Juntendo Medical Journal
Online ISSN : 2188-2134
Print ISSN : 0022-6769
ISSN-L : 0022-6769
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Volume 40, Issue 2
Displaying 1-18 of 18 articles from this issue
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Contents
  • Changes in bradykinin by membrane plasmapheresis
    MASAKAZU YOKOYAMA, HIROSHI TSUDA
    1994 Volume 40 Issue 2 Pages 183-188
    Published: September 05, 1994
    Released on J-STAGE: November 18, 2014
    DOIhttps://doi.org/10.14789/pjmj.40.183
    JOURNAL FREE ACCESS
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    Recently, there have been some reports that one of the causes of shock during plasmapheresis (PP) is bradykinin (BK). We examined BK during PP using membrane filters. We treated five patients (rheumatoid arthritis: three patients, systemic lupus erythematosus: two patients) using single filtration PP and investigated the BK level at three points: pre-filter, post-filter, and in the filtrated plasma. We used three filters: polyethylene (OP), and two kinds of polysulfone filters (PS and FS). As an anticoagulant, we used heparin (HP) or nafamostat mesilate (NM). The initial dose of HP was 2000 units, and we used HP at 1100 units per hour during PP, while NM was used at 40 mg per hour during PP. In the patients receiving HP, after 15 minutes, the BK level was increased slightly using OP, and was increased remarkably using PS or FS. After 600 ml of plasma filtration, the BK level was increased slightly using OP, PS, or FS. In the patients receiving NM, after 15 minutes and after 600 ml blood of circulation, the BK level was not increased. We investigated the influence of anticoagulants on BK, which is suggested to be a cause of shock in PP. With HP, BK was increased remarkably post-filter. We considered that BK was activated by the filter when using HP, while BK was not activated by NM.
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  • Diversity of human smooth muscle myosin heavy chains
    -Significance as markers for vascular development and atherosclerosis-
    MASANORI AIKAWA
    1994 Volume 40 Issue 2 Pages 189-199
    Published: September 05, 1994
    Released on J-STAGE: November 18, 2014
    DOIhttps://doi.org/10.14789/pjmj.40.189
    JOURNAL FREE ACCESS
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    Rabbit smooth muscle contains at least three types of myosin heavy chain (MHC) isoforms; SM1, SM2 and SMemb. SM1 and SM2 are specific to smooth muscle, but SMemb is a nonmuscle-type MHC abundantly expressed in the embryonic aorta. These three MHC isoforms are differentially expressed in the rabbit during normal vascular development and in experimental arterio- and atherosclerosis. This study investigated whether expression of human smooth muscle MHC isoforms is regulated in developing arteries and in atherosclerotic lesions. To accomplish this cDNA clones encoding human SM 1, SM2 and SMemb were isolated. The expression of SM2 mRNA in the fetal aorta was significantly lower compared to SM1 mRNA, but ratio of SM2- to SM1-mRNA in the aorta decreased after birth, but appeared to increase in the aged. In immunohistological studies using three antibodies against human MHC isoforms, SM1 was constitutively positive from the fetal stage to adulthood in the apparently normal media of the aorta and coronary arteries, whereas SM2 was negative in fetal arteries at an early gestational stage. In the human aorta or coronary arteries, unlike the rabbit, SMemb was detected even in the adult. Diffuse intimal thickening in the major coronary arteries was composed of smooth muscle cells, reacting equally to three antibodies for MHC isoforms, but reactivities with anti-SM2 antibody were reduced with aging. With progression of atherosclerosis, intimal smooth muscle diminished the expression of not only SM2 but also SM1, whereas α-smooth muscle actin was preserved. These results suggest that smooth muscle MHC isoforms are important molecular markers for studying human vascular smooth muscle cell differentiation as well as the cellular mechanisisms of atherosclerosis.
