PMID- 12818967
OWN - NLM
STAT- MEDLINE
DCOM- 20030717
LR  - 20190704
IS  - 0003-2999 (Print)
IS  - 0003-2999 (Linking)
VI  - 97
IP  - 1
DP  - 2003 Jul
TI  - Dobutamine inhibits monocyte chemoattractant protein-1 production and chemotaxis 
      in human monocytes.
PG  - 205-9, table of contents
AB  - It has been reported that, in patients with acute myocardial infarction or 
      congestive heart failure, monocyte chemoattractant protein-1 (MCP-1) plays an 
      important role in the development of inflammatory responses and that the level of 
      MCP-1 is correlated with the severity of the disease. We conducted this study to 
      investigate the effects of dobutamine and dopamine on lipopolysaccharide 
      (LPS)-induced MCP-1 production in human monocytic THP-1 cells. Monocytes were 
      incubated in vitro with LPS for 16 h at 37 degrees C in the presence or absence 
      of dobutamine or dopamine. Enzyme-linked immunosorbent assay was used to examine 
      the effect of dobutamine on MCP-1 synthesis, with the MCP-1 messenger RNA 
      expression examined by reverse transcriptase-polymerase chain reaction. 
      Dobutamine inhibited LPS-induced production of MCP-1, as well as messenger RNA 
      expression, in a dose-dependent manner, whereas dopamine had no significant 
      effect. Furthermore, we demonstrated that dobutamine suppressed MCP-1-induced 
      chemotaxis and peak [Ca(2+)](i) in monocytic THP-1 cells. These findings suggest 
      that dobutamine may modulate monocyte activation, such as chemotaxis and 
      [Ca(2+)](i), as well as MCP-1 production, during therapy for congestive heart 
      failure. IMPLICATIONS: Monocyte chemoattractant protein-1 (MCP-1) plays important 
      roles in the inflammatory processes associated with pathogenesis of 
      cardiovascular diseases. In this study, dobutamine was found to inhibit 
      lipopolysaccharide-induced MCP-1 production and messenger RNA expression, as well 
      as MCP-1-induced chemotaxis and peak [Ca(2+)](i), in human monocytes.
FAU - Li, Chi-Yuan
AU  - Li CY
AD  - Department of Anesthesiology, Tri-Service General Hospital, Taipei, Taiwan, 
      Republic of China. cyli@ndmctsgh.edu.tw
FAU - Tsai, Chien-Sung
AU  - Tsai CS
FAU - Chueh, Sheau-Huei
AU  - Chueh SH
FAU - Hsu, Ping-Ching
AU  - Hsu PC
FAU - Wang, Jia-Yi
AU  - Wang JY
FAU - Wong, Chih-Shung
AU  - Wong CS
FAU - Ho, Shung-Tai
AU  - Ho ST
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Anesth Analg
JT  - Anesthesia and analgesia
JID - 1310650
RN  - 0 (Adrenergic beta-Agonists)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
RN  - 3S12J47372 (Dobutamine)
RN  - QF8SVZ843E (Albuterol)
RN  - SY7Q814VUP (Calcium)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Adrenergic beta-Agonists/*pharmacology
MH  - Albuterol/pharmacology
MH  - Calcium/metabolism
MH  - Cell Movement/drug effects
MH  - Chemokine CCL2/*antagonists & inhibitors/*biosynthesis
MH  - Chemotaxis/*drug effects
MH  - Depression, Chemical
MH  - Dobutamine/*pharmacology
MH  - Dopamine/pharmacology
MH  - Electrophoresis, Polyacrylamide Gel
MH  - Humans
MH  - In Vitro Techniques
MH  - Lipopolysaccharides/pharmacology
MH  - Monocytes/*drug effects/*metabolism
MH  - RNA, Messenger/biosynthesis
MH  - Reverse Transcriptase Polymerase Chain Reaction
EDAT- 2003/06/24 05:00
MHDA- 2003/07/18 05:00
CRDT- 2003/06/24 05:00
PHST- 2003/06/24 05:00 [pubmed]
PHST- 2003/07/18 05:00 [medline]
PHST- 2003/06/24 05:00 [entrez]
AID - 10.1213/01.ane.0000066013.34263.54 [doi]
PST - ppublish
SO  - Anesth Analg. 2003 Jul;97(1):205-9, table of contents. doi: 
      10.1213/01.ane.0000066013.34263.54.