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1 xydecanoate) during exposure to hyperkalemic cardioplegia.
2 ia or underwent preperfusion with HIT before cardioplegia.
3 in the coronary microcirculation after blood 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 ugh highly protective, cardiac surgery using cardioplegia and cardiopulmonary bypass (CP/CPB) subject
39                                              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 0 year old) sheep were randomized to receive cardioplegia based on the hyperpolarizing ATP-sensitive
55 plemented blood (RSR13-BC) to standard blood cardioplegia (BC).
56 O(-) may exist between crystalloid and blood cardioplegia (BCP) environments.
57 d the hypothesis that ADO-supplemented blood cardioplegia (BCP) or ADO administered during reperfusio
58 and hearts subjected to preconditioning plus cardioplegia before 35 minutes of ischemia.
59  intraoperative administration of cold blood cardioplegia, blood cardioplegia containing 500 microM a
60 s that ONOO(-) is cardiotoxic in crystalloid cardioplegia but cardioprotective in BCP in ischemically
61 r to that previously noted with hyperkalemic cardioplegia, but did not alter volume change secondary
62 a(2)-AR, n=15) were administered through the cardioplegia cannula immediately after arrest and were a
63 s C; then 10 minutes of reperfusion); or PCO/cardioplegia (cardioplegia supplemented with 100 micromo
64                                              Cardioplegia-cardiopulmonary bypass (C/CPB) is associate
65    Cardioplegic arrest (CA) using cold blood cardioplegia (CBC) has been reported to reduce ischemia-
66 r 30 minutes (37 degrees C) with crystalloid cardioplegia (CCP).
67 ion and examined myocardial morphology after cardioplegia, comparing RSR13 (1.75 mmol/L)-supplemented
68                                              Cardioplegia consisted of Krebs-Henseleit solution eithe
69                In 1 group (CP+GSH, n=5), the cardioplegia contained 500 micromol/L GSH, whereas 1 gro
70 ic storage only or standard cardioplegia, or cardioplegia containing 1 mg/kg D-Ala2-Leu5-enkaphalin (
71 a containing 500 microM adenosine, and blood cardioplegia containing 2 mM adenosine.
72 nistration of cold blood cardioplegia, blood cardioplegia containing 500 microM adenosine, and blood
73 urs of hypothermic ischemia with crystalloid cardioplegia containing adenosine 0, 0.01, 0.25, or 5 mm
74  there was an added benefit of adding Ran to cardioplegia (CP) in a model of global ischemia/reperfus
75 les within the myocardium during crystalloid cardioplegia (CP) infusion and ischemia-reperfusion (I-R
76 ) as an alternative, adjunct, or additive to cardioplegia (CP).
77 ring, and after cold storage with or without cardioplegia (CP).
78 llowing solutions: Tyrode, isolation buffer, cardioplegia (CPG)+/-DZX+/-ATP-sensitive potassium chann
79      Hence, protective interventions such as cardioplegia delay ischemic contracture and improve post
80 However, preconditioning accelerated whereas cardioplegia delayed ischemic contracture; preconditioni
81        Although preconditioning accelerates, cardioplegia delays, and preconditioning plus cardiopleg
82 ardial protection compared with dilute (4:1) cardioplegia delivered in a continuous retrograde modali
83 ally based system achieves aortic occlusion, cardioplegia delivery, and left ventricular decompressio
84 sease, cardiac arrhythmias and the method of cardioplegia delivery.
85                           GSH in crystalloid cardioplegia detoxifies ONOO(-) and forms cardioprotecti
86 d whether intermittent blood and crystalloid cardioplegia differentially affect myocardial apoptosis
87 lood cardioplegia (AB group) or dilute blood cardioplegia (Dil group).
88 rdioplegia, longer maximum intervals between cardioplegia doses, lower cardioplegia volume per anasto
89 ing activation adjuvant to hypothermic blood cardioplegia enhances postischemic contractile recovery,
90 othermic ischemia after infusion of 50 mL of cardioplegia, followed by 30 minutes of reperfusion.
