PMID- 1380615
OWN - NLM
STAT- MEDLINE
DCOM- 19920924
LR  - 20031114
IS  - 0160-2446 (Print)
IS  - 0160-2446 (Linking)
VI  - 20 Suppl 1
DP  - 1992
TI  - Molecular biology of the coronary vascular and myocardial responses to ischemia.
PG  - S23-31
AB  - To understand the complex mechanism(s) involved in molecular responses to 
      ischemia, we developed two experimental models in pigs. In a "stunning" model of 
      repetitive ischemia and reperfusion, we studied the mRNA expression of immediate 
      early genes like c-fos, c-myc and heat shock protein-70 (HSP-70). Myocardial 
      stunning was achieved by two cycles of 10-min left anterior descending coronary 
      artery (LAD) occlusion and 30 min reperfusion. We observed several-fold enhanced 
      expression of c-fos and HSP-70 mRNA in the stunned myocardium as compared with 
      the control, whereas c-myc mRNA levels remained almost unchanged. In the second 
      model, we examined the expression of the peptide mitogens heparin-binding growth 
      factor 1 (HBGF-1) and transforming growth factor beta 1 (TGF-beta 1) after a 
      chronic coronary artery occlusion leading to myocardial collateralization. 
      Progredient stenosis of the circumflex coronary artery was induced by implanting 
      a hygroscopic ameroid constrictor ring around it and occlusion was verified by in 
      vivo angiography. Using polymerase chain reaction (PCR) and Northern 
      hybridization techniques, we observed significantly enhanced expression of HBGF-1 
      and TGF-beta 1 in collateralized myocardium as compared with normal. In situ 
      techniques revealed the localization of HBGF-1 transcripts in the blood vessel 
      wall, and TGF-beta 1 in cardiac myocytes and Purkinje cells. Our results clearly 
      indicate that myocardial stunning stimulates the expression of transcription 
      factors which might be involved in regulation of certain growth factors like 
      HBGF-1 and TGF-beta 1 which may play a significant role in the development of a 
      collateral circulation.
FAU - Sharma, H S
AU  - Sharma HS
AD  - Department of Experimental Cardiology, Max-Planck Institute, Bad Nauheim, 
      Germany.
FAU - Wunsch, M
AU  - Wunsch M
FAU - Brand, T
AU  - Brand T
FAU - Verdouw, P D
AU  - Verdouw PD
FAU - Schaper, W
AU  - Schaper W
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Cardiovasc Pharmacol
JT  - Journal of cardiovascular pharmacology
JID - 7902492
RN  - 0 (Heat-Shock Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transforming Growth Factor beta)
RN  - 104781-85-3 (Fibroblast Growth Factor 1)
SB  - IM
GS  - c-fos
GS  - c-myc
MH  - Animals
MH  - Blotting, Northern
MH  - Coronary Disease/genetics/*metabolism
MH  - Coronary Vessels/*metabolism
MH  - Disease Models, Animal
MH  - Fibroblast Growth Factor 1/genetics
MH  - Gene Expression
MH  - Genes, fos
MH  - Genes, myc
MH  - Heat-Shock Proteins/biosynthesis
MH  - Male
MH  - Myocardial Reperfusion
MH  - Myocardium/*metabolism
MH  - Neovascularization, Pathologic/*metabolism
MH  - Polymerase Chain Reaction
MH  - RNA, Messenger/analysis/genetics
MH  - Swine
MH  - Transcription, Genetic
MH  - Transforming Growth Factor beta/genetics
EDAT- 1992/01/01 00:00
MHDA- 1992/01/01 00:01
CRDT- 1992/01/01 00:00
PHST- 1992/01/01 00:00 [pubmed]
PHST- 1992/01/01 00:01 [medline]
PHST- 1992/01/01 00:00 [entrez]
PST - ppublish
SO  - J Cardiovasc Pharmacol. 1992;20 Suppl 1:S23-31.