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(Circulation Research. 2003;93:e25.)
© 2003 American Heart Association, Inc.

Letter to the Editor

Priority of Experimental Evidence

Shigeru Nishizawa

Hamamatsu, Japan, nisizawa@hama-med.ac.jp

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

The authors of a recent article that appeared in Circulation Research¹ described that "there is no information available regarding the mechanism by which SAH activates the Rho/Rho kinase or PKC pathways" (page 810). I would like to say that such a description is incorrect. There is a history of experiments to identify the relationship between the roles of protein kinase C (PKC) and the mechanism of vasospasm after subarachnoid hemorrhage (SAH). In particular, we have extensively investigated the roles of PKC in the development and maintenance of vasospasm after SAH, as listed in the References.^2–5 Wickman et al¹ should have discussed the history of the experiments regarding "the mechanism by which SAH activates PKC pathways." Since we clarified the roles of PKC in the mechanism of vasospasm, we carefully examined which PKC isoforms are expressed in canine basilar artery and which ones are involved in the development and maintenance of vasospasm with Western blotting analysis, just as the authors did. We detected four PKC isoforms in canine basilar artery (PKC, , , ). Among these four PKC isoforms, PKC is closely related with the initiation and PKC with the maintenance of vasospasm in a "two-hemorrhage" canine model (in situ 1-week study). Because the antibodies for PKC isoforms are derived from a different space (rat brain), we showed the specificity of the bands expressed in Western blotting by elimination of these bands using antibody-specific synthetic peptides. I believe that it is not good enough to show the . . . [Full Text of this Article]