Ultrastructural Study on the Venous Sphincter in the Sublobular Vein of the Canine Liver

Yamamoto, Kōji

doi:10.1006/mvre.1998.2080

Cited by 14 publications

(10 citation statements)

References 21 publications

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“…Organ-specific variation (Aird, 2007b) also occurs and certain specialised endothelia, such as alveolar capillary endothelial cells, lack VWF and therefore possess no WPBs (Pusztaszeri et al, 2006). Finally VWF expression levels (and thus presumably WPB number) vary with vessel type, veins exhibiting higher message levels than arteries (Chi et al, 2003;Yamamoto, 1998).…”

Section: Variations In Wpbsmentioning

confidence: 99%

Formation and function of Weibel-Palade bodies

Metcalf,

Nightingale,

Zenner

et al. 2008

Journal of Cell Science

136

140

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Weibel-Palade bodies (WPBs) are secretory organelles used for post-synthesis storage in endothelial cells that can, very rapidly, be triggered to release their contents. They carry a variety of bioactive molecules that are needed to mount a rapid response to the complex environment of cells that line blood vessels. They store factors that are essential to haemostasis and inflammation, as well as factors that modulate vascular tonicity and angiogenesis. The number of WPBs and their precise content vary between endothelial tissues, reflecting their differing physiological circumstances. The particular functional demands of the highly multimerised haemostatic protein von Willebrand Factor (VWF), which is stored in WPBs as tubules until release, are responsible for the cigar shape of these granules. How VWF tubules drive the formation of these uniquely shaped organelles, and how WPB density increases during maturation, has recently been revealed by EM analysis using high-pressure freezing and freeze substitution. In addition, an AP1/clathrin coat has been found to be essential to WPB formation. Following recruitment of cargo at the TGN, there is a second wave of recruitment that delivers integral and peripheral membrane proteins to WPBs, some of which is AP3 dependent.

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Section: Variations In Wpbsmentioning

confidence: 99%

Formation and function of Weibel-Palade bodies

Metcalf,

Nightingale,

Zenner

et al. 2008

Journal of Cell Science

136

140

View full text Add to dashboard Cite

show abstract

“…In addition, the rat hepatic constrictive site of the distal portal venules may not be applied to other species, such as dogs. Actually, in dogs, the post-sinusoidal hepatic veins contract at the sublobular sphincter in response to vasoconstrictors (21). In the portal venography of the present study, the different vessel images of vanishment, stenosis, dilatation, and no change were observed in the 4th and 5th generation branches.…”

