patients receiving the potassium binder

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

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

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

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

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

29 humans lead to a Mendelian hypertensive and hyperkalemic disease pseudohypoaldosteronism type II (PH

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

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

32 Affected subjects had an early onset of a hyperkalemic hyperchloremic phenotype, but normal blood

33 Familial hyperkalemic hypertension (FHHt) is a monogenic disease

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

35 ) 1 (WNK1) gene are responsible for Familial Hyperkalemic Hypertension (FHHt), a rare form of human h

36 , or Cullin 3 (CUL3), can result in familial hyperkalemic hypertension (FHHt), a rare Mendelian form

37 and WNK4 genes are responsible for familial hyperkalemic hypertension (FHHt), a rare, inherited diso

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

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

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

41 lin 3 (CUL3) gene cause the disease familial hyperkalemic hypertension (FHHt).

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

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

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

45 WNKs-SPAK kinase cascade underlies Familial Hyperkalemic Hypertension, but it remains unknown whethe

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

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

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

49 In the current 6-wk trial, 26 hyperkalemic patients with CKD stage 4-5 not on dialysis

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

51 Hyperkalemic periodic paralysis (HyperKPP) is an autosom

52 Hyperkalemic periodic paralysis (HyperKPP) produces myot

53 Hyperkalemic periodic paralysis (HyperPP) is a disorder

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

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

56 paralysis (hypokalemic periodic paralysis or hyperkalemic periodic paralysis).

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

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

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

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

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

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

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

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

65 lightly lower plasma potassium but were more hyperkalemic with prolonged high potassium intake and mo