Letter to the editor: Do neutrophils contribute to the clearance of injured cardiomyocytes in reperfusion injury?
✍ Scribed by Beranek, J. T.
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 19 KB
- Volume
- 183
- Category
- Article
- ISSN
- 0022-3417
No coin nor oath required. For personal study only.
✦ Synopsis
As a student of cardiac reperfusion 1 , I was intrigued by Fig. in the article by Seko et al. about the expression and the role of sialyl Lewis X antigen (SLe X ) in heart reperfusion injury. Their photograph visualizes not only the expression of SLe X , but also the extensive destruction and disappearance of cardiomyocytes evidenced by enormously enlarged interstitial spaces and by the bizarre contours of remaining atrophic cardiomyocytes. Since the authors do not discuss this fact, their article creates the impression that the interaction between SLe X , selectins, and neutrophils contributed decisively not only to the death of cardiomyocytes, but also to their elimination.
In myocardial infarcts, neutrophils do not inflict any histologically recognizable injury on cardiomyocytes. How, then, are the destruction and disappearance of cardiomyoctes in Fig. 2 to be explained?
There is only one plausible answer to this question: the terminal complement-complex lysed ischaemic cardiomyocytes into 'eosinophilic droplets' which were eliminated subsequently by lymphatic flow and/or proteolysis. This proposition is corroborated by Shandelya et al., who found that complement, even though not needed for the adhesion of neutrophils to endothelial surfaces, is indispensable for their activation in the ischaemic heart and that the terminal complement-complex was deposited in the reperfused heart. With this information in mind, it would be most interesting to know whether the anti-SLe X monoclonal antibody treatment 2 reduced the disappearance of cardiomyocytes seen in Fig. J. T. B