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1 ia or underwent preperfusion with HIT before cardioplegia.
2 in the coronary microcirculation after blood cardioplegia.
3 xydecanoate) during exposure to hyperkalemic cardioplegia.
4 hat presents a significant limitation to PCO cardioplegia.
5 anged appropriately during administration of cardioplegia.
6 red with control and was as effective as KCl cardioplegia.
7 placed in the coronary sinus for delivery of cardioplegia.
8 y be superior to the use of standard K+/Mg2+ cardioplegia.
9 G (with or without valve surgery) with blood cardioplegia.
10 signaling is altered in cardiomyocytes after cardioplegia.
11 atric patients protected by cold-crystalloid cardioplegia.
12 rol nonarrested hearts even after 4 hours of cardioplegia.
13 respect to the use of blood and crystalloid cardioplegia.
14 =0.02) than did those who received antegrade cardioplegia.
15 ystolic function when present in crystalloid cardioplegia.
16 ATP)) channel after exposure to hyperkalemic cardioplegia.
17 myocardial protection, which is additive to cardioplegia.
18 shown to improve endothelial function after cardioplegia.
19 ypass, followed by 75 minutes of hypothermic cardioplegia (13 degrees C) with either BC (n=6) or RSR1
20 .9 +/- 0.8 minutes; and preconditioning plus cardioplegia 15.4 +/- 2.4 minutes (P<.05 preconditioning
21 nutes; preconditioning, 6.2 +/- 0.3 minutes; cardioplegia 23.9 +/- 0.8 minutes; and preconditioning p
22 (cell culture media, 2 hours, 37 degrees C); cardioplegia (24 mEq/L K+, 2 hours, 4 degrees C; then 10
23 erfusion and rewarming (n = 62); and (3) PCO/cardioplegia: 5 minutes of PCO treatment (50 mumol/L, SR
24 eischemic value: preconditioning, 44 +/- 2%; cardioplegia, 53 +/- 3%; preconditioning plus cardiopleg
25 ardioplegia, 53 +/- 3%; preconditioning plus cardioplegia, 54 +/- 4% and control, 26 +/- 6%, P<.05).
27 ry bypass and randomized to either all-blood cardioplegia (AB group) or dilute blood cardioplegia (Di
29 aland White rabbits were treated with either cardioplegia alone or delta-opiate drugs (fentanyl, morp
31 d the effect of ischemic preconditioning and cardioplegia (alone and in combination) on ischemic cont
32 ming improved myocyte function compared with cardioplegia-alone values (31.7 +/- 2.2 versus 24.7 +/-
33 ntly improved myocyte function compared with cardioplegia-alone values (53.5 +/- 1.7, 57.6 +/- 2.0 ve
39 ugh highly protective, cardiac surgery using cardioplegia and cardiopulmonary bypass (CP/CPB) subject
42 ntegrade potassium all-blood or dilute blood cardioplegia and maintained with tepid retrograde corona
43 utralizing anti-rabbit TNF-alpha antibody to cardioplegia and perfusate solutions restored postischem
46 from patients (n=15) before and after blood cardioplegia and short-term reperfusion under conditions
47 early death (6% crystalloid versus 4% blood cardioplegia) and late death (24% crystalloid versus 21%
48 rdiopulmonary bypass, aortic cross-clamping, cardioplegia, and a thoracotomy or sternotomy and, there
51 cclusion of the ascending aorta, delivery of cardioplegia, aortic root venting, and pressure measurem
52 plegia and combined antegrade and retrograde cardioplegia are superior to crystalloid and antegrade c
54 rocess in 5 interdependent stages, including cardioplegia, back-table preparation, static cold storag
55 0 year old) sheep were randomized to receive cardioplegia based on the hyperpolarizing ATP-sensitive
58 d the hypothesis that ADO-supplemented blood cardioplegia (BCP) or ADO administered during reperfusio
60 intraoperative administration of cold blood cardioplegia, blood cardioplegia containing 500 microM a
61 s that ONOO(-) is cardiotoxic in crystalloid cardioplegia but cardioprotective in BCP in ischemically
62 r to that previously noted with hyperkalemic cardioplegia, but did not alter volume change secondary
63 a(2)-AR, n=15) were administered through the cardioplegia cannula immediately after arrest and were a
64 s C; then 10 minutes of reperfusion); or PCO/cardioplegia (cardioplegia supplemented with 100 micromo
66 Cardioplegic arrest (CA) using cold blood cardioplegia (CBC) has been reported to reduce ischemia-
68 ion and examined myocardial morphology after cardioplegia, comparing RSR13 (1.75 mmol/L)-supplemented
71 ic storage only or standard cardioplegia, or cardioplegia containing 1 mg/kg D-Ala2-Leu5-enkaphalin (
73 nistration of cold blood cardioplegia, blood cardioplegia containing 500 microM adenosine, and blood
74 urs of hypothermic ischemia with crystalloid cardioplegia containing adenosine 0, 0.01, 0.25, or 5 mm
75 there was an added benefit of adding Ran to cardioplegia (CP) in a model of global ischemia/reperfus
76 les within the myocardium during crystalloid cardioplegia (CP) infusion and ischemia-reperfusion (I-R
79 llowing solutions: Tyrode, isolation buffer, cardioplegia (CPG)+/-DZX+/-ATP-sensitive potassium chann
81 However, preconditioning accelerated whereas cardioplegia delayed ischemic contracture; preconditioni
83 ardial protection compared with dilute (4:1) cardioplegia delivered in a continuous retrograde modali
84 ally based system achieves aortic occlusion, cardioplegia delivery, and left ventricular decompressio
87 d whether intermittent blood and crystalloid cardioplegia differentially affect myocardial apoptosis
89 rdioplegia, longer maximum intervals between cardioplegia doses, lower cardioplegia volume per anasto
90 ing activation adjuvant to hypothermic blood cardioplegia enhances postischemic contractile recovery,
91 othermic ischemia after infusion of 50 mL of cardioplegia, followed by 30 minutes of reperfusion.
