Reviewer's report
 Adenosine preconditioning attenuates hepatic reperfusion injury in the rat by preventing the Title:
down-regulation of endothelial nitric oxide synthase
Authors:
Ferdinand Serracino-Inglott (fsinglott@hotmail.com )
Ioannis T Virlos (itvirlos@hotmail.com )
Nagy A Habib (nagy.habib@ic.ac.uk )
Robin C Willianson (r.williamson@ic.ac.uk )
Robert T Mathie (rmathie@trusthomeopathy.org )
 1  31 May 2002 Version: Date:
 Dr Gina Hotter Reviewer:
 A paper whose findings are important to those with closely related research interests Level of interest:
 Accept after discretionary revisions Advice on publication:
This study is an extension of the author's previous work on the preconditioning field with eemphasis on 
possible applications of adenosine in preventing liver ischemia reperfusion injury. The mechanism is 
postulated to involve endothelial nitric oxide synthase. Although the findings appear to confrirm the 
stated hypothesis, some aspects of the experimental design leave room for discussion. 
Comments 
Results of the present study reveals that the decrease in the inmunoreactivity of endothelial nitric oxide 
synthase ( eNOS) and liver injury after hepatic ischemia reperfusion could be both modulated by adenosine treatment. In addition, the use of L-NNA (an irreversible inhibitor of constitutive NOS as well 
as reversible inhibitor of inducible NOS) leads to the inhibition of the protection confered by adenosine. 
From these results authors conclude that the protective role of adenosine is mediated by upregulation 
of endothelial NOS. 
Authors should use a more specific inhibitor of endothelial NOS to be sure that the inhibition of this NOS
isoform reduces the protection confered by adenosine preconditioning, or alternatively report data ( 
inmunohistochemistry of other specific isoforms) indicative of the non-existence of any NOS up-regulation. 
Competing interests:
None declared.
Reviewer's report
 Adenosine preconditioning attenuates hepatic reperfusion injury in the rat by preventing the Title:
down-regulation of endothelial nitric oxide synthase
Authors:
Ferdinand Serracino-Inglott (fsinglott@hotmail.com )
Ioannis T Virlos (itvirlos@hotmail.com )
Nagy A Habib (nagy.habib@ic.ac.uk )
Robin C Willianson (r.williamson@ic.ac.uk )
Robert T Mathie (rmathie@trusthomeopathy.org )
 1  31 May 2002 Version: Date:
 Dr Gina Hotter Reviewer:
 A paper whose findings are important to those with closely related research interests Level of interest:
 Accept after discretionary revisions Advice on publication:
This study is an extension of the author's previous work on the preconditioning field with eemphasis on 
possible applications of adenosine in preventing liver ischemia reperfusion injury. The mechanism is 
postulated to involve endothelial nitric oxide synthase. Although the findings appear to confrirm the 
stated hypothesis, some aspects of the experimental design leave room for discussion. 
Comments 
Results of the present study reveals that the decrease in the inmunoreactivity of endothelial nitric oxide 
synthase ( eNOS) and liver injury after hepatic ischemia reperfusion could be both modulated by adenosine treatment. In addition, the use of L-NNA (an irreversible inhibitor of constitutive NOS as well 
as reversible inhibitor of inducible NOS) leads to the inhibition of the protection confered by adenosine. 
From these results authors conclude that the protective role of adenosine is mediated by upregulation 
of endothelial NOS. 
Authors should use a more specific inhibitor of endothelial NOS to be sure that the inhibition of this NOS
isoform reduces the protection confered by adenosine preconditioning, or alternatively report data ( 
inmunohistochemistry of other specific isoforms) indicative of the non-existence of any NOS up-regulation. 
Competing interests:
None declared.
Please review this paper.
user
Reviewer's report
 Adenosine preconditioning attenuates hepatic reperfusion injury in the rat by preventing the Title:
down-regulation of endothelial nitric oxide synthase
Authors:
Ferdinand Serracino-Inglott (fsinglott@hotmail.com )
Ioannis T Virlos (itvirlos@hotmail.com )
Nagy A Habib (nagy.habib@ic.ac.uk )
Robin C Willianson (r.williamson@ic.ac.uk )
Robert T Mathie (rmathie@trusthomeopathy.org )
 1  31 May 2002 Version: Date:
 Dr Gina Hotter Reviewer:
 A paper whose findings are important to those with closely related research interests Level of interest:
 Accept after discretionary revisions Advice on publication:
This study is an extension of the author's previous work on the preconditioning field with eemphasis on 
possible applications of adenosine in preventing liver ischemia reperfusion injury. The mechanism is 
postulated to involve endothelial nitric oxide synthase. Although the findings appear to confrirm the 
stated hypothesis, some aspects of the experimental design leave room for discussion. 
Comments 
Results of the present study reveals that the decrease in the inmunoreactivity of endothelial nitric oxide 
synthase ( eNOS) and liver injury after hepatic ischemia reperfusion could be both modulated by adenosine treatment. In addition, the use of L-NNA (an irreversible inhibitor of constitutive NOS as well 
as reversible inhibitor of inducible NOS) leads to the inhibition of the protection confered by adenosine. 
From these results authors conclude that the protective role of adenosine is mediated by upregulation 
of endothelial NOS. 
Authors should use a more specific inhibitor of endothelial NOS to be sure that the inhibition of this NOS
isoform reduces the protection confered by adenosine preconditioning, or alternatively report data ( 
inmunohistochemistry of other specific isoforms) indicative of the non-existence of any NOS up-regulation. 
Competing interests:
None declared.
assistant