Effects of Hct and norepinephrine on segmental vascular resistance distribution in isolated perfused rat livers

Kamikado, Chiaki; Shibamoto, Toshishige; Hongo, Minoru; Koyama, Shozo

doi:10.1152/ajpheart.01136.2002

Cited by 6 publications

(8 citation statements)

References 27 publications

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“…On the other hand, renal sympathetic nerve activity was reported to increase in pentobarbital-anesthetized rats suffering from ovalbumin-induced anaphylactic hypotension (15). Furthermore, norepinephrine, the neurotransmitter released from the sympathetic nerve endings, can constrict presinusoidal vessel almost selectively, as demonstrated in the perfused rat livers with the vascular occlusion method (9). In addition, plasma levels of epinephrine and norepinephrine increased 14-and 4-fold baseline, respectively, at 2.5 min after antigen injection in a similar sensitized rat (23).…”

Section: Discussionmentioning

confidence: 99%

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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Section: Discussionmentioning

confidence: 99%

Portal venular constriction during anaphylactic shock in anesthetized rats

et al. 2013

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“…The methods for isolated perfused rat livers were described previously [18]. A catheter was placed in the right carotid artery.…”

Section: Isolated Liver Preparationmentioning

confidence: 99%

“…In other words, the rapid changes in Ppv and Phv with simultaneous inflow and outflow occlusion (double occlusion) represent the pressure drops across the portal and hepatic venous relatively indistensible (low compliant) vessels. We designated the pressure to which Ppv rapidly decreased during double occlusion maneuver as the portal occlusion pressure (Ppo), and the pressure to which Phv rapidly increased as the hepatic venous occlusion pressure (Phvo) [18].…”

Section: Measurement Of Ppo and Phvo From Double Occlusionmentioning

confidence: 99%

“…However, further physiological studies which aimed at identifying the resistance sites in liver cirrhosis have not been reported. On the other hand, we have recently developed new double occlusion method, which occludes simultaneously both the inflow and outflow perfusion lines of isolated perfused rat livers, to determine hepatic vascular resistances of three segments in series, i.e., portal, sinusoidal and hepatic venous segments in isolated perfused rat livers [18].…”

Section: Introductionmentioning

confidence: 99%

“…Thus, the first purpose of the present study was to determine using the double occlusion technique [18] hepatic vascular resistance distribution in isolated portally perfused cirrhotic rat livers. Portal-hepatic venous resistance (Rt) was assigned to three segments of the portal (Rpv), sinusoidal (Rsinus), and hepatic venous (Rhv) resistances.…”

Section: Introductionmentioning

confidence: 99%

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Increased sinusoidal resistance is responsible for the basal state and endothelin-induced venoconstriction in perfused cirrhotic rat liver

Shibamoto

Kamikado

Koyama³

2008

Pflugers Arch - Eur J Physiol

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The localization of increased intrahepatic vascular resistance and the segmental vascular responsiveness to endothelin-1 are not well known in liver cirrhosis. We determined the segmental vascular resistances and their response to endothelin-1 of isolated portally perfused bile duct ligation (BDL)-induced cirrhotic rat livers. The portal occlusion pressure (Ppo) and the hepatic venous occlusion pressure (Phvo) were obtained by analyzing the profiles of the portal (Ppv) and hepatic venous (Phv) pressures during the double occlusion maneuver of simultaneous occlusions of the inflow and outflow perfusion lines. From the pressure gradients among Ppv, Ppo, Phvo, and Phv, the portal-hepatic venous resistance was assigned to three segments of the portal [Rpv = (Ppv - Ppo)/blood flow (Q)], sinusoidal [Rsinus = (Ppo - Phvo)/Q] and hepatic venous [Rhv = (Phvo - Phv)/Q] resistances. Rsinus, but not Rpv or Rhv, was significantly greater in BDL livers than in sham livers. Endothelin-1 (0.1-1 nM) increased Rpv and Rsinus to a similar magnitude, but not Rhv, in both sham and BDL. At 3 nM, the responsiveness of Rpv was smaller in BDL than in sham, but that of Rsinus were similar between in BDL and sham. In conclusion, increased sinusoidal resistance accounts for increased intrahepatic resistance of BDL-induced liver cirrhosis. Endothelin-1 contracts portal veins and sinusoids, but not hepatic veins, in both sham and cirrhotic livers. Sinusoidal contractility to endothelin-1 is not impaired in cirrhotic livers.

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Effects of Hct on L-NAME-induced Potentiation of Anaphylactic Presinusoidal Constriction in Perfused Rat Livers

Cui

Shibamoto²,

Liu³

et al. 2006

Journal of Cardiovascular Pharmacology

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Effects of hematocrit (Hct) on N-nitro-L-arginine methyl ester (L-NAME)-induced modulation of anaphylactic venoconstriction were determined in isolated perfused rat livers. The rats were sensitized with ovalbumin (1 mg), and the livers were excised 2 weeks later and perfused portally and recirculatingly under constant flow at Hct of 0%, 5%, 16%, and 22%. The hepatic sinusoidal pressure was estimated via the double occlusion pressure (Pdo), and the presinusoidal resistance (Rpre) and the postsinusoidal resistance (Rhv) were calculated. The antigen of ovalbumin 0.1 mg was injected into the reservoir at 10 minutes after pretreatment with L-NAME (100 microM) or D-NAME (100 microM). Perfusate viscosity, a determinant of vascular resistance and shear stress, was increased in parallel with Hct. In the D-NAME groups, antigen caused predominant presinusoidal constriction. The magnitude of venoconstriction was significantly smaller at Hct 0% than at Hct 5% to 22%, whereas no significant differences were found among Hct 5% to 22%. L-NAME potentiated the antigen-induced increase in Rpre, but not in Rpost at Hct 5% to 22% as compared with D-NAME. But the augmentative effects of L-NAME were similar in magnitude among Hct 5% to 22%. These findings suggest that hepatic anaphylaxis increases production of nitric oxide, which consequently attenuates anaphylactic presinusoidal constriction in rat livers, and that these effects are independent of perfusate Hct or viscosity in blood-perfused rat livers.

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Effects of Hct and norepinephrine on segmental vascular resistance distribution in isolated perfused rat livers

Cited by 6 publications

References 27 publications

Portal venular constriction during anaphylactic shock in anesthetized rats

Portal venular constriction during anaphylactic shock in anesthetized rats

Increased sinusoidal resistance is responsible for the basal state and endothelin-induced venoconstriction in perfused cirrhotic rat liver

Effects of Hct on L-NAME-induced Potentiation of Anaphylactic Presinusoidal Constriction in Perfused Rat Livers

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