Hepatic venous resistance site in the dog: localization and validation of intrahepatic pressure measurements

1987 ◽  
Vol 65 (3) ◽  
pp. 352-359 ◽  
Author(s):  
Dallas J. Legare ◽  
W. Wayne Lautt
Keyword(s):  
Blood Volume ◽  
Nerve Stimulation ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Vena Cava ◽  
Pressure Rise ◽  
Vascular Occlusion ◽  
Portal Venous Pressure ◽  
Hepatic Veins ◽  
Venous Resistance

Intrahepatic pressure (9.4 ± 0.3 mmHg; 1 mmHg = 133.32 Pa), measured proximal to a hepatic venous resistance site, was insignificantly different from portal venous pressure (9.6 ± 0.4 mmHg). This lobar venous pressure is not wedged hepatic venous pressure as it is measured from side holes in a catheter with a sealed tip. Validation of the lobar venous pressure measurement was done in a variety of ways and using different sizes and configurations of catheters. The site of hepatic venous resistance in the dog is localized to a narrow sphincterlike region about 0.5 cm in length and within 1–2 cm (usually within 1 cm) of the junction of the vena cava and hepatic veins. Sinusoidal and portal venous resistance appears insignificant in the basal state and large increases in liver blood volume (histamine infusion or passive vena caval occlusion) or large decreases in liver blood volume (passive vascular occlusion) do not alter the insignificant pressure gradient between portal and lobar venous pressures. Norepinephrine infusion (1.25 μg∙kg−1∙min−1 intraportal) and hepatic sympathetic nerve stimulation (10 Hz) led to a significantly greater rise in portal venous pressure than in lobar venous pressure, indicating some presinusoidal (and (or) sinusoidal) constriction and this indicates that lobar venous pressure cannot be assumed under all conditions to accurately reflect portal pressure. However, most of the rise in portal venous pressure induced by intraportal infusion of norepinephrine or nerve stimulation and virtually all of the pressure rise induced by histamine could be attributed to the postsinusoidal resistance site. This site was highly localized since 62% of the pressure drop from the portal vein to the inferior vena cava in the basal state occurred over a 0.5-cm length. However, the anatomical position of this site was different in the dog compared with the cat.

Effect of hepatic venous sphincter contraction on transmission of central venous pressure to lobar and portal pressure

1987 ◽  
Vol 65 (11) ◽  
pp. 2235-2243 ◽  
Author(s):  
W. Wayne Lautt ◽  
Dallas J. Legare ◽  
Clive V. Greenway
Keyword(s):  
Vascular Resistance ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Vena Cava ◽  
Pressure Rise ◽  
Portal Venous Pressure ◽  
Small Rise ◽  
Venous Resistance ◽  
Small Increments ◽  
Control State

In dogs anesthetized with pentobarbital, central vena caval pressure (CVP), portal venous pressure (PVP), and intrahepatic lobar venous pressure (proximal to the hepatic venous sphincters) were measured. The objective was to determine some characteristics of the intrahepatic vascular resistance sites (proximal and distal to the hepatic venous sphincters) including testing predictions made using a recent mathematical model of distensible hepatic venous resistance. The stimulus used was a brief rise in CVP produced by transient occlusion of the thoracic vena cava in control state and when vascular resistance was elevated by infusions of norepinephrine or histamine, or by nerve stimulation. The percent transmission of the downstream pressure rise to upstream sites past areas of vascular resistance was elevated. Even small increments in CVP are partially transmitted upstream. The data are incompatible with the vascular waterfall phenomenon which predicts that venous pressure increments are not transmitted upstream until a critical pressure is overcome and then further increments would be 100% transmitted. The hepatic sphincters show the following characteristics. First, small rises in CVP are transmitted less than large elevations; as the CVP rises, the sphincters passively distend and allow a greater percent transmission upstream, thus a large rise in CVP is more fully transmitted than a small rise in CVP. Second, the amount of pressure transmission upstream is determined by the vascular resistance across which the pressure is transmitted. As nerves, norepinephrine, or histamine cause the hepatic sphincters to contract, the percent transmission becomes less and the distensibility of the sphincters is reduced. Similar characteristics are shown for the "presinusoidal" vascular resistance and the hepatic venous sphincter resistance. Finally, a unit of pressure rise in downstream pressure will be more completely transmitted upstream as the basal starting downstream pressure is increased. These data fulfill the predictions of the distensible hepatic venous sphincter model developed for the cat liver and are incompatible with the Starling resistor – vascular waterfall theory. The distensible hepatic venous resistance allows the splanchnic blood volume to most efficiently buffer the largest changes in CVP by transmitting proportionately more pressure to the highly compliant splanchnic vessels. In addition the distensible sphincters serve to autoregulate portal venous pressure. As portal flow changes, the passively distensible sphincters minimize changes in PVP.

Nonlinear resistances in hepatic microcirculation

1995 ◽  
Vol 269 (6) ◽  
pp. H1922-H1930 ◽  
Author(s):  
R. Maass-Moreno ◽  
C. F. Rothe
Keyword(s):  
Portal Vein ◽  
Blood Volume ◽  
Venous Pressure ◽  
Vena Cava ◽  
Portal Venous Pressure ◽  
Hepatic Microcirculation ◽  
Nonlinear Characteristics ◽  
Nonlinear Mode ◽  
Pressure Transmission ◽  
Liver Surface

The liver provides a reservoir available for mobilizing large amounts of blood, but if a change in downstream (outflow) pressure below a certain magnitude (break pressure) does not change upstream pressures, blood volume redistribution may be limited. For downstream pressures larger than the break pressure, the upstream pressures change proportionately. We tested the hypothesis that this nonlinear mode of pressure transmission could be found from the abdominal vena cava to the hepatic microcirculation and from the hepatic microcirculation to the portal vein. Using a servo-null micropipette technique, we measured microvascular pressures at the liver surface of rabbits. In 16 of 30 measurements, increasing the pressure at the liver outflow, by partially occluding the caudal thoracic vena cava, caused an increase in hepatic venular pressure only after the abdominal vena caval pressure exceeded a break pressure of 2.85 +/- 0.92 mmHg. In 13 of 31 measurements, portal venous pressure was not changed until the hepatic venular pressure exceeded a break pressure of 3.36 +/- 0.54 mmHg. Similar behavior and values were obtained for sinusoids and portal venules. When present, the sharp inflection in the upstream-downstream pressure plots suggests that this may be caused by a Starling resistor-type mechanism. When the break was absent, the downstream pressure may have been larger than the break pressure. We conclude that significant hepatic resistances with nonlinear characteristics exist upstream and downstream to the central venules, sinusoids, and portal venules.

Norepinephrine on venous compliance and unstressed volume in cat liver

1985 ◽  
Vol 248 (4) ◽  
pp. H468-H476 ◽  
Author(s):  
C. V. Greenway ◽  
K. L. Seaman ◽  
I. R. Innes
Keyword(s):  
Blood Volume ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Hepatic Veins ◽  
Venous Compliance ◽  
Inferior Vena Caval ◽  
Unstressed Volume ◽  
True Blood ◽  