91                                            1 cardioplegia for 4 hours at 4 degrees C, and reperfused
92 ested with normothermic oxygenated potassium cardioplegia for 5 minutes, followed by 60 minutes of no
93 ntained with tepid retrograde coronary sinus cardioplegia for a total of 1 hour.
94 d ischemic contracture; preconditioning plus cardioplegia gave an intermediate result.
95 tion of CPB when compared with the untreated cardioplegia group (1.72 +/- 0.07, P < 0.05).
96 nd 75% of the placebo and low-dose adenosine cardioplegia group (p < 0.05).
97  the slope of the PRSWR was depressed in the cardioplegia group compared with baseline with separatio
98 hest tube removal in the high-dose adenosine cardioplegia group was 68%, 76%, and 75% of the placebo
99 o received combined antegrade and retrograde cardioplegia had significantly less inotrope use (71% ve
100                                 Hyperkalemic cardioplegia has been the gold standard for myocardial p
101 ardioplegia delays, and preconditioning plus cardioplegia has little effect on ischemic contracture,
102       Both all-blood cardioplegia and dilute cardioplegia have disadvantages, but these do not have a
103                                          The cardioplegia hematocrit for the Dil group was lower than
104 ardioplegia (iC-CCP; n=8) or with cold blood cardioplegia (iC-BCP; n=6) administered intermittently.
105 rrested for 60 minutes with cold crystalloid cardioplegia (iC-CCP; n=8) or with cold blood cardiopleg
106 reased from normothermia during hyperkalemic cardioplegia in control (81+/-4 to 145+/-7 nmol/L) and C
107 d tolerance of adenosine when added to blood cardioplegia in increasing doses to enhance myocardial p
108  myocardial protection with cold-crystalloid cardioplegia in pediatric open heart surgery is dependen
109                      The advantages of blood cardioplegia include the oxygen-carrying capacity, super
110 2 hours at 37 degrees C (n=60); hyperkalemic cardioplegia, incubation for 2 hours in hypothermic hype
111 kalemic cardioplegic solution (n=60); or PCO/cardioplegia, incubation in cardioplegic solution contai
112 o 35 kg) were assigned to the following: (1) cardioplegia: institution of cardiopulmonary bypass (CPB
113 perfusion and rewarming (n = 8); and (2) PCO/cardioplegia: institution of CPB, antegrade myocardial P
114 l alternative to hyperkalemic (depolarizing) cardioplegia is arrest in a "hyperpolarized" or "polariz
115           Elective temporary cardiac arrest (cardioplegia) is often required during cardiac surgery.
116 ere perfused with KHB for 90 minutes without cardioplegia ischemia.
117                        A 60-minute period of cardioplegia-ischemia was followed by rewarming, separat
118 rdioplegia (iW-CCP) (n=8) or with warm blood cardioplegia (iW-BCP) (n=8) administered intermittently.
119 minutes with warm (37 degrees C) crystalloid cardioplegia (iW-CCP) (n=8) or with warm blood cardiople
120 ntrol: 37 degrees C x 2 hours (n = 116); (2) cardioplegia: K+ 24 mEq/L, 4 degrees C x 2 hours followe
121 ad shorter clamp and bypass times, antegrade cardioplegia, longer maximum intervals between cardiople
