PMID- 31427970
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200929
IS  - 1663-9812 (Print)
IS  - 1663-9812 (Electronic)
IS  - 1663-9812 (Linking)
VI  - 10
DP  - 2019
TI  - The Effect of Glycemic Control on Endothelial and Cardiac Dysfunction Induced by 
      Red Blood Cells in Type 2 Diabetes.
PG  - 861
LID - 10.3389/fphar.2019.00861 [doi]
LID - 861
AB  - Red blood cells (RBCs) from patients with type 2 diabetes mellitus (T2DM) induce 
      endothelial dysfunction and impair cardiac function following ischemia via 
      increase in RBC arginase and oxidative stress. Here, we aimed to elucidate 
      whether the effect of RBC-mediated cardiac impairment following ischemia and 
      endothelial dysfunction in T2DM is dependent on glycemic control. Patients with 
      T2DM at poor glycemic control (T2DM PGC) and at improvement in glycemic control 
      (T2DM IGC) and healthy subjects were recruited. Isolated RBCs from subjects were 
      incubated with aortic rings from healthy wild-type rats with subsequent 
      evaluation of endothelium-dependent relaxation (EDR) using wire myograph. 
      Moreover, RBCs were administered to isolated wild-type rat hearts with subsequent 
      evaluation of left ventricular developed pressure (LVDP) during reperfusion using 
      Langendorff setup. In separate experiments, RBCs were preincubated with an 
      arginase inhibitor before perfusion. Blood glucose and glycated hemoglobin were 
      33 and 26%, respectively, lower in T2DM IGC compared with those in T2DM PGC. RBCs 
      from T2DM PGC and T2DM IGC impaired EDR to a similar magnitude compared with RBCs 
      from healthy subjects. LVDP was significantly impaired in hearts given RBCs from 
      T2DM PGC as compared with those from healthy subjects. The impairment of LVDP 
      induced by T2DM PGC was attenuated by RBCs from T2DM IGC. Arginase inhibition 
      improved LVDP to a similar extent between T2DM PGC and IGC groups. These 
      observations indicate that glycemic control abrogate the impairment in 
      postischemic recovery but not endothelial dysfunction induced by RBCs from T2DM. 
      Moreover, inhibition of RBC arginase improves cardiac function irrespective of 
      glycemic control.
FAU - Mahdi, Ali
AU  - Mahdi A
AD  - Division of Cardiology, Department of Medicine, Karolinska Institutet, Karolinska 
      University Hospital, Stockholm, Sweden.
FAU - Jiao, Tong
AU  - Jiao T
AD  - Division of Cardiology, Department of Medicine, Karolinska Institutet, Karolinska 
      University Hospital, Stockholm, Sweden.
FAU - Yang, Jiangning
AU  - Yang J
AD  - Division of Cardiology, Department of Medicine, Karolinska Institutet, Karolinska 
      University Hospital, Stockholm, Sweden.
FAU - Kovamees, Oskar
AU  - Kovamees O
AD  - Division of Cardiology, Department of Medicine, Karolinska Institutet, Karolinska 
      University Hospital, Stockholm, Sweden.
FAU - Alvarsson, Michael
AU  - Alvarsson M
AD  - Division of Endocrinology and Diabetology, Department of Molecular Medicine and 
      Surgery, Karolinska Institutet, Karolinska University Hospital, Stockholm, 
      Sweden.
FAU - von Heijne, Maaria
AU  - von Heijne M
AD  - Department of Clinical Sciences, Karolinska Institutet, Danderyd Hospital, 
      Danderyd, Sweden.
FAU - Zhou, Zhichao
AU  - Zhou Z
AD  - Division of Cardiology, Department of Medicine, Karolinska Institutet, Karolinska 
      University Hospital, Stockholm, Sweden.
FAU - Pernow, John
AU  - Pernow J
AD  - Division of Cardiology, Department of Medicine, Karolinska Institutet, Karolinska 
      University Hospital, Stockholm, Sweden.
LA  - eng
PT  - Journal Article
DEP - 20190802
PL  - Switzerland
TA  - Front Pharmacol
JT  - Frontiers in pharmacology
JID - 101548923
PMC - PMC6688094
OTO - NOTNLM
OT  - diabetes
OT  - endothelial dysfunction
OT  - glycemic control
OT  - ischemia
OT  - red blood cells
OT  - reperfusion
EDAT- 2019/08/21 06:00
MHDA- 2019/08/21 06:01
PMCR- 2019/08/02
CRDT- 2019/08/21 06:00
PHST- 2019/03/25 00:00 [received]
PHST- 2019/07/05 00:00 [accepted]
PHST- 2019/08/21 06:00 [entrez]
PHST- 2019/08/21 06:00 [pubmed]
PHST- 2019/08/21 06:01 [medline]
PHST- 2019/08/02 00:00 [pmc-release]
AID - 10.3389/fphar.2019.00861 [doi]
PST - epublish
SO  - Front Pharmacol. 2019 Aug 2;10:861. doi: 10.3389/fphar.2019.00861. eCollection 
      2019.