PMID- 20400115
OWN - NLM
STAT- MEDLINE
DCOM- 20120109
LR  - 20141120
IS  - 1095-8673 (Electronic)
IS  - 0022-4804 (Linking)
VI  - 171
IP  - 1
DP  - 2011 Nov
TI  - Protection of human myocardium by bone marrow cells: role of long-term 
      administration of the mitochondrial K(ATP) channel opener nicorandil.
PG  - 66-70
LID - 10.1016/j.jss.2009.12.029 [doi]
AB  - BACKGROUND: We have previously demonstrated that bone marrow cells (BMCs) afford 
      myocardial protection as potent as ischemic preconditioning (IP) and also that 
      the myocardium of patients treated with the mitoK(ATP) channel opener nicorandil 
      cannot be protected by IP. Here, we investigated whether nicorandil influences 
      the cardioprotection elicited by BMCs and whether any loss in protection can be 
      rescued by naive allogenic BMCs. MATERIALS AND METHODS: BMCs and right atrial 
      appendage were obtained from patients on long-term treatment and nontreated with 
      nicorandil. The atrial myocardium was subjected to 90 min ischemia/120 min 
      reoxygenation at 37 degrees C in the presence and absence of autologous and allogenic 
      BMCs. Some muscles were subjected to IP prior to ischemia and served as positive 
      controls. Tissue injury was assessed by creatine kinase released during 
      reoxygenation, and cell necrosis and apoptosis were determined by propidium 
      iodide and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). 
      RESULTS: Creatine kinase (CK) release and cell necrosis and apoptosis induced by 
      ischemia were not significantly reduced by IP in the myocardium from nicorandil 
      subjects and values were also unaffected by the co-incubation with autologous or 
      allogenic BMCs from subjects not treated with nicorandil (naive BMCs). However, 
      when the myocardium from subjects not treated with nicorandil was co-incubated 
      with autologous BMCs or with allogenic BMCs from subjects treated with 
      nicorandil, there was a similar significant reduction in CK release, cell 
      necrosis and apoptosis. CONCLUSIONS: The cardioprotective properties of BMCs from 
      subjects treated with the mitoK(ATP) channel opener nicorandil are preserved; 
      however, the myocardium of these patients cannot benefit from the 
      cardioprotective effect of BMCs due to an unresponsive myocardium.
CI  - Copyright (c) 2011 Elsevier Inc. All rights reserved.
FAU - Lai, Vien Khach
AU  - Lai VK
AD  - Cardiac Surgery Unit, Department of Cardiovascular Sciences, University of 
      Leicester, United Kingdom.
FAU - Galinanes, Manuel
AU  - Galinanes M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100125
PL  - United States
TA  - J Surg Res
JT  - The Journal of surgical research
JID - 0376340
RN  - 0 (Cardiotonic Agents)
RN  - 0 (Potassium Channels)
RN  - 0 (Vasodilator Agents)
RN  - 0 (mitochondrial K(ATP) channel)
RN  - 260456HAM0 (Nicorandil)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Apoptosis/drug effects
MH  - Atrial Appendage/*drug effects/pathology
MH  - Bone Marrow Cells/*cytology
MH  - Cardiotonic Agents/pharmacology
MH  - Cell Communication/drug effects
MH  - Humans
MH  - In Vitro Techniques
MH  - Middle Aged
MH  - Myocardial Ischemia/*drug therapy/pathology
MH  - Necrosis
MH  - Nicorandil/*pharmacology
MH  - Potassium Channels/*agonists/physiology
MH  - Vasodilator Agents/pharmacology
EDAT- 2010/04/20 06:00
MHDA- 2012/01/10 06:00
CRDT- 2010/04/20 06:00
PHST- 2009/09/14 00:00 [received]
PHST- 2009/11/30 00:00 [revised]
PHST- 2009/12/28 00:00 [accepted]
PHST- 2010/04/20 06:00 [entrez]
PHST- 2010/04/20 06:00 [pubmed]
PHST- 2012/01/10 06:00 [medline]
AID - S0022-4804(09)01352-3 [pii]
AID - 10.1016/j.jss.2009.12.029 [doi]
PST - ppublish
SO  - J Surg Res. 2011 Nov;171(1):66-70. doi: 10.1016/j.jss.2009.12.029. Epub 2010 Jan 
      25.