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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).
26 ile function when compared with hyperkalemic cardioplegia (58+/-4 microm/s, P<.05).
27 ry bypass and randomized to either all-blood cardioplegia (AB group) or dilute blood cardioplegia (Di
28 ia are superior to crystalloid and antegrade cardioplegia alone for postoperative morbidity.
29 aland White rabbits were treated with either cardioplegia alone or delta-opiate drugs (fentanyl, morp
30 e, and pentazocine groups when compared with cardioplegia alone.
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
34                    The higher dose adenosine cardioplegia also prevented translocation of PKC from cy
35 of 10 degrees C antegrade intermittent blood cardioplegia and 30 minutes of reperfusion.
36          In this study, the effects of blood cardioplegia and brief reperfusion on vascular reactivit
37                                              Cardioplegia and cardiopulmonary bypass (CP/CPB) leads t
38                                              Cardioplegia and cardiopulmonary bypass (CP/CPB) subject
39 ugh highly protective, cardiac surgery using cardioplegia and cardiopulmonary bypass (CP/CPB) subject
40                                        Blood cardioplegia and combined antegrade and retrograde cardi
41                               Both all-blood cardioplegia and dilute cardioplegia have disadvantages,
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
44 y endothelium and to systolic function after cardioplegia and reperfusion.
45                                 Hyperkalemic cardioplegia and rewarming caused a significant reductio
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
49                       Anesthesia, perfusion, cardioplegia, and surgical techniques were standardized.
50 ed by the choice of anesthesia, hypothermia, cardioplegia, and traumatic myocardial injury.
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
53                                          PCO cardioplegia attenuated the intracellular increase in fr
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
56 plemented blood (RSR13-BC) to standard blood cardioplegia (BC).
57 O(-) may exist between crystalloid and blood cardioplegia (BCP) environments.
58 d the hypothesis that ADO-supplemented blood cardioplegia (BCP) or ADO administered during reperfusio
59 and hearts subjected to preconditioning plus cardioplegia before 35 minutes of ischemia.
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
65                                              Cardioplegia-cardiopulmonary bypass (C/CPB) is associate
66    Cardioplegic arrest (CA) using cold blood cardioplegia (CBC) has been reported to reduce ischemia-
67 r 30 minutes (37 degrees C) with crystalloid cardioplegia (CCP).
68 ion and examined myocardial morphology after cardioplegia, comparing RSR13 (1.75 mmol/L)-supplemented
69                                              Cardioplegia consisted of Krebs-Henseleit solution eithe
70                In 1 group (CP+GSH, n=5), the cardioplegia contained 500 micromol/L GSH, whereas 1 gro
71 ic storage only or standard cardioplegia, or cardioplegia containing 1 mg/kg D-Ala2-Leu5-enkaphalin (
72 a containing 500 microM adenosine, and blood cardioplegia containing 2 mM adenosine.
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
77 ) as an alternative, adjunct, or additive to cardioplegia (CP).
78 ring, and after cold storage with or without cardioplegia (CP).
79 llowing solutions: Tyrode, isolation buffer, cardioplegia (CPG)+/-DZX+/-ATP-sensitive potassium chann
80      Hence, protective interventions such as cardioplegia delay ischemic contracture and improve post
81 However, preconditioning accelerated whereas cardioplegia delayed ischemic contracture; preconditioni
82        Although preconditioning accelerates, cardioplegia delays, and preconditioning plus cardiopleg
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
85 sease, cardiac arrhythmias and the method of cardioplegia delivery.
86                           GSH in crystalloid cardioplegia detoxifies ONOO(-) and forms cardioprotecti
87 d whether intermittent blood and crystalloid cardioplegia differentially affect myocardial apoptosis
88 lood cardioplegia (AB group) or dilute blood cardioplegia (Dil group).
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.
92                                            1 cardioplegia for 4 hours at 4 degrees C, and reperfused
93 ested with normothermic oxygenated potassium cardioplegia for 5 minutes, followed by 60 minutes of no
94 ntained with tepid retrograde coronary sinus cardioplegia for a total of 1 hour.
95 d ischemic contracture; preconditioning plus cardioplegia gave an intermediate result.
96 tion of CPB when compared with the untreated cardioplegia group (1.72 +/- 0.07, P < 0.05).
97 nd 75% of the placebo and low-dose adenosine cardioplegia group (p < 0.05).
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
101                                 Hyperkalemic cardioplegia has been the gold standard for myocardial p
102 ardioplegia delays, and preconditioning plus cardioplegia has little effect on ischemic contracture,
103       Both all-blood cardioplegia and dilute cardioplegia have disadvantages, but these do not have a
104                                          The cardioplegia hematocrit for the Dil group was lower than
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
110                      The advantages of blood cardioplegia include the oxygen-carrying capacity, super
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
116           Elective temporary cardiac arrest (cardioplegia) is often required during cardiac surgery.
117 ere perfused with KHB for 90 minutes without cardioplegia ischemia.
118                        A 60-minute period of cardioplegia-ischemia was followed by rewarming, separat
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.
124            Thus, preconditioning adjuvant to cardioplegia may provide a novel means of protecting myo
125  segment exposed to cold, hyperkalemic blood cardioplegia (mean, 60 minutes) and a brief period (10 m
126             Stress (exposure to hyperkalemic cardioplegia, metabolic inhibition, or osmotic) results
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-
134                     During hypothermic blood cardioplegia, oxygen delivery to myocytes is minimal wit
135 y bypass grafting (P=0.003), and use of warm cardioplegia (P=0.02) were inversely associated with cTn
136  60 minutes of intermittent cold crystalloid cardioplegia (Plegisol) and 2 hours of reperfusion.
137                                  Hypothermic cardioplegia provides myocellular protection, yet postis
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
140                                              Cardioplegia-reperfusion was associated with a 4 +/- 2-f
141  microvessels to bFGF were not altered after cardioplegia-reperfusion, and there was no increase in b
142 cardial edema, and vascular remodeling after cardioplegia-reperfusion.
143                     Hypothermic hyperkalemic cardioplegia results in significant myocyte swelling and
144 avenous infusion (0.1 mg/kg/min; 7 h) and in cardioplegia solution (placebo or acadesine; 5 microg/ml
145                                          The cardioplegia solution contained 5 micromol/L authentic O
146                       ONOO(-) in crystalloid cardioplegia solution induces injury to coronary endothe
147  infusion for 7 continuous hours and via the cardioplegia solution.
148 ere perfused with 3 mmol/L L-arginine in the cardioplegia solution.
149       NO has been advocated as an adjunct to cardioplegia solutions.
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
153                     During administration of cardioplegia, TEE showed movement of the balloon away fr
154 nutes of CPB, with 45 minutes of crystalloid cardioplegia, then 90 minutes of post-CPB reperfusion.
155 4 +/- 2.4 minutes (P<.05 preconditioning and cardioplegia versus control).
156               Patients receiving crystalloid cardioplegia versus those receiving blood cardioplegia w
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
159                                              Cardioplegia was administered via the distal port of the
160                   A new method of retrograde cardioplegia was developed.
161  to 34.0 degrees C and retrograde cold blood cardioplegia was infused continuously.
162                      Contractility after PCO cardioplegia was similar to normothermic values in contr
163                 Patients receiving adenosine cardioplegia were also given an infusion of adenosine (2
164 id cardioplegia versus those receiving blood cardioplegia were found to have significantly more opera
165 ing open heart surgery with cold-crystalloid cardioplegia were included in the study.
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
169 /L GSH, whereas 1 group received crystalloid cardioplegia without GSH (CCP, n=6).

 
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