Vascular perfusion limits mesenteric lymph flow during anaphylactic hypotension in rats

Zhang, Wei; Shibamoto, Toshishige; Kuda, Yuhichi; Kurata, Yasutaka; Shinomiya, Shohei; Kida, Masahiro; Tsuchida, Hideaki

doi:10.1152/ajpregu.00695.2011

Cited by 8 publications

(10 citation statements)

References 26 publications

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“…An interesting finding of the present study is that the femoral arterial vasodilatation, as evidenced by increased FBF and decreased FVR, occurred immediately after the antigen injection, and simultaneously with the initial fall of SAP. The similar vasodilatation is observed in the arteries of other vascular beds, such as the hepatic artery and mesenteric artery during anaphylaxis in anaesthetized rats [ 26 , 27 ]. This vasodilatation was quickly followed by return to the basal levels [ 26 , 27 ], as observed in the present study.…”

Section: Discussionsupporting

confidence: 57%

The Role of Lumbar Sympathetic Nerves in Regulation of Blood Flow to Skeletal Muscle during Anaphylactic Hypotension in Anesthetized Rats

et al. 2016

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During hypovolemic shock, skeletal muscle blood flow could be redistributed to vital organs via vasoconstriction in part evoked by activation of the innervating sympathetic nerve activity. However, it is not well known whether this mechanism operates during anaphylactic shock. We determined the femoral artery blood flow (FBF) and lumbar sympathetic nerve activity (LSNA) mainly regulating the hindquater muscle blood flow during anaphylactic hypotension in anesthetized rats. Anesthetized Sprague-Dawley rats were randomly allocated to the following groups (n = 7/group): (1) non-sensitized, (2) anaphylaxis, (3) anaphylaxis-lumbar sympathectomy (LS) and (4) anaphylaxis-sinoaortic denervation (SAD) groups. Anaphylaxis was induced by an intravenous injection of the ovalbumin antigen to the sensitized rats. The systemic arterial pressure (SAP), heart rate (HR), central venous pressure (CVP), FBF and LSNA were continuously measured. In the anaphylaxis group, LSNA and HR increased, while SAP and FBF decreased after antigen injection. In the anaphylaxis-SAD group, LSNA did not significantly change during the early phase, but the responses of SAP and FBF were similar to those in the anaphylaxis group. In the anaphylaxis-LS group, both FBF and SAP decreased similarly to the anaphylaxis group during anaphylactic hypotension. These results indicated that LSNA increased via baroreceptor reflex, but this sympathoexcitation or LS did not affect antigen-induced decreases in FBF or SAP. Lumbar sympathetic nerves are not involved in regulation of the blood flow to the hindlimb or systemic blood pressure during anaphylactic hypotension in anesthetized rats.

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Section: Discussionsupporting

confidence: 57%

The Role of Lumbar Sympathetic Nerves in Regulation of Blood Flow to Skeletal Muscle during Anaphylactic Hypotension in Anesthetized Rats

et al. 2016

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“…Taken together, these findings suggest that hepatic venoconstriction occurs over a wide range of portal veins with the diameter up to 420 μm, and markedly in the portal venules with diameters less than 70 μm during anaphylactic hypotension in anesthetized rats. According to Ohm's law (V = IR), as applied to hemodynamic systems, the antigen-induced increase in Ppv in this study is accounted for by an increase in the R, but not the Q, because the blood flow to the liver decreases in this rat anaphylaxis model (22). Based on Pouseuille's law, R = 8ηL/πr 4 , where η = Fig.…”

Section: Discussionmentioning

confidence: 79%

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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“…The amount of change in each indicator was represented by Δ, which was calculated as the difference between each time point and baseline. The TPR and PVR were calculated using the following equations (Zhang, Shibamoto, Kuda, Ohmukai, & Kurata, 2011a;Zhang, et al, 2012):…”

