Effects of platelet-activating factor and thromboxane A2 on isolated perfused guinea pig liver

Ruan, Zonghai; Shibamoto, Toshishige; Shimo, Tomohiro; Koizumi, Tomonobu; Tsuchida, Hideaki; Kurata, Yasutaka; Ogura, Toshitsugu; Kubo, Keishi

doi:10.1016/j.prostaglandins.2003.11.002

Cited by 21 publications

(17 citation statements)

References 32 publications

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“…Although PAF substantially increased P pv in isolated perfused mouse livers (Fig. 3), the increase was much smaller than that in rats (6), dogs (29), and guinea pigs (22): the peak R t after PAF was 1.4 times baseline in mice, 3.7 times baseline in rats (6), 3.3 times baseline in dogs (29), and 5.1 times baseline in guinea pigs (22). Further studies on structural and functional mechanisms for weak reactivity of the mouse hepatic vessels are required to determine the amount and distribution of vascular smooth muscle cells and receptors for anaphylactic vasoactive substances and vasoreactivity to those individual substances in the mouse portal and hepatic veins.…”

Section: Discussionmentioning

confidence: 75%

Involvement of splanchnic vascular bed in anaphylactic hypotension in anesthetized BALB/c mice

Liu¹,

Takano²,

Shibamoto³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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August 22, 2007; doi:10.1152/ajpregu.00904.2006.-Using in vivo and isolated perfused liver preparations of BALB/c mice, we determined the roles of the liver and splanchnic vascular bed in anaphylactic hypotension. Intravenous injection of ovalbumin antigen into intact-sensitized mice decreased systemic arterial pressure (Psa) from 92 Ϯ 2 to 39 Ϯ 3 (SE) mmHg but only slightly increased portal venous pressure (Ppv) from 6.4 Ϯ 0.1 cmH2O to the peak of 9.9 Ϯ 0.5 cmH2O at 3.5 min after antigen. Elimination of the splanchnic vascular beds by ligation of the celiac and mesenteric arteries, combined with total hepatectomy, attenuated anaphylactic hypotension. Ligation of these arteries alone, but not partial hepatectomy (70%), similarly attenuated anaphylactic hypotension. In contrast, isolated sensitized mouse liver perfused portally at constant flow did not show anaphylactic venoconstriction but, rather, substantial constriction in response to the anaphylaxisassociated platelet-activating factor, indicating that venoconstriction in mice in vivo may be induced by mediators released from extrahepatic tissues. These results suggest that splanchnic vascular beds are involved in BALB/c mouse anaphylactic hypotension. They presumably act as sources of chemical mediators to cause the anaphylaxisinduced portal hypertension, which induced splanchnic congestion, resulting in a decrease in circulating blood volume and, thus, systemic arterial hypotension. Mouse hepatic anaphylactic venoconstriction may be induced by factors outside the liver, but not by anaphylactic reaction within the liver. anaphylactic shock; hepatic circulation; portal hypertension; splanchnic congestion ANAPHYLACTIC HYPOTENSION appears to be caused primarily by a decrease in blood flow to the heart, because left ventricular function is relatively well preserved during anaphylactic shock (1, 2). Peripheral circulatory collapse is ascribed to hypovolemia, which results from a decrease in effective circulating blood volume. The latter could be due to vasodilation with the peripheral pooling and increased vascular permeability with a shift of intravascular fluid to the extravascular space (1, 2).In canine experimental models of anaphylactic shock, an increase in resistance to venous return is important in the pathogenesis of circulatory collapse (27): increased venous resistance decreases venous return, with a resultant decrease in stroke volume and systemic arterial pressure. Indeed, eviscerated dogs did not develop anaphylactic shock (19). In addition, Enjeti et al. (9) reported that the severity of the anaphylactic shock could be decreased by occlusion of the descending aorta. In dogs, the anaphylaxis-induced increase in venous resistance is partly caused by constriction of the hepatic veins (27, 30), which induces pooling of blood in the liver, as well as in upstream splanchnic organs. In addition, we recently demonstrated that the liver and splanchnic vascular beds are involved in rat anaphylactic hypotension by showing that elimination of splanchnic ci...

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Section: Discussionmentioning

confidence: 75%

Involvement of splanchnic vascular bed in anaphylactic hypotension in anesthetized BALB/c mice

Liu¹,

Takano²,

Shibamoto³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…For example, with respect to PAF, which caused a substantial increase in PPV in isolated perfused mouse livers, 1,4 the increase was much smaller than that in rats, 6 dogs, 18 and guinea pigs 9 : the peak portal-to-hepatic vein resistance levels after PAF injection were 1.4-fold the baseline in mice, 1 3.7-fold in rats, 6 3.3-fold in dogs, 19 and 5.1-fold in guinea pigs. 9 One of the limitations of the present study is that the same size catheter was used for PPV measurement in different size of mouse and rats. Although the resistance due to catheter itself at the insert portion of the portal vein should be relatively larger in mouse than in rat, the length of the catheter inserted was as short as 5 mm.…”