Section: Discussionmentioning

confidence: 70%

Portal venular constriction during anaphylactic shock in anesthetized rats

et al. 2013

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Hepatic venoconstriction occurs in rat anaphylactic hypotension. However, the exact venoconstrictive site remains unknown, and we therefore attempted to determine its location by using hepatic venography and histology. Anaphylaxis was induced in anesthetized Sprague-Dawley rats by i.v. administration of ovalbumin antigen. Venography of the portal vein (n = 8) was obtained at baseline and maximal hepatic venoconstriction. We separately examined photomicrographs of the liver sections. Along with systemic hypotension, portal venous pressure increased to a peak of 28 ± 3 cm-H 2 O at 2 min after antigen injection. Post-antigen portal venography revealed that 40% of portal venules (76 vessels/total 188 vessels) with diameters from 160 to 300 μm were not visualized, suggesting that stenosis or obliteration occurred distally. The corresponding upstream portal vessels exhibited markedly bulging. Stenosis was also observed in some portal branches with diameters from 180 to 420 μm (9%; 17 vessels/total 188 vessels). Light microscopically, most portal venules with an estimated baseline diameter less than 110 μm showed stenosis, but statistically significant stenosis was found in those with baseline diameters of 20-70 μm. In conclusion, anaphylactic hepatic venoconstriction occurs over a wide range of portal veins with diameters less than 420 μm, and occurs markedly in portal venules with diameters less than 70 μm in anesthetized rats.Anaphylactic hypotension is in part caused by a decrease in effective circulating blood volume, which could be caused by vasodilation in conjunction with the peripheral blood pooling, as well as by a shift of intravascular fluid to the extravascular space due to increased vascular permeability (2). In canine anaphylactic shock, hepatic venoconstriction, especially selective constriction of the postsinusoidal hepatic veins, induces pooling of blood in the upstream splanchnic organs, as well as in the liver itself (5,6,20). Likewise, in rat anaphylactic hypotension, hepatic venoconstriction occurs, although the liver blood volume decreases rather than increasing (8,16,19). This anaphylactic hepatic venoconstriction plays a significant role in the genesis of blood pressure fall, based on the finding that the elimination of acute portal hypertension by means of surgical perturbations or portacaval shunting attenuates the antigen-induced systemic hypotension in anesthetized rats (10, 16). However, detailed information on the anaphylactic hepatic venoconstriction which causes acute portal hypertension is limited. The anatomical site for anaphylactic venoconstriction of the liver remains unknown. In a previous work using the hepatic vascular occlusion method, we reported that the portal veins are the primary site of anaphylactic hepatic venoconstriction in isolated perfused rat livers (16). Recently this notion was reinforced by measuring the hepatic venular pressure with a servo-null micropipette pressure measurement technique: anaphylactic venoconstriction in the liver venous circulation occ...

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“…Histamine is known as a mediator that causes smooth muscle contraction 31 in addition to increasing microvascular permeability, by loosening the endothelium 32 . In dog liver, the sphincter muscles are periodically located along the hepatic veins 25,33,34 , and they elevate portal vein pressure by contraction following histamine release 35 . Therefore, the release of histamine by liposomes caused hypertension of the sub-lobular vessel and increased the permeability of the blood vessels.…”

Section: Discussionmentioning

confidence: 99%

Dog-specific hemorrhagic changes induced by liposomal formulations, in the liver and the gallbladder

et al. 2020

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Although several liposomal drugs, including liposomal doxorubicin, have been approved, the etiology of the pathological responses caused by their physicochemical properties remains unknown. Herein, we investigated the pathological changes in the liver and the gallbladder of dogs following a single injection of liposomal doxorubicin (1 or 2.5 mg/kg) or an empty liposomal formulation (i.e., liposomal formulation without doxorubicin, ca. 21 mg/kg as lipid content). Injection of liposomal doxorubicin or the empty liposomal formulation induced hemorrhagic changes in the liver and the gallbladder. These changes were accompanied by minimal cellular infiltration with no obvious changes in the blood vessels. As there were no differences in the incidence and severity of hemorrhage between the groups administered comparable amounts of total lipid, the physicochemical properties of the liposomal formulation rather than an active pharmacological ingredient, doxorubicin, were associated with the hemorrhagic changes. Furthermore, decreased cytoplasmic granules with low electron density in mast cells beneath the endothelium of the hepatic vein were observed in the liver of dogs treated with liposomal doxorubicin or empty liposomal formulation. Injection of compound 48/80, a histamine releaser induced comparable hemorrhage in dogs, implying that hemorrhage caused by injection of liposomal doxorubicin or the empty liposomal formulation could be attributed to the histamine released from mast cells. The absence of similar hemorrhagic lesions in other species commonly used in toxicology studies (i.e., rats and monkeys), as well as humans, is due to the lack of mast cells beneath the endothelium of the hepatic vein in these species.

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Ultrastructural Study on the Venous Sphincter in the Sublobular Vein of the Canine Liver

Cited by 14 publications

References 21 publications

Formation and function of Weibel-Palade bodies

Formation and function of Weibel-Palade bodies

Portal venular constriction during anaphylactic shock in anesthetized rats

Dog-specific hemorrhagic changes induced by liposomal formulations, in the liver and the gallbladder

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