Section: Experimental Data Acquisitionmentioning

confidence: 99%

“…We used atenolol (Bogaert, Rosseel, & Lefebvre, 1984;Prachi, Komal, & Priti, 2017), ICI 118,551 (Baker, 2010;Propping, Newe, Kaumann, Wirth, & Ravens, 2015) and propranolol (Hoffmann, Leitz, Oberdorf-Maass, Lohse, & Klotz, 2004;Tan & Yang, 2016;Zhang et al, 2011b) as the selective β 1 -AR, selective β 2 -AR and non-selective β-AR antagonists, respectively. The doses of the β-AR antagonists were selected according to our previous experimental data, which were shown to be the optimal doses for stable monitoring of haemodynamics (Zhang et al, 2011a(Zhang et al, , 2012. MAP decreased from the baseline of 96.1 ± 9.9 mmHg to 77.7 ± 21.1 and 88.0 ± 5.3 mmHg at 10 min after the antagonist challenge in the propranolol and atenolol groups, respectively, along with reductions in ABF, HR and PAP (Table 3; Figure 2a).…”

Section: Changes In Haemodynamic Indexesmentioning

confidence: 99%

Effects of β‐adrenoceptor activation on haemodynamics during hypoxic stress in rats

Zhang

Cao

et al. 2020

Experimental Physiology

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New Findings What is the central question of this study?The acute hypoxic compensatory reaction is based on haemodynamic changes, and β‐adrenoceptors are involved in haemodynamic regulation. What is the role of β‐adrenoceptors in haemodynamics during hypoxic exposure? What is the main finding and its importance?Activation of β2‐adrenoceptors attenuates the increase in pulmonary artery pressure during hypoxic exposure. This compensatory reaction activated by β2‐adrenoceptors during hypoxic stress is very important to maintain the activities of normal life. Abstract The acute hypoxic compensatory reaction is accompanied by haemodynamic changes. We monitored the haemodynamic changes in rats undergoing acute hypoxic stress and applied antagonists of β‐adrenoceptor (β‐ARs) subtypes to reveal the regulatory role of β‐ARs on haemodynamics. Sprague–Dawley rats were randomly divided into control, atenolol (β1‐AR antagonist), ICI 118,551 (β2‐AR antagonist) and propranolol (non‐selective β‐AR antagonist) groups. Rats were continuously recorded for changes in haemodynamic indexes for 10 min after administration. Then, a hypoxic ventilation experiment [15% O2, 2200 m a.sl., 582 mmHg (0.765 Pa), PnormalO2 87.3 mmHg; Xining, China] was conducted, and the indexes were monitored for 5 min after induction of hypoxia. Plasma catecholamine concentrations were also measured. We found that, during normoxia, the mean arterial pressure, heart rate, ascending aortic blood flow and pulmonary artery pressure were reduced in the propranolol and atenolol groups. Catecholamine concentrations were increased significantly in the atenolol group compared with the control group. During hypoxia, mean arterial pressure and total peripheral resistance were decreased in the control, propranolol and ICI 118,551 groups. Pulmonary arterial pressure and pulmonary vascular resistance were increased in the propranolol and ICI 118,551 groups. During hypoxia, catecholamine concentrations were increased significantly in the control group, but decreased in β‐AR antagonist groups. In conclusion, the β2‐AR is involved in regulation of pulmonary haemodynamics in the acute hypoxic compensatory reaction, and the activation of β2‐ARs attenuates the increase in pulmonary arterial pressure during hypoxic stress. This compensatory reaction activated by β2‐ARs during hypoxic stress is very important to maintain activities of normal life.

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Vascular perfusion limits mesenteric lymph flow during anaphylactic hypotension in rats

Cited by 8 publications

References 26 publications

The Role of Lumbar Sympathetic Nerves in Regulation of Blood Flow to Skeletal Muscle during Anaphylactic Hypotension in Anesthetized Rats

The Role of Lumbar Sympathetic Nerves in Regulation of Blood Flow to Skeletal Muscle during Anaphylactic Hypotension in Anesthetized Rats

Portal venular constriction during anaphylactic shock in anesthetized rats

Effects of β‐adrenoceptor activation on haemodynamics during hypoxic stress in rats

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