ライフサイエンスコーパス: superfusate

1 d 4-aminopyridine (4-AP) were applied in the superfusate.

2 4 h of recovery with an FBP-free oxygenated superfusate.

3 roM bovine type II carbonic anhydrase to the superfusate.

4 oupling agents were added to the brain slice superfusate.

5 d VIP-LI material released in the ganglionic superfusate.

6 in myeloperoxidase activity in the tracheal superfusate.

7 molar concentration range in vascular tissue superfusates.

8 ular ATP or off-site measurement of ATP from superfusates.

9 roteolytic activity is also increased in the superfusates.

10 Following removal of Mg2+ from the superfusate a further excitatory component was identifie

11 MMA) and N G-nitro L-arginine (L-NNA) to the superfusate abolished the positive correlation between P

12 inistration had no effect on basal levels of superfusate amino acids and reduced basal levels of lino

13 ) elicited a rapid increase in the levels of superfusate amino acids; aspartate, glutamate, GABA, gly

14 e, glutamate, GABA and taurine into cortical superfusates, and also elevated L-lactate levels above t

15 umens had the most divergent pH from luminal superfusates; (b) qualitatively similar results were obs

16 entaenoic acid (EPA: 5-15 micromol/L) to the superfusate before adding the toxins prevented the expec

17 urons with and without Mg(2+) present in the superfusate but had no significant effect on either (1S,

18 s similar in Hepes- or 5% CO2/HCO3--buffered superfusates but, in both cases, was approximately 0.1 p

19 ynamic pH(i) changes during displacements of superfusate CO(2) concentration are also spatially coinc

20 ble FKN (sFKN) contents are increased in the superfusates collected after noxious-like electrical sti

21 se (cADPR) and ADPR were also present in the superfusates collected during EFS of CMA (2.5 +/- 0.9 an

22 of glucose and lactate in cerebral cortical superfusates during four-vessel occlusion-elicited globa

23 de results in increased CatS activity in the superfusates, followed by increased sFKN contents.

24 s present in low molecular weight (Mr, <500) superfusate fractions.

25 ble of superfusing a single islet and mixing superfusate from each islet online with fluorescein isot

26 Lactate levels in cortical superfusates from EIPA-treated animals rose more rapidly

27 ed contracting cardiac myocytes treated with superfusates from pressure-overloaded and control hearts

28 re-overloaded hearts but was normal with the superfusates from the control hearts.

29 otion was depressed in myocytes treated with superfusates from the pressure-overloaded hearts but was

30 nts were made of tissue glycogen content and superfusate glucose and lactate concentrations.

31 tid body chemoafferents showed that reducing superfusate glucose concentration from 10 mM to 2 mM red

32 not affected, and did not increase when the superfusate [glucose] was lowered from 10 mm to 2 mm by

33 Cl- and taurocholate, isohydric reduction of superfusate HCO3- concentration from 50 to 25 mM resulte

34 In addition, HPLC analysis of the superfusates indicated that GABA and glutamate accumulat

35 A raised superfusate [K+] also induced a Ca2+ transient, due to t

36 Addition of 25 microM taurocholate to the superfusate led to a rapid fall in pHi in induced (-0.03

37 dehydrogenase inhibitor, on cortical window superfusate levels of amino acids, glucose and L-lactate

38 mia caused significant increases in cortical superfusate levels of aspartate, glutamate, GABA, taurin

39 Cerebral ischemia elicited increased superfusate levels of aspartate, glutamate, phosphoethan

40 Superfusate levels of aspartate, glutamate, taurine, GAB

41 Superfusate levels of glucose, which decline to near zer

42 determined by measuring the efflux into the superfusate of 5-carboxyfluorescein (CF) applied to the

43 s, when heptanol (2 mmol/L) was added to the superfusate of monolayers loaded with CTP-RXP-E, action

44 ent increase of [3H] dopamine release in the superfusate of striatum slices.

45 The superfusates of hypoxic endothelial cells induced rapid,

46 Levels of beta-NAD in superfusates of muscles after nerve stimulation exceed A

47 the removal of extracellular Ca(2+) from the superfusate or by the addition of either Ni(2+) (2 mM) o

48 c oxide synthase inhibitor, 10(-5) mol/L) in superfusate over the arteries (16.1+/-5% increase, P=NS

49 chamber designed to allow controlled flow of superfusate over the culture.

50 With superfusate oxygen level raised from 0 to 21%, 2A arteri

51 +] ([Ca2+]i) were measured during changes to superfusate PCO2 and/or [NaHCO3].

52 Changes to superfusate PCO2 produced sustained changes to pHi and [

53 etion by the stomach in response to changing superfusate pH from 5 to 3.

54 the basal discharge induced by reducing the superfusate PO2 led to proportional decreases in the tim

55 acin (30 micromol l-1) to both perfusate and superfusate reduced the positive correlation between PK

56 Hypoxic endothelial superfusate reduced unloaded shortening velocity of huma

57 Superfusate removed from the trachea 8 h after antigen c

58 The adenosine level in the superfusate, representing adenosine overflow from the re

59 Confocal imaging of Fura-Red dye in luminal superfusate shows a localized extracellular Ca(2+) incre

60 as were first induced, adding the EPA to the superfusate terminated the arrhythmias.

61 In Na(+)-free superfusate, the 5-HT-induced depolarization was convert

62 antagonists were applied exogenously via the superfusate to dissect the synaptic pathways pharmacolog

63 inucleotide (beta-NAD) is released in tissue superfusates upon EFS of canine mesenteric artery (CMA),

64 Catecholamine release was measured from the superfusates using fast cyclic voltammetry before, durin

65 Cell loading (with increasing superfusate viscosity from 1 cp to 300 cp) also did not

66 prevented when the Ca2+ concentration in the superfusate was doubled (from 2.2 to 4.4 mM).

67 [(3)H]-acetylcholine (ACh) released into the superfusate was monitored.

68 e and 3-[13C]lactate peak intensities in the superfusate were measured using 13C-NMR spectroscopy.

69 Samples of superfusate were taken at 10 s intervals during the 60 s

70 Cell superfusates were buffered either with a 5% CO2-HCO3- sy

71 m Hg) physiological buffer solution, and the superfusates were reequilibrated to a PO2 of approximate

72 replacing Hepes buffer in the extracellular superfusate with a 5 % CO(2)/HCO(3)(-) buffer system (at

73 ate, GABA and taurine effluxes into cortical superfusates, with non-significant effects on the efflux

74 acid and free fatty acid levels in cortical superfusates, withdrawn at 10-min intervals from bilater

75 Free fatty acid levels in cortical superfusates, withdrawn at 10-min intervals from bilater