Section: Discussionmentioning

confidence: 93%

“…1 In addition, we previously demonstrated that the response of PPV in isolated perfused mouse liver to the vasoactive substances of norepinephrine (NE), 3 histamine, 3 PAF, 1,4 and thromboxane A 2 analogue 5 was much weak as compared with that in other mammals such as rat, 4-7 rabbit, 8 and guinea pig. 4,5,7,9 The passive blood mobilization to and from the liver, which influences the venous return to the heart, is critically dependent on the location and magnitude of intrahepatic vascular resistances, the changes of which could be produced by hepatic venoconstriction. 10 Thus, it is important to investigate the characteristics of the hepatic venoconstriction in response to physiological vasoactive agonists in mice.…”

Section: Introductionmentioning

confidence: 99%

Mouse Hepatic Portal Venoconstrictive Response to Vasoconstrictors Is Much Weaker Than That in Rat

Zhao

Shibamoto²,

Tsutsumi³

et al. 2009

Journal of Cardiovascular Pharmacology

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We previously reported that the portal venous pressure (PPV) response of perfused mouse livers to various vasoactive agents was much weaker than that of other mammals such as rat, rabbit, and guinea pigs. The purpose of this study was to determine the responsiveness of PPV in in vivo BALB/c mouse to intraportal injections of the 3 major vasoconstrictors of angiotensin II, norepinephrine, and endothelin-1 in comparison with that in Sprague-Dawley rats. In anesthetized spontaneously breathing animals, PPV, systemic arterial pressure, and central venous pressure were directly and continuously measured. The above-mentioned vasoconstrictors were injected into the portal vein as a bolus repetitively at the doses ranging 0.01-100 nmol/kg. A dose-dependent increase in systemic arterial pressure in response to each vasoconstrictor was observed similarly in both mice and rats. All vasoconstrictors also caused a dose-dependent increase in PPV in both species, but the peak levels in mouse did not reach higher than 7 mm Hg, whereas it reached as high as 15-24 mm Hg in rats. Immunostaining for alpha-smooth muscle actin revealed that smooth muscles were distributed substantially in portal venules of rat but scarcely in that of mouse. In conclusion, PPV response to various vasoconstrictors was limited in anesthetized BALB/c mice, as compared with the anesthetized Sprague-Dawley rats, presumably due to small amount of vascular smooth muscle in mouse portal venules.

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“…In guinea pig livers, the anaphylactic presinusoidal constriction may be caused mainly by PAF, whereas the postsinusoidal constriction is caused by cysteinyl leukotrienes (19). Actually, PAF predominantly contracts presinusoidal vessels in guinea pig livers (17). However, effects of anaphylaxis-related vasoactive substances are not currently known on the segmental vascular resistances of rat livers.…”

Section: Discussionmentioning

confidence: 98%

Hepatic venoconstriction is involved in anaphylactic hypotension in rats

Shibamoto

Cui

Ruan

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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We determined the roles of liver and splanchnic vascular bed in anaphylactic hypotension in anesthetized rats and the effects of anaphylaxis on hepatic vascular resistances and liver weight in isolated perfused rat livers. In anesthetized rats sensitized with ovalbumin (1 mg), an intravenous injection of 0.6 mg ovalbumin caused not only a decrease in systemic arterial pressure from 120 +/- 9 to 43 +/- 10 mmHg but also an increase in portal venous pressure that persisted for 20 min after the antigen injection (the portal hypertension phase). The elimination of the splanchnic vascular beds, by the occlusions of the celiac and mesenteric arteries, combined with total hepatectomy attenuated anaphylactic hypotension during the portal hypertension phase. For the isolated perfused rat liver experiment, the livers derived from sensitized rats were hemoperfused via the portal vein at a constant flow. Using the double-occlusion technique to estimate the hepatic sinusoidal pressure, presinusoidal (R(pre)) and postsinusoidal (R(post)) resistances were calculated. An injection of antigen (0.015 mg) caused venoconstriction characterized by an almost selective increase in R(pre) rather than R(post) and liver weight loss. Taken together, these results suggest that liver and splanchnic vascular beds are involved in anaphylactic hypotension presumably because of anaphylactic presinusoidal contraction-induced portal hypertension, which induced splanchnic congestion resulting in a decrease in circulating blood volume and thus systemic arterial hypotension.

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Effects of platelet-activating factor and thromboxane A2 on isolated perfused guinea pig liver

Cited by 21 publications

References 32 publications

Involvement of splanchnic vascular bed in anaphylactic hypotension in anesthetized BALB/c mice

Involvement of splanchnic vascular bed in anaphylactic hypotension in anesthetized BALB/c mice

Mouse Hepatic Portal Venoconstrictive Response to Vasoconstrictors Is Much Weaker Than That in Rat

Hepatic venoconstriction is involved in anaphylactic hypotension in rats

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