PMID- 9659449
OWN - NLM
STAT- MEDLINE
DCOM- 19980730
LR  - 20190512
IS  - 0008-6363 (Print)
IS  - 0008-6363 (Linking)
VI  - 37
IP  - 3
DP  - 1998 Mar
TI  - The low molecular weight heparin, enoxaparin, limits infarct size at reperfusion 
      in the dog.
PG  - 656-66
AB  - OBJECTIVE: Heparin (HEP) is used in the post-thrombolytic state to prevent vessel 
      reocclusion, thereby aiding myocardial salvage. Side effects limit its benefits, 
      but besides anticoagulant activity HEP has diffuse actions that may be 
      potentially beneficial to jeopardized reperfused myocardium. This study compares 
      the effect of therapeutic doses of HEP and enoxaparin (ENOX), a low molecular 
      weight heparin, and to streptokinase (SK), on infarct size. METHODS: The left 
      anterior descending coronary artery was occluded in dogs for 90 min, followed by 
      6 h of reperfusion with a residual critical stenosis in place. Five min before 
      reperfusion, HEP (2800 IU) was injected i.v., and perfused at 500 IU/h until 
      sacrifice in group 2, while groups 3 and 4 received ENOX (2128 anti-Xa IU i.v.) 
      followed by 380 anti-Xa IU/h. Group 4 was also given 500,000 IU SK over 30 min 
      before reperfusion beginning at 55 min of occlusion (ENOX + SK), while group 5 
      received only SK. Controls (CON, group 1) received saline. P-selectin mediated 
      platelet-neutrophil rosettes formation was also tested in vitro in the presence 
      of HEP and ENOX. RESULTS: The area at risk delimited by dye perfusion was 
      statistically similar among groups. Covariance analysis between infarct size (% 
      of area at risk) delimited with triphenyltetrazolium and collateral flow measured 
      with radioactive microspheres confirmed that groups given ENOX (21.6 +/- 5.5%) 
      and ENOX + SK (24.9 +/- 3.9%) developed smaller infarcts (P < 0.05) than CON 
      (48.1 +/- 4.5%), as opposed to HEP (32.2 +/- 3.6%) and SK (46.8 +/- 3.4%) groups. 
      111In-platelet counts in the infarct were reduced significantly by 64% in the 
      ENOX group as compared to CON, and to a lesser extent (42%, n.s.) in the ENOX + 
      SK group, but were not reduced by HEP and SK treatments. Neutrophil accumulation 
      in the infarcts was decreased significantly and by more than 75% in the ENOX and 
      ENOX + SK groups versus CON, but not in the HEP and SK groups. Also, only ENOX 
      (10-100 micrograms/ml) significantly inhibited platelet-neutrophil rosettes 
      formation in a plasmatic milieu. CONCLUSIONS: The ENOX treatment, as opposed to 
      that of HEP, reduces myocardial platelet and neutrophil accumulations, and limits 
      infarct size when given just before and during reperfusion. The benefits of ENOX 
      on infarct size were not modified by SK, and may be related, at least in part, to 
      an interaction with P-selectin-mediated cell adhesion.
FAU - Libersan, D
AU  - Libersan D
AD  - Laboratory of Experimental Pathology, Montreal Heart Institute, Canada.
FAU - Khalil, A
AU  - Khalil A
FAU - Dagenais, P
AU  - Dagenais P
FAU - Quan, E
AU  - Quan E
FAU - Delorme, F
AU  - Delorme F
FAU - Uzan, A
AU  - Uzan A
FAU - Latour, J G
AU  - Latour JG
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Cardiovasc Res
JT  - Cardiovascular research
JID - 0077427
RN  - 0 (Anticoagulants)
RN  - 0 (Enoxaparin)
RN  - 9005-49-6 (Heparin)
RN  - EC 3.4.- (Streptokinase)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Anticoagulants/*therapeutic use
MH  - Blood Platelets/pathology
MH  - Cells, Cultured
MH  - Dogs
MH  - Enoxaparin/*therapeutic use
MH  - Erythrocytes/pathology
MH  - Female
MH  - Heparin/therapeutic use
MH  - Male
MH  - Myocardial Ischemia/drug therapy/pathology
MH  - Myocardial Reperfusion Injury/pathology/*prevention & control
MH  - Myocardium/pathology
MH  - Neutrophils/pathology
MH  - Platelet Adhesiveness/drug effects
MH  - Streptokinase/therapeutic use
MH  - *Thrombolytic Therapy
EDAT- 1998/07/11 00:00
MHDA- 1998/07/11 00:01
CRDT- 1998/07/11 00:00
PHST- 1998/07/11 00:00 [pubmed]
PHST- 1998/07/11 00:01 [medline]
PHST- 1998/07/11 00:00 [entrez]
AID - S0008-6363(97)00292-7 [pii]
AID - 10.1016/s0008-6363(97)00292-7 [doi]
PST - ppublish
SO  - Cardiovasc Res. 1998 Mar;37(3):656-66. doi: 10.1016/s0008-6363(97)00292-7.