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  • 1
    ISSN: 1615-5947
    Keywords: Chylous ascites ; ascites ; abdominal aortic operations
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Three patients, two women, one man (mean age 74 years), who had abdominal aortic aneurysms (2) or aortobifemoral surgery (1), developed chylous ascites postoperatively. They were studied to determine their clinical course and develop a plan for management of this complication. In each patient, the ascites was not manifest until abdominal swelling developed two weeks after operation, and the problem was confirmed by the finding of milky fluid on paracentesis. A low serum albumin (mean 2.6 gm) was also characteristic. The ascites was not altered by parenteral nutrition or reduction of dietary fat and ingestion of medium chain triglycerides. In one patient (man, age 93) the ascites resolved spontaneously two months after abdominal aortic aneurysm surgery. Another (woman, age 70) was cured following operative ligation of a lymphatic fistula identified at operation five weeks after abdominal aortic aneurysm repair. In the third (woman, age 60), the ascites resolved immediately following placement of a peritoneal venous shunt six weeks after an aortobifemoral bypass. Chylous ascites is rare after aortic surgery and manifests itself about two weeks after operation, at times after discharge from hospital. It has an indolent course, but may resolve spontaneously up to two months after operation. Its course appears not to be foreshortened by diet, including omission of fat, but can be successfully treated surgically with a shunt or fistula ligation. If done early a protracted hospital course may be avoided.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2013
    Keywords: Key words Ca2+ entry ; Kinetics ; Thapsigargin ; Parotid cells ; Fura-2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The molecular mechanism(s) involved in mediating Ca2+ entry into rat parotid acinar and other non-excitable cells is not known. In this study we have examined the kinetics of Ca2+ entry in fura-2-loaded parotid acinar cells, which were treated with thapsigargin to deplete internal Ca2+ pools (Ca2+-pool-depleted cells). The rate of Ca2+ entry was determined by measuring the initial increase in free cytosolic [Ca2+] ([Ca2+]i) in Ca2+-pool-depleted, and control (untreated), cells upon addition of various [Ca2+] to the medium. In untreated cells, a low-affinity component was detected with K Ca = 3.4 ± 0.7 mM (where K Ca denotes affinity for Ca2+) and V max = 9.8 ± 0.4 nM [Ca2+]i /s. In thapsigargin-treated cells, two Ca2+ influx components were detected with K Ca values of 152 ±  79 μM (V max = 5.1 ± 1.9 nM [Ca2+]i/s) and 2.4 ±  0.9 mM (V max = 37.6 ± 13.6 nM [Ca2+]i/s), respectively. We have also examined the effect of Ca2+ and depolarization on these two putative Ca2+ influx components. When cells were treated with thapsigargin in a Ca2+-free medium, Ca2+ influx was higher than into cells treated in a Ca2+-containing medium and, while there was a 46% increase in the V max of the low-affinity component (no change in K Ca), the high-affinity component was not clearly detected. In depolarized Ca2+-pool-depleted cells (with 50 mM KCl in the medium) the high-affinity component was considerably decreased while there was an apparent increase in the K Ca of the low-affinity component, without any change in the V max. These results demonstrate that Ca2+ influx into parotid acinar cells (1) is increased (four- to five-fold) upon internal Ca2+ pool depletion, and (2) is mediated via at least two components, with low and high affinities for Ca2+.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-2013
    Keywords: Ca2+ influx ; G-protein ; Muscarinic receptor ; Carbachol ; Thapsigargin ; Salivary gland cells
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the human submandibular ductal cell line (HSG) thapsigargin and carbachol stimulated Ca2+ release from the internal Ca2+ pool, resulting in the activation of capacitatively regulated Ca2+ entry (CRCE). This entry pathway was permeant to both Ca2+ and Mn2+, blocked by Ni2+ and insensitive to the muscarinic antagonist, atropine. Carbachol also stimulated an increase in cytosolic [Ca2+] in internal Ca2+-pool-depleted (i.e.thapsigargin-treated) cells which was dependent on the presence of external Ca2+ and blocked by Ni2+, demonstrating that it was due to Ca2+ entry. However, under the same experimental conditions, carbachol was unable to stimulate Mn2+ entry. Additionally, this latter carbachol-stimulated Ca2+ entry pathway was blocked by atropine. Pretreatment of HSG cells with AlF4-increased basal rates of Mn2+ entry due to CRCE activation, but attenuated carbachol-stimulated Ca2+ entry into thapsigargin-treated cells. The data suggest that two distinct divalent cation entry pathways are activated in muscarinic-receptor-stimulated HSG cells; a CRCE mechanism, permeable to both Mn2+ and Ca2+, and a second entry mechanism, permeable only to Ca2+. The latter does not depend on internal pool depletion, but appears to be regulated via G-protein activation.
    Type of Medium: Electronic Resource
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