The Keio Journal of Medicine
Online ISSN : 1880-1293
Print ISSN : 0022-9717
ISSN-L : 0022-9717
Volume 63, Issue 1
Displaying 1-2 of 2 articles from this issue
ORIGINAL ARTICLE
  • Koichiro Homma, Koichi Hayashi, Shu Wakino, Hirobumi Tokuyama, Takeshi ...
    Article type: Original Article
    2014 Volume 63 Issue 1 Pages 1-12
    Published: 2014
    Released on J-STAGE: April 01, 2014
    Advance online publication: January 16, 2014
    JOURNAL FREE ACCESS
    Renal afferent arterioles (AFF) regulate glomerular capillary pressure through two main mechanisms: the myogenic response (MYO) and tubuloglomerular feedback (TGF). Because Rho-kinase and nitric oxide synthase (NOS) are established factors that modulate vascular tone, we examined the role of these factors in pressure-induced AFF tone in Wistar-Kyoto rats and in spontaneously hypertensive rats (SHR) using an intravital CCD camera. Elevated renal perfusion pressure elicited marked AFF constriction that was partially inhibited by gadolinium, furosemide and fasudil, which inhibit MYO, TGF and Rho-kinase, respectively; however, this AFF constriction was completely blocked by combined treatment with fasudil+gadolinium or fasudil+furosemide. S-methyl-L-thiocitrulline (SMTC) partially reversed the fasudil-induced inhibition of TGF-mediated, but not that of MYO-mediated, AFF constriction. In SHR, the pressure-induced AFF response was enhanced, and MYO- and TGF-induced constriction were exaggerated. In the presence of gadolinium, SMTC partially mitigated the fasudil-induced inhibition of TGF-mediated AFF constriction. Immunoblot analyses demonstrated that both Rho-kinase activity and neuronal NOS were augmented in SHR kidneys. In conclusion, Rho-kinase contributes to MYO- and TGF-mediated AFF responses, and these responses are enhanced in SHR. Furthermore, neuronal NOS-induced nitric oxide modulates the TGF mechanism. This mechanism constitutes a target for Rho-kinase in TGF-mediated AFF constriction.
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CASE REPORT
  • Takeshi Morioka, Takayuki Honma, Kiyohisa Ogawa
    Article type: Case Report
    2013 Volume 63 Issue 1 Pages 13-17
    Published: 2013
    Released on J-STAGE: April 01, 2014
    Advance online publication: December 10, 2013
    JOURNAL FREE ACCESS
    Two percent of scapular fractures occur as a result of indirect trauma caused by traction of the muscles and ligaments attached to the scapula. We present two cases involving adults with incomplete avulsion fractures of the scapular spine caused by violent voluntary contraction of the deltoid muscle. These cases are the first reported avulsion fractures confined to the scapular spine medial to the spinoglenoid notch. Although the fractures were incomplete, one patient had a typical symptom of scapular fracture − pseudo-rupture of the rotator cuff characterized by clinical signs of a complete rupture of the musculotendinous cuff. Although this symptom is generally thought to be caused by massive hemorrhaging under the rotator-cuff muscle bellies, it may develop from modest bleeding through the formation of an intramuscular hematoma and a resultant elevation in intramuscular pressure. Confirming the presence of tenderness on the scapular spine and performing appropriate imaging investigation constitute a clinically effective method for preventing misdiagnosis.
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