93 ested with normothermic oxygenated potassium cardioplegia for 5 minutes, followed by 60 minutes of no
98 the slope of the PRSWR was depressed in the cardioplegia group compared with baseline with separatio
99 hest tube removal in the high-dose adenosine cardioplegia group was 68%, 76%, and 75% of the placebo
100 o received combined antegrade and retrograde cardioplegia had significantly less inotrope use (71% ve
102 ardioplegia delays, and preconditioning plus cardioplegia has little effect on ischemic contracture,
105 ardioplegia (iC-CCP; n=8) or with cold blood cardioplegia (iC-BCP; n=6) administered intermittently.
106 rrested for 60 minutes with cold crystalloid cardioplegia (iC-CCP; n=8) or with cold blood cardiopleg
107 reased from normothermia during hyperkalemic cardioplegia in control (81+/-4 to 145+/-7 nmol/L) and C
108 d tolerance of adenosine when added to blood cardioplegia in increasing doses to enhance myocardial p
109 myocardial protection with cold-crystalloid cardioplegia in pediatric open heart surgery is dependen
111 2 hours at 37 degrees C (n=60); hyperkalemic cardioplegia, incubation for 2 hours in hypothermic hype
112 kalemic cardioplegic solution (n=60); or PCO/cardioplegia, incubation in cardioplegic solution contai
113 o 35 kg) were assigned to the following: (1) cardioplegia: institution of cardiopulmonary bypass (CPB
114 perfusion and rewarming (n = 8); and (2) PCO/cardioplegia: institution of CPB, antegrade myocardial P
115 l alternative to hyperkalemic (depolarizing) cardioplegia is arrest in a "hyperpolarized" or "polariz
119 rdioplegia (iW-CCP) (n=8) or with warm blood cardioplegia (iW-BCP) (n=8) administered intermittently.
120 minutes with warm (37 degrees C) crystalloid cardioplegia (iW-CCP) (n=8) or with warm blood cardiople
121 ntrol: 37 degrees C x 2 hours (n = 116); (2) cardioplegia: K+ 24 mEq/L, 4 degrees C x 2 hours followe
122 ad shorter clamp and bypass times, antegrade cardioplegia, longer maximum intervals between cardiople
123 They also suggest that preconditioning and cardioplegia may act through very different mechanisms.
125 segment exposed to cold, hyperkalemic blood cardioplegia (mean, 60 minutes) and a brief period (10 m
127 without the use of cardiopulmonary bypass or cardioplegia (off-pump CABG, or OPCAB) is superior to th
128 rmine the effect, if any, of adenosine blood cardioplegia on blood component usage after heart surger
129 effects of cardiopulmonary bypass (CPB) and cardioplegia on gene expressions of VEGF protein and the
130 nformation regarding the effect of adenosine cardioplegia on venous plasma adenosine concentrations,
131 lated rabbit hearts received either standard cardioplegia or HIT in the cardioplegia or underwent pre
132 d either standard cardioplegia or HIT in the cardioplegia or underwent preperfusion with HIT before c
133 either hypothermic storage only or standard cardioplegia, or cardioplegia containing 1 mg/kg D-Ala2-
135 y bypass grafting (P=0.003), and use of warm cardioplegia (P=0.02) were inversely associated with cTn
138 tested the hypothesis that all-blood (66:1) cardioplegia provides superior myocardial protection com
139 hat the administration of adenosine (ADO) in cardioplegia reduces myocardial ischemic injury, but thi
141 microvessels to bFGF were not altered after cardioplegia-reperfusion, and there was no increase in b
144 avenous infusion (0.1 mg/kg/min; 7 h) and in cardioplegia solution (placebo or acadesine; 5 microg/ml
150 late death (24% crystalloid versus 21% blood cardioplegia) statistics were not significantly differen
151 ckade, myocytes were exposed to hyperkalemic cardioplegia (stress) with and without a K(ATP) channel
152 inutes of reperfusion); or PCO/cardioplegia (cardioplegia supplemented with 100 micromol/L of the PCO
154 nutes of CPB, with 45 minutes of crystalloid cardioplegia, then 90 minutes of post-CPB reperfusion.
157 yocardial protection afforded by crystalloid cardioplegia, volatile anesthesia and hypothermia during
158 intervals between cardioplegia doses, lower cardioplegia volume per anastomosis or minute of ischemi
164 id cardioplegia versus those receiving blood cardioplegia were found to have significantly more opera
166 tricular biopsies obtained at surgery before cardioplegia were separated into free and polymerized tu
167 ts preserved by single dose cold crystalloid cardioplegia with greater than 8 hours of cold ischemia.
168 35 minutes of ischemia, hearts subjected to cardioplegia with St Thomas' solution infused for 1 minu