ライフサイエンスコーパス: cardioplegic

1 wed by 60 minutes of normothermic continuous cardioplegic administration with left anterior descendin

2 oss-bridge cycle and to learn more about the cardioplegic agent BDM (2,3-butanedione monoxime), its e

3 ay be due to a lack of clear criteria that a cardioplegic agent should meet at a cellular level and,

4 tempt to define the criteria for the optimal cardioplegic agent.

5 and clinical potential of previously-studied cardioplegic agents and suggest cellular targets, partic

6 (PCOs) aprikalim and pinacidil are effective cardioplegic agents but exhibit toxicity at high doses.

7 ver the last two decades to establish better cardioplegic agents have mainly remained limited to anim

8 diastolic function after 3 hr of hypothermic cardioplegic arrest (114+/-4 mm Hg vs. 83+/-4 mm Hg gene

9 esponses to cardiopulmonary bypass (CPB) and cardioplegic arrest (C) in patients with and without dia

10 elin-1 (ET-1) is released after hyperkalemic cardioplegic arrest (CA) and reperfusion and may contrib

11 Cardioplegic arrest (CA) using cold blood cardioplegia (

12 Cardioplegic arrest (CP) followed by reperfusion after c

13 titution of cardiopulmonary bypass (CPB) and cardioplegic arrest (K+ 24 mEq/L, 4 degrees C x 2 hours)

14 mumol/L, SR47063, 37 degrees C), followed by cardioplegic arrest (n = 6).

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

16 ed for 90 minutes, followed by 45 minutes of cardioplegic arrest and 180 minutes of reperfusion.

17 lamb hearts underwent 2 hours of hypothermic cardioplegic arrest and 2 hours of reperfusion.

18 the present study tested the hypothesis that cardioplegic arrest and activation of KATP channels by a

19 ely characterized in the setting of surgical cardioplegic arrest and ischemia/reperfusion.

20 Cardioplegic arrest and preconditioning induced by pinac

21 We investigated the effects of cardioplegic arrest and reperfusion (CP/Rep) on myocardi

22 ing and myocyte contractile dysfunction with cardioplegic arrest and reperfusion.

23 Cardioplegic arrest and rewarming caused a decline in st

24 yte velocity of shortening was reduced after cardioplegic arrest and rewarming compared with normothe

25 eluent from endothelial cultures followed by cardioplegic arrest and rewarming improved myocyte funct

26 beneficial effects of preconditioning during cardioplegic arrest and rewarming remain unclear.

27 ioning on myocyte contractile processes with cardioplegic arrest and rewarming were examined in a fin

28 thermic reperfusion; and (3) preconditioning/cardioplegic arrest and rewarming, hypoxia (20 minutes)

29 um (37 degrees C) for 2 hours; (2) simulated cardioplegic arrest and rewarming, incubated in crystall

30 ygenation (20 minutes) followed by simulated cardioplegic arrest and rewarming.

31 means of endogenous cardioprotection during cardioplegic arrest and rewarming.

32 eans of protecting myocardial function after cardioplegic arrest and rewarming.

33 yocyte contractile function during simulated cardioplegic arrest and rewarming.

34 ytes, which were then subjected to simulated cardioplegic arrest and rewarming.

35 , SR47063, 37 degrees C; n = 94) followed by cardioplegic arrest and rewarming.

36 LV) dysfunction can occur after hyperkalemic cardioplegic arrest and subsequent reperfusion and rewar

37 ary sinus blood samples were obtained before cardioplegic arrest and then obtained at 1 and 15 min af

38 tion remained increased until after ischemic cardioplegic arrest and was also higher than with placeb

39 ression analysis identified CPB inclusive of cardioplegic arrest as the only independent predictor of

40 llular calcium increased during hyperkalemic cardioplegic arrest compared with baseline values (147+/

41 Cardioplegic arrest followed by reperfusion after cardio

42 urgery with cardiopulmonary bypass (CPB) and cardioplegic arrest has been associated with myocardial

43 ess technique for cardiopulmonary bypass and cardioplegic arrest has been developed for use in cardia

44 23), respectively, and before/after ischemic cardioplegic arrest in CABG patients.

45 dence was observed of ischemic stress during cardioplegic arrest in children and infants as shown by

46 the role of cardiopulmonary bypass (CPB) and cardioplegic arrest in the pathogenesis of this complica

47 Preconditioning during cardioplegic arrest is agent specific, feasible at cold

48 Cardiovascular surgery with ischemic cardioplegic arrest is only a surrogate of acute myocard

49 CPB inclusive of cardioplegic arrest is the main independent predictor of

50 Ischemic cardioplegic arrest led to an increase of left ventricul

51 (40 to 77) years)] with normothermic CPB and cardioplegic arrest of the heart or (2) off-pump surgery

52 PCO-augmented cardioplegic arrest preserved myocyte contractility and

53 In Beating Heart Against Cardioplegic Arrest Study (BHACAS) 1, we excluded patien

54 herens junctions after regional ischemia and cardioplegic arrest through a mechanism potentially invo

55 AT5) increased from baseline before ischemic cardioplegic arrest to 10 minutes of reperfusion with RI

56 ulations with respect to preconditioning and cardioplegic arrest was examined.

57 In situ cardioplegic arrest was followed by an ischemic time of

58 Cardioplegic arrest with PCO supplementation significant

59 Cardioplegic arrest with simultaneous activation of KATP

60 ther PCO supplementation during hyperkalemic cardioplegic arrest would provide protective effects on

61 full sternotomy, cardiopulmonary bypass, and cardioplegic arrest) has been the treatment of choice fo

62 before cardioplegic arrest, effective during cardioplegic arrest, and detrimental during reperfusion.

63 rginine is most beneficial when given before cardioplegic arrest, effective during cardioplegic arres

64 By using cardiopulmonary bypass and cardioplegic arrest, intracoronary delivery of adenovira

65 ariate analysis showed that CPB inclusive of cardioplegic arrest, postoperative inotropic support, in

66 ing for NO supplementation in the setting of cardioplegic arrest, regional ischemia, and reperfusion.

67 nd to protect the myocardium during ischemic cardioplegic arrest.

68 in a porcine model of regional ischemia and cardioplegic arrest.

69 to 45 minutes of normothermic ischemia with cardioplegic arrest.

70 nary surgery with cardiopulmonary bypass and cardioplegic arrest.

71 ompared with control hearts after 4 hours of cardioplegic arrest.

72 prevents LV dysfunction induced by prolonged cardioplegic arrest.

73 by aortic cross-clamping with 30 minutes of cardioplegic arrest.

74 ontractile function in an in vitro system of cardioplegic arrest.

75 ventricular (LV) and myocyte function after cardioplegic arrest.

76 t could be translated to an in vivo model of cardioplegic arrest.

77 on LV myocyte contractility after simulated cardioplegic arrest.

78 ation of myocyte contractile function during cardioplegic arrest.

79 y a contributory role in preconditioning for cardioplegic arrest.

80 ecreased LV contractility after hyperkalemic cardioplegic arrest.

81 cyte contractile dysfunction associated with cardioplegic arrest.

82 ith 3 mmol/L L-arginine for 5 minutes before cardioplegic arrest.

83 oss-clamping, sternotomy or thoracotomy, and cardioplegic cardiac arrest, and are associated with sig

84 ttractive options for the development of new cardioplegic drugs.

85 fused and exposed to 40-minute normothermic, cardioplegic global ischemia and 30 minutes of reperfusi

86 tracellular increase in free Ca2+ during the cardioplegic interval in control (110+/-6 nmol/L) and CH

87 Two hours of 10 degrees C cardioplegic ischemia was induced in 40 isolated, blood-

88 (n=6) were perfused for 120 minutes without cardioplegic ischemia.

89 stered for 15 min at 2 mmol, 25 min prior to cardioplegic ischemia.

90 (MIMVS) approach avoiding cross-clamping and cardioplegic myocardial arrest using a small (5 cm) righ

91 Current cardioplegic protection techniques used in pediatric car

92 an ideal group to benefit most from optimal cardioplegic protection.

93 in myocytes exposed to the PCO-supplemented cardioplegic solution (109+/-4 nmol/L, P<.05).

94 rest and rewarming, incubated in crystalloid cardioplegic solution (24 mEq/L K+, 4 degrees C) for 2 h

95 maged following isolation and perfusion with cardioplegic solution (n = 6), imaged in vivo (n = 6), o

96 tion for 2 hours in hypothermic hyperkalemic cardioplegic solution (n=60); or PCO/cardioplegia, incub

97 olerance to ischemia, adenosine-supplemented cardioplegic solution also may reduce bleeding after car

98 storage hearts were flushed with St Thomas' cardioplegic solution and stored in ice.

99 n (n=60); or PCO/cardioplegia, incubation in cardioplegic solution containing 100 micromol/L of the P

100 monary artery were occluded with snares, and cardioplegic solution containing histamine was injected

101 es with age and is influenced by the type of cardioplegic solution used.

102 Cardioplegic solution was visualized in the aortic root,

103 ed after the infusion of St Thomas' Hospital cardioplegic solution, stored at 4 degrees C for 4 hours

104 There is controversy regarding which cardioplegic solution, temperature, and route of adminis

105 d for 1 hour with a hyperkalemic, cold blood cardioplegic solution.

106 erfusion followed by isolated perfusion with cardioplegic solution.

107 Hypothermic hyperkalemic cardioplegic solutions are currently used for donor hear

108 Addition of blood to cardioplegic solutions has been shown to improve endothe

109 iC-BCP is superior to the other cardioplegic solutions in increasing the phosphorylation

110 dilution of blood in 4:1 (blood:crystalloid) cardioplegic solutions may nullify these advantages and

111 the 1970 s, the development of hyperkalaemic cardioplegic solutions revolutionised cardiac surgery by

112 assium channels were activated by augmenting cardioplegic solutions with adenosine (200 mumol/L) or t

113 for 7 hours) or placebo (both also added to cardioplegic solutions) beginning just before anesthesia

114 rmacological agents in order to offer better cardioplegic solutions.

115 Despite remaining the most widely-used cardioplegic technique, hyperkalaemia can have detriment

116 urgical myocardial protection using advanced cardioplegic technologies, some patients require inotrop

117 nnaire was sent to surgeons requesting blood cardioplegic temperature and route.