Active hepatic capacitance responses to neural and humoral stimuli in dogs

Bennett, Tom; MacAnespie, C. L.; Rothe, Carl F.

doi:10.1152/ajpheart.1982.242.6.h1000

Cited by 30 publications

(25 citation statements)

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“…We added new evidence that a similar response to norepinephrine was observed in isolated mouse livers. It is well known that norepinephrine causes a reduction in liver blood volume in cats [20], dogs [9,21], rabbits [4,19], guinea pigs [11], and rats [11]. In this respect, the present study showed that mouse livers also respond to norepinephrine with a reduction of liver weight, suggesting a decrease in liver blood volume.…”

Section: Discussionsupporting

confidence: 67%

Effects of Norepinephrine and Histamine on Vascular Resistance in Isolated Perfused Mouse Liver

Shibamoto¹,

Cui²,

Ruan³

et al. 2005

JJP

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Mice have frequently been used for a variety of physiological studies because of the development of genetic engineering. However, the characteristics of hepatic vessels such as the vascular resistance distribution and the reactivity to various vasoconstrictors are not known in mice. We therefore determined the basal levels of segmental vascular resistances and the effects of histamine and norepinephrine on the vascular resistance distribution of mice. The liver of male non-inbred ddY mice was excised and perfused via the portal vein with 5% bovine albumin-Krebs solution at a constant flow rate. The sinusoidal pressure was measured by the double occlusion pressure and used to de-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 in relation to the compliances [1]. There are species differences in the distribution of the hepatic vascular resistance. In canine livers, the presinusoidal resistance comprises approximately 50% of the total liver vascular resistance [2], but it comprises 56% and 59% in guinea pig [3] and rabbit livers [4][5][6], respectively, and more than 60% in rat livers [7,8]. However, the basal hepatic vascular resistance distribution of mouse livers is not known, although mouse has been frequently used in physiological studies because of the development of genetic engineering.Species differences are also found in the primary site of hepatic vasoconstriction. By using the vascular occlusion methods for measurement of the hepatic sinusoidal pressure [2, 9], we have recently shown that the hepatic longitudinal vascular responsiveness to vasoactive substances differs among different species, such as dogs, rabbits, rats, and guinea pigs [4][5][6][9][10][11]. Histamine termine the presinusoidal (R pre ) and postsinusoidal (R post ) resistances. The basal R post comprised 53 ± 1% of the total hepatic vascular resistance. The norepinephrine and histamine increased R pre in a greater magnitude than R post with liver weight loss. However, the response to histamine was weaker than that to norepinephrine. Moreover, histamine-induced vasoconstriction showed tachyphylaxis. In conclusion, the presinusoidal and postsinusoidal resistances of mouse livers were similar in magnitude. The presinusoidal vessels predominantly contract in response to norepinephrine and histamine in mouse livers. [The Japanese Journal of Physiology 55: [143][144][145][146][147][148] 2005] Key words: double occlusion pressure, isolated perfused mouse liver, sinusoidal pressure.predominantly contracts the postsinusoidal veins with resultant hepatic congestion in dogs [9, 10] and guinea pigs [11], but this substance constricts presinusoidal vessels in rabbits [4]. In rat livers, histamine did not contract or dilate hepatic vessels [11]. On the other hand, norepinephrine predominantly contracts the presinusoidal veins over the postsinusoidal veins in dogs, rabbits, rats, and guinea pigs [...

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Section: Discussionsupporting

confidence: 67%

Effects of Norepinephrine and Histamine on Vascular Resistance in Isolated Perfused Mouse Liver

Shibamoto¹,

Cui²,

Ruan³

et al. 2005

JJP

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“…However, with the exception of the study by Bennett et al (1982), the investigations of changes in liver blood volume did not carefully control the hepatic inflows and hepatic venous pressure making the interpretation of volume changes difficult. Ours is the first study to have made comparisons of changes in hepatic blood volume during constant portal venous and hepatic arterial inflows with the changes occurring when both pressures were controlled and flows allowed to change.…”

Section: Discussionmentioning

confidence: 99%

Blood mobilization from the liver of the anaesthetized dog

Noble¹,

Drinkhill²,

Myers³

et al. 1998

Experimental Physiology

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SUMMARYThe abdominal circulation contains a high proportion of the total blood volume and this can change either passively in response to changes in vascular distending pressure or actively (termed a capacitance response) to changes in sympathetic nervous activity. The liver is the largest abdominal organ and this study was designed to evaluate its potential contribution to overall vascular capacitance and compliance. In chloralose anaesthetized dogs, the liver was vascularly isolated, perfused through the portal vein and hepatic artery at either constant pressures or constant flows and drained from the hepatic veins at constant pressure. Changes in vascular resistance were assessed from changes in inflow pressures or flows and hepatic blood volume was determined by differences between net inflow and outflow. During constant flow perfusion the change in hepatic volume (capacitance change) in response to supramaximal stimulation of sympathetic nerves at 16 Hz was (mean + S.E.M.) -2-40 + 0-61 ml (kg body weight)-'. This response was not significantly different during constant pressure perfusion. The changes in portal venous and hepatic arterial pressures during stimulation at constant flow perfusion were +0-67 + 0.13 and +4-92 + 0-67 kPa, respectively. The compliance of the liver, assessed as the change in volume to a change in hepatic venous pressure, was +544 + 0-18 ml kg-' kPa-. These results indicate that the liver has a major capacitance role, comparable to that of the canine spleen and, in addition, is highly compliant. No evidence was found to suggest that a sphincter on the hepatic outflow exists. Assuming similar responses occur in humans, who do not possess a large contractile spleen, the liver would be the most important controllable blood reservoir in the body.

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“…As another mechanism, increased sympathetic nerve activity in response to a fall of Psa induced by systemic anaphylaxis may account for a decrease in liver volume (3). Electrical stimulation of the hepatic sympathetic nerves causes a decrease in liver volume in dogs (10,11) and cats (8). Hepatic nerve stimulation expels up to 50% of hepatic blood volume (3,8,11).…”

Section: Discussionmentioning

confidence: 99%

“…The plethysmographic technique was applied to relative large animals such as cats and dogs (1,2,8,10,11) but not small animals of rats or mice because of the inherent technical difficulty. In contrast, ultrasonic crystals were used to measure the liver thickness as an indicator of the liver volume by measuring the distance of each of the pair of crystals attached on the liver surface (9).…”

Section: Introductionmentioning

confidence: 99%

Liver Volume, as Assessed by Four Ultrasonic Crystals Arranged to Form a Tetrahedron, Decreases During Anaphylactic Shock in Anesthetized Rats

Takano¹,

Shibamoto²,

Zhang³

et al. 2010

Shock

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We determined the hepatic volume change in anaphylactic hypotension by using four ultrasonic crystals in anesthetized rats. The hepatic volume was measured with four ultrasonic crystals arranged to form a tetrahedron on the liver surface. Before in vivo experiments, using isolated perfused rat liver preparations, we compared the measured liver volume changes with the whole-liver weight changes during hepatic blood flow rate changes and venoconstriction induced by norepinephrine. The measured relative change of the tetrahedron volume (V[utc]; percentage changes of the initial volume) was closely correlated with the liver weight change (W; percentage changes of the initial liver weight): V(utc) = 0.85W - 4.11 (r² = 0.67). Then, we measured the liver weight and the tetrahedron volume during hepatic anaphylaxis in isolated perfused liver excised from the rats sensitized with ovalbumin. An injection of the antigen into the perfusate caused anaphylactic venoconstriction, liver weight loss (1.1 ± 0.3 g; 9% ± 1%), and the tetrahedron volume reduction (12% ± 4%). Finally, we measured the liver volume change during anaphylactic hypotension in anesthetized ovalbumin-sensitized rats. When the antigen was i.v. injected into anesthetized rats, along with systemic hypotension and hepatic venoconstriction, the liver tetrahedron volume decreased by 6% ± 2% from baseline. In conclusion, we established a method to measure the hepatic volume by using four ultrasonic crystals forming a tetrahedron. Using this ultrasonic crystal method, we demonstrated that liver volume decreases during anaphylactic hypotension in anesthetized rats.

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Active hepatic capacitance responses to neural and humoral stimuli in dogs

Cited by 30 publications

References 0 publications

Effects of Norepinephrine and Histamine on Vascular Resistance in Isolated Perfused Mouse Liver

Effects of Norepinephrine and Histamine on Vascular Resistance in Isolated Perfused Mouse Liver

Blood mobilization from the liver of the anaesthetized dog

Liver Volume, as Assessed by Four Ultrasonic Crystals Arranged to Form a Tetrahedron, Decreases During Anaphylactic Shock in Anesthetized Rats

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