ライフサイエンスコーパス: crystalloid cardioplegia

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1 ompared with respect to the use of blood and crystalloid cardioplegia.

2 nction and systolic function when present in crystalloid cardioplegia.

3 jury in pediatric patients protected by cold-crystalloid cardioplegia.

4 he hypothesis that ONOO(-) is cardiotoxic in crystalloid cardioplegia but cardioprotective in BCP in

5 arrested for 30 minutes (37 degrees C) with crystalloid cardioplegia (CCP).

6 arts to 8 hours of hypothermic ischemia with crystalloid cardioplegia containing adenosine 0, 0.01, 0

7 in microbubbles within the myocardium during crystalloid cardioplegia (CP) infusion and ischemia-repe

8 GSH in crystalloid cardioplegia detoxifies ONOO(-) and forms ca

9 investigated whether intermittent blood and crystalloid cardioplegia differentially affect myocardia

10 earts were arrested for 60 minutes with cold crystalloid cardioplegia (iC-CCP; n=8) or with cold bloo

11 Extent of myocardial protection with cold-crystalloid cardioplegia in pediatric open heart surgery

12 sted for 60 minutes with warm (37 degrees C) crystalloid cardioplegia (iW-CCP) (n=8) or with warm blo

13 followed by 60 minutes of intermittent cold crystalloid cardioplegia (Plegisol) and 2 hours of reper

14 ONOO(-) in crystalloid cardioplegia solution induces injury to coro

15 wed by 60 minutes of CPB, with 45 minutes of crystalloid cardioplegia, then 90 minutes of post-CPB re

16 Patients receiving crystalloid cardioplegia versus those receiving blood ca

17 to enhance myocardial protection afforded by crystalloid cardioplegia, volatile anesthesia and hypoth

18 sis) undergoing open heart surgery with cold-crystalloid cardioplegia were included in the study.

19 y donor hearts preserved by single dose cold crystalloid cardioplegia with greater than 8 hours of co

20 500 micromol/L GSH, whereas 1 group received crystalloid cardioplegia without GSH (CCP, n=6).

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