PMID- 22099599
OWN - NLM
STAT- MEDLINE
DCOM- 20120514
LR  - 20120328
IS  - 1095-8673 (Electronic)
IS  - 0022-4804 (Linking)
VI  - 174
IP  - 1
DP  - 2012 May 1
TI  - The effect of diabetes and poor left ventricular function on bone marrow 
      cell-induced myocardial protection.
PG  - e1-e10
LID - 10.1016/j.jss.2011.09.050 [doi]
AB  - OBJECTIVES: The myocardium of patients with diabetes and poor left ventricular 
      (LV) function cannot be protected by interventions such as ischemic 
      preconditioning (IP). We investigated whether these clinical conditions influence 
      the protection elicited by the paracrine effect of bone marrow cells (BMCs) and 
      whether the cause for loss in protection resides in the BMCs, the myocardium, or 
      both. METHODS: BMCs and right atrial appendage were obtained from patients with 
      and without diabetes and from poor (EF < 30%) and preserved LV function 
      undergoing elective cardiac surgery. Muscles (n = 6/group) were co-cultured with 
      BMCs and subjected to 90 min ischemia/120 min reoxygenation at 37 degrees C. The degree 
      of protection was assessed by measuring creatine kinase (CK) released, and 
      myocardial cell necrosis and apoptosis. RESULTS: Ischemia-induced CK release, 
      cell necrosis, and apoptosis in the diabetic myocardium were not significantly 
      affected by IP or by co-incubation with autologous or non-diabetic allogenic 
      BMCs. Conversely, significant reduction in CK release, cell necrosis, and 
      apoptosis were observed when non-diabetic myocardium was co-incubated with 
      allogenic diabetic BMCs. Interestingly, while allogenic BMCs from subjects with 
      preserved LV function exerted a modest but significant reduction in CK leakage 
      and cell necrosis, but not apoptosis, on failing myocardium, the BMCs from 
      patients with poor LV function failed to protect their own and the allogenic 
      myocardium from subjects with normal LV function. CONCLUSIONS: The failure to 
      protect the myocardium of patients with poor LV function against 
      ischemia/reoxygenation-induced injury is mainly due to a deficit in their BMCs 
      and the myocardium itself, whereas in patients with diabetes the deficit remains 
      within the myocardium and not in the BMCs.
CI  - Copyright (c) 2012 Elsevier Inc. All rights reserved.
FAU - Lai, Vien Khach
AU  - Lai VK
AD  - Cardiac Surgery Unit, Department of Cardiovascular Sciences, University of 
      Leicester, UK.
FAU - Linares-Palomino, Jose
AU  - Linares-Palomino J
FAU - Treumann, Achim
AU  - Treumann A
FAU - Saeed, Muhammad
AU  - Saeed M
FAU - Nadal-Ginard, Bernardo
AU  - Nadal-Ginard B
FAU - Galinanes, Manuel
AU  - Galinanes M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20111018
PL  - United States
TA  - J Surg Res
JT  - The Journal of surgical research
JID - 0376340
SB  - IM
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Bone Marrow Cells/*physiology
MH  - Diabetes Mellitus/*physiopathology
MH  - Humans
MH  - *Ischemic Preconditioning, Myocardial
MH  - Middle Aged
MH  - Myocardial Reperfusion Injury/*prevention & control
MH  - *Ventricular Function, Left
EDAT- 2011/11/22 06:00
MHDA- 2012/05/15 06:00
CRDT- 2011/11/22 06:00
PHST- 2011/05/05 00:00 [received]
PHST- 2011/09/15 00:00 [revised]
PHST- 2011/09/23 00:00 [accepted]
PHST- 2011/11/22 06:00 [entrez]
PHST- 2011/11/22 06:00 [pubmed]
PHST- 2012/05/15 06:00 [medline]
AID - S0022-4804(11)00811-0 [pii]
AID - 10.1016/j.jss.2011.09.050 [doi]
PST - ppublish
SO  - J Surg Res. 2012 May 1;174(1):e1-e10. doi: 10.1016/j.jss.2011.09.050. Epub 2011 
      Oct 18.