122   They also suggest that preconditioning and cardioplegia may act through very different mechanisms.
123            Thus, preconditioning adjuvant to cardioplegia may provide a novel means of protecting myo
124  segment exposed to cold, hyperkalemic blood cardioplegia (mean, 60 minutes) and a brief period (10 m
125             Stress (exposure to hyperkalemic cardioplegia, metabolic inhibition, or osmotic) results
126 without the use of cardiopulmonary bypass or cardioplegia (off-pump CABG, or OPCAB) is superior to th
127 rmine the effect, if any, of adenosine blood cardioplegia on blood component usage after heart surger
128  effects of cardiopulmonary bypass (CPB) and cardioplegia on gene expressions of VEGF protein and the
129 nformation regarding the effect of adenosine cardioplegia on venous plasma adenosine concentrations,
130 lated rabbit hearts received either standard cardioplegia or HIT in the cardioplegia or underwent pre
131 d either standard cardioplegia or HIT in the cardioplegia or underwent preperfusion with HIT before c
132  either hypothermic storage only or standard cardioplegia, or cardioplegia containing 1 mg/kg D-Ala2-
133                     During hypothermic blood cardioplegia, oxygen delivery to myocytes is minimal wit
134 y bypass grafting (P=0.003), and use of warm cardioplegia (P=0.02) were inversely associated with cTn
135  60 minutes of intermittent cold crystalloid cardioplegia (Plegisol) and 2 hours of reperfusion.
136                                  Hypothermic cardioplegia provides myocellular protection, yet postis
137  tested the hypothesis that all-blood (66:1) cardioplegia provides superior myocardial protection com
138 hat the administration of adenosine (ADO) in cardioplegia reduces myocardial ischemic injury, but thi
139                                              Cardioplegia-reperfusion was associated with a 4 +/- 2-f
140  microvessels to bFGF were not altered after cardioplegia-reperfusion, and there was no increase in b
141 cardial edema, and vascular remodeling after cardioplegia-reperfusion.
142                     Hypothermic hyperkalemic cardioplegia results in significant myocyte swelling and
143 avenous infusion (0.1 mg/kg/min; 7 h) and in cardioplegia solution (placebo or acadesine; 5 microg/ml
144                                          The cardioplegia solution contained 5 micromol/L authentic O
145                       ONOO(-) in crystalloid cardioplegia solution induces injury to coronary endothe
146  infusion for 7 continuous hours and via the cardioplegia solution.
147 ere perfused with 3 mmol/L L-arginine in the cardioplegia solution.
148       NO has been advocated as an adjunct to cardioplegia solutions.
149 late death (24% crystalloid versus 21% blood cardioplegia) statistics were not significantly differen
150 ckade, myocytes were exposed to hyperkalemic cardioplegia (stress) with and without a K(ATP) channel
151 inutes of reperfusion); or PCO/cardioplegia (cardioplegia supplemented with 100 micromol/L of the PCO
152                     During administration of cardioplegia, TEE showed movement of the balloon away fr
153 nutes of CPB, with 45 minutes of crystalloid cardioplegia, then 90 minutes of post-CPB reperfusion.
154 4 +/- 2.4 minutes (P<.05 preconditioning and cardioplegia versus control).
155               Patients receiving crystalloid cardioplegia versus those receiving blood cardioplegia w
156 yocardial protection afforded by crystalloid cardioplegia, volatile anesthesia and hypothermia during
157  intervals between cardioplegia doses, lower cardioplegia volume per anastomosis or minute of ischemi
158                                              Cardioplegia was administered via the distal port of the
159                   A new method of retrograde cardioplegia was developed.
160                      Contractility after PCO cardioplegia was similar to normothermic values in contr
161                 Patients receiving adenosine cardioplegia were also given an infusion of adenosine (2
162 id cardioplegia versus those receiving blood cardioplegia were found to have significantly more opera
163 ing open heart surgery with cold-crystalloid cardioplegia were included in the study.
164 tricular biopsies obtained at surgery before cardioplegia were separated into free and polymerized tu
165 ts preserved by single dose cold crystalloid cardioplegia with greater than 8 hours of cold ischemia.
166  35 minutes of ischemia, hearts subjected to cardioplegia with St Thomas' solution infused for 1 minu
167 /L GSH, whereas 1 group received crystalloid cardioplegia without GSH (CCP, n=6).

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