Hepatic venoconstriction is involved in anaphylactic hypotension in rats

Shibamoto, Toshishige; Cui, Sen; Ruan, Zonghai; Liu, Wei; Takano, Haruo; Kurata, Yasutaka

doi:10.1152/ajpheart.00368.2005

Cited by 51 publications

(89 citation statements)

References 20 publications

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“…We speculate that anaphylaxis causes hepatic venoconstriction and portal hypertension, resulting in congestion of the upstream splanchnic organs, with a resultant decrease in venous return and effective circulating blood volume, and finally augmentation of anaphylactic hypotension. Indeed, elimination of the liver and splanchnic circulation by total hepatectomy combined with ligation of the celiac and mesenteric arteries attenuates anaphylactic hypotension in anesthetized rats (5). More recently, the same surgical procedures (hepatectomy and elimination of the splanchnic vascular bed) have been shown to attenuate mouse anaphylactic hypotension (6).…”

Section: Discussionmentioning

confidence: 99%

NG-Nitro-L-arginine Methyl Ester, but Not Methylene Blue, Attenuates Anaphylactic Hypotension in Anesthetized Mice

et al. 2007

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Abstract. To clarify the role of NO in mouse anaphylactic hypotension, effects of a nitric oxide (NO) synthase inhibitor, N G -nitro-L-arginine methyl ester (L-NAME), on antigen-induced hypotension and portal hypertension were determined in anesthetized BALB / c mice. Systemic arterial pressure (Psa), central venous pressure (Pcv), and portal venous pressure (Ppv) were directly and simultaneously measured. Mice were first sensitized with ovalbumin, and then the injection of antigen was used to decrease Psa and increase Ppv. Pretreatment with L-NAME (1 mg / kg) attenuated this antigen-induced systemic hypotension, but not the increase in Ppv. The effect of inhibitors of soluble guanylate cyclase on anaphylactic hypotension were studied with either methylene blue (3.0 mg / kg) or 1H-[1,2,4]oxadiazole[4,3-a]quinoxalin-1-one (10 mg / kg). Neither modulated any antigen-induced changes. Furthermore, methylene blue did not improve systemic hypotension induced by Compound 48 / 80 (4.5 mg/ kg), a mast cell degranulator, which can produce non-immunological anaphylactoid reactions. These data show in anesthetized BALB/ c mice that L-NAME attenuated anaphylactic hypotension without affecting portal hypertension. This beneficial effect of L-NAME appears not to depend on the soluble guanylate cyclase pathway.

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Section: Discussionmentioning

confidence: 99%

NG-Nitro-L-arginine Methyl Ester, but Not Methylene Blue, Attenuates Anaphylactic Hypotension in Anesthetized Mice

et al. 2007

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“…Rats in the anaphylaxis group, but not in the 2 other groups, were actively sensitized by the subcutaneous injection of an emulsion made by mixing equal volumes of complete Freund's adjuvant (0.5 mL) with 1 mg ovalbumin (grade V; Sigma Chemical Company, St. Louis, MO), as described previously [14].…”

Section: Antigen Sensitizationmentioning

confidence: 99%

Major Contribution of Vasospasm-Induced Coronary Blood Flow Reduction to Anaphylactic Ventricular Dysfunction Assessed in Isolated Blood-Perfused Rat Heart

et al. 2013

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“…2 and 3, Rspl and HBF dose- The results of the isolated perfused rat livers suggest that vasopressin causes venoconstriction albeit only slightly: the increase in the hepatic vascular resistance was only 6% of the baseline. This hepatic venoconstriction was accompanied by a liver weight loss, suggesting presinusoidal constriction (15). This vasopressin, Psa and Rspl dose-dependently increased, where both HBF and Ppv decreased.…”

Section: Anesthetized Rat Experimentsmentioning

confidence: 86%

“…The basic methods for isolated perfused rat livers were described previously (15). Five rats (250 ± 5 g) were anesthetized with pentobarbital.…”

Section: Animalsmentioning

confidence: 99%

The responses of the hepatic and splanchnic vascular beds to vasopressin in rats

et al. 2012

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Vasopressin, a vasoactive peptide, causes vasoconstriction via V1a vasopressin receptors. Unlike other vasoconstrictor agents, vasopressin also has vasodilatory properties. The purpose of this study was to determine the effect of vasopressin on hepatic and splanchnic circulation in SpragueDawley rats. The experiments were conducted in not only isolated blood-and constant flowperfused livers but also anesthetized spontaneously breathing rats. In anesthetized rats, portal venous pressure (Ppv), systemic arterial pressure (Psa), central venous pressure, and hepatic blood flow (HBF) of combined portal venous and hepatic arterial blood flow were continuously measured, and splanchnic vascular bed resistance (Rspl) defined by (Psa − Ppv) / HBF was determined. In perfused livers, vasopressin at 0.1-1,000 nM caused weak venoconstriction as evidenced by small increase in Ppv. In anesthetized rats, when vasopressin was injected into the portal vein as a bolus consecutively at 0.01-100 nmol/kg, Psa increased dose-dependently with the peak increment of 60 ± 18 mmHg at 100 nmol/kg. Ppv and HBF decreased, with resultant increase in Rspl, indicating splanchnic vasoconstriction. In conclusion, hepatic venoconstrictor action of vasopressin was weak in rats. Vasopressin causes splanchnic vasoconstriction, resulting in a decrease in HBF and Ppv in anesthetized rats.Vasopressin, a vasoactive peptide, causes vasoconstriction via V1a vasopressin receptor of vascular smooth muscle cells (1, 5). Vasopressin has been a well-established therapeutic agent controlling severe hypotension such as hemorrhagic shock due to gastrointestinal bleeding (21), septic shock (6, 8), and anaphylactic shock (13). Its beneficial effects on hypotension are usually ascribed to its strong arteriolar constrictor activity in most peripheral vascular beds, especially splanchnic vascular beds. Vasopressin-induced vasoconstriction in the intestinal and splenic vascular beds results in a reduction of portal blood flow with a fall in hepatic portal venous pressure (Ppv). Vasopressin causes vasoconstriction in most vascular beds. Paradoxically, vasopressin has also been demonstrated to cause vasodilation in numerous vascular beds (2,3,9,10,12,16,17,19), a feature not shared by other vasoconstrictor agents. For rats which are one of the most frequently used animals for experiments, the investigations on the effect of vasopressin on the splanchnic vascular bed in vivo are limited (11): blood flow to liver was not measured, although a decrease in Ppv was reported. A decrease in Ppv could be theoretically induced by vasodilation, rather than vasoconstriction, in the hepatic vessels. On the other hand, there are reports on the hepatic vascular response of perfused rat livers to vasopressin, indicating absence of constriction or dilatation (14,18). However, these experiments

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Hepatic venoconstriction is involved in anaphylactic hypotension in rats

Cited by 51 publications

References 20 publications

NG-Nitro-L-arginine Methyl Ester, but Not Methylene Blue, Attenuates Anaphylactic Hypotension in Anesthetized Mice

NG-Nitro-L-arginine Methyl Ester, but Not Methylene Blue, Attenuates Anaphylactic Hypotension in Anesthetized Mice

Major Contribution of Vasospasm-Induced Coronary Blood Flow Reduction to Anaphylactic Ventricular Dysfunction Assessed in Isolated Blood-Perfused Rat Heart

The responses of the hepatic and splanchnic vascular beds to vasopressin in rats

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