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81.
Platelet adherence at high wall shear rates requires plasma von Willebrand factor (vWF). Clinically, the ristocetin cofactor (RCof) activity is the only widely available assay for vWF function. When purified vWF is treated with neuraminidase to yield asialo-vWF (AS- vWF), its RCof activity is increased by 20% to 40%. AS-vWF binds to normal human platelets independently of ristocetin and induces platelet aggregation in the presence of fibrinogen. To determine whether AS-vWF also shows an enhanced capacity to support platelet adherence to subendothelium, we used the Baumgartner technique. Intact vWF, AS-vWF, or AS-vWF treated with beta-galactosidase (asialo, agalacto-vWF; AS,AG- vWF) was added to normal citrated whole blood before perfusion over human umbilical artery segments (wall shear rate, 2,600 sec-1). Four micrograms per milliliter AS-vWF caused a 69% reduction in total platelet adherence compared with citrated whole blood (P less than .001), and 4 micrograms/mL AS,AG-vWF led to a 48% reduction (P less than .005). With 4 micrograms/mL intact vWF, the platelet adherence values were not significantly different from the controls. No significant differences in subendothelial platelet thrombi or postperfusion platelet counts were evident among any of the groups. In reconstituted afibrinogenemic perfusates, 4 micrograms/mL AS-vWF caused a 42% reduction in platelet adherence (P less than .05). Thus, AS-vWF is a potent inhibitor of platelet adherence, despite its enhanced RCof specific activity. Abnormalities in vWF carbohydrate may play a role in impaired primary hemostasis in some patients with von Willebrand's disease. 相似文献
82.
Nitric oxide (NO) is a paramagnetic gas that has been implicated in a wide range of biologic functions. The common pathway to evoke the functional response frequently involves the formation of an iron- nitrosyl complex in a target (heme) protein. In this study, we report on the interactions between NO and cobalt-containing vitamin B12 derivatives. Absorption spectroscopy showed that of the four Co(III) derivatives (cyanocobalamin [CN-Cbl], aquocobalamin [H2O-Cbl], adenosylcobalamin [Ado-Cbl], and methylcobalamin [MeCbl]), only the H2O- Cbl combined with NO. In addition, electron paramagnetic resonance spectroscopy of H2O-Cbl preparations showed the presence of a small amount of Cob-(II)alamin that was capable of combining with NO. The Co(III)-NO complex was very stable, but could transfer its NO moiety to hemoglobin (Hb). The transfer was accompanied by a reduction of the Co(III) to Co(II), indicating that NO+ (nitrosonium) was the leaving group. In accordance with this, the NO did not combine with the Hb Fe(II)-heme, but most likely with the Hb cysteine-thiolate. Similarly, the Co(III)-NO complex was capable of transferring its NO to glutathione. Ado-Cbl and Me-Cbl were susceptible to photolysis, but CN- Cbl and H2O-Cbl were not. The homolytic cleavage of the Co(III)-Ado or Co(III)-Me bond resulted in the reduction of the metal. When photolysis was performed in the presence of NO, formation of NO-Co(II) was observed. Co(II)-nitrosyl oxidized slowly to form Co(III)-nitrosyl. The capability of aquocobalamin to combine with NO had functional consequences. We found that nitrosylcobalamin had diminished ability to serve as a cofactor for the enzyme methionine synthase, and that aquocobalamin could quench NO-mediated inhibition of cell proliferation. Our in vitro studies therefore suggest that interactions between NO and cobalamins may have important consequences in vivo. 相似文献
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U PODDAR Y CHAWLA RK DHIMAN K VAIPHEI RK VASISHTA JB DILAWARI 《Journal of gastroenterology and hepatology》1998,13(1):109-111
Ascites may be associated with fulminant hepatic failure (FHF), but spontaneous bacterial peritonitis (SBP) is an extremely rare complication. We report on two patients with FHF who developed SBP. One patient died and the other recovered. 相似文献
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In vitro and in vivo selectin-blocking activities of sulfated lipids and sulfated sialyl compounds 总被引:2,自引:0,他引:2
Mulligan MS; Warner RL; Lowe JB; Smith PL; Suzuki Y; Miyasaka M; Yamaguchi S; Ohta Y; Tsukada Y; Kiso M; Hasegawa A; Ward PA 《International immunology》1998,10(5):569-575
There is accumulating evidence that sulfated lipids, sulfated
oligosaccharides and other sulfated compounds are reactive with selectins
in a manner that interferes with selectin interactions with their natural
ligands. In the report we describe the ability of sulfated lipids
(sulfatides and gangliosides) and multimeric forms of sulfated sialic acid
to block binding of P- and E-selectin-Ig to neutrophils. The in vivo
ability of these compounds to block lung injury in rats following i.v.
infusion of purified cobra venom factor (CVF), which induces injury that is
L- and P-selectin dependent, was also determined as well as effects on
recruitment of neutrophils, as measured by lung myeloperoxidase. There was
a significant correlation between the ability of sulfated lipids and sialyl
compounds to interfere in vitro with P-selectin-Ig binding to neutrophils
and to protect against P-selectin-dependent acute lung injury induced by
CVF. The biological effects of these sulfated compounds were also
associated with diminished accumulation of neutrophils. The protective
effects of these compounds may be linked to their ability to interfere with
P- selectin binding to counter-receptors on neutrophils.
相似文献
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