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  • The role of ejection velocity in the oxygen-wasting effect to a change in contractility
    Yoshitaka HAYASHI
    1994 Volume 40 Issue 2 Pages 200-209
    Published: September 05, 1994
    Released on J-STAGE: November 18, 2014
    DOIhttps://doi.org/10.14789/pjmj.40.200
    JOURNAL FREE ACCESS
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    Recent studies have shown that left ventricular oxygen consumption (VO2) linearly correlates with systolic pressure-volume area (PVA), and VO2 is predicted by the empirical equation VO2=A·PVA+B·Emax+C. When PVA is maintained at zero in an unloaded condition, unloaded VO2 increases with increases in contractility (Ema), which indicates oxygen-wasting due to changes in contractility. To investigate the role of ejection velocity in the oxygen-wasting (Vmax) -unloaded VO2 relation in normal and hyperthyroid rabbit hearts. Thyrotoxic stress in the rabbit is known to alter the myosin isoform component from predominantly V3 (low mobility) to predominantly V1 (high mobility). Afer the establishment of retrograde coronary perfusion, the heart was isolated and a latex balloon was inserted into the left ventricular cavity. Then, the balloon was connected to a volume controller. Ejection velocity was measured using an isovelocity method under different coronary perfusions. Emax, PVA, VO2 were also measured under different coronary perfusions, The Vmax-unloaded VO2 relation and the Emax-unloaded VO2 relation was linear in normal heart. By contrast, in the hyperthyroid heart, the Emax-unloaded VO2 relasion was linear under lower coronary perfusion, but became steeper under higher coronary perfusion. When the slope of the Emax-unloaded VO2 became steeper, Vmax showed further increase. Our results suggest that increases in ejection velocity are largely responsible for the oxygen-wastiong effect in the hyperthyroid heart.
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  • Sigmoidcolocystoplasty for the patients with spina bifida
    -Clinical analysis of 40 children-
    ARATA MORIOKA, TAKESHI MIYANO, HIROSHI SHIMOMURA, SATOSHI SEKI, KIYOHI ...
    1994 Volume 40 Issue 2 Pages 210-220
    Published: September 05, 1994
    Released on J-STAGE: November 18, 2014
    DOIhttps://doi.org/10.14789/pjmj.40.210
    JOURNAL FREE ACCESS
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    We performed sigmoidcolocystoplasty in 40 patients with neurogenic bladder who had refractory clean intermittent catheterization, medication and non-surgical treatment. Forty pediatric myelomeningocele patients were studied. In this series, many patients with defunctionalized bladder showed urinary incontience, small capacity, low compliance and/or vesicoureteral reflux. An excellent surgical result was obtained in 89 percent of these patients who became asymptomatic and obtained urinary continence after sigmoidcolocystoplasty. Forty-eight percent of the patients achieved complete bladder emptying, 45 percent were able to void with minimal post-void residual urine. Twenty-three patients with vesicoureteral reflux were all improved by antireflux procedure using the Cohen, Leadbetter-Politano technique, or using an implanted colon cap through the submucosal tunnel technique. This study, included 7 patients developed late complications. In one child, a mechanical small bowel obstruction developed (required surgical adhenolysis). Two ureters of 2 children showed ureteral obstruction after antireflux procedure. Stone formation occurred in 4 patients.
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  • Serum thrombomodulin levels in rheumatic diseases
    -A study for a maker of endothelial injury and correlation with anticardiolipin antibodies-
    MITSUHIKO TANAKA, SHIGETO KOBAYASHI, NAOTO TAMURA, HIROSHI HASHIMOTO, ...
    1994 Volume 40 Issue 2 Pages 221-229
    Published: September 05, 1994
    Released on J-STAGE: November 18, 2014
    DOIhttps://doi.org/10.14789/pjmj.40.221
    JOURNAL FREE ACCESS
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    To investigate the serological marker of vascular involvement in rheumatic diseases, serum thrombomodulin (TM) levels were determined. Serum TM levels were significantly elevated in 15 patients with vasculitis syndrome (39.4±33.1ng/ ml; p<0.01), 22 patients with systemic lupus erythematosus (SLE) (26.8±15.8ng/ ml; p<0.01) and 15 patients with progressive systemic sclerosis (PSS) compared to those in healthy controls. In addition serum TM levels increased with the exacerbation of vascular involvement. Since anticardiolipin antibody (aCL) is one of the causes of thrombosis in patients with rheumatic diseases, aCL levels were determined in the presence of a cofactor (β2 glycoprotein I) using aCL ELISA. aCL was significantly elevated in SLE patients (p<0.01) compared to patients with other rheumatic diseases and that of healthy controls. Among these 22 SLE patients, TM levels correlated with aCL levels (r=-0.565; p<0.01). Our findings indicated that the serum TM level is an excellent maker of the vascular involvement in rheumatic diseases and might directly reflect the degree of endothelial injury due to aCL in SLE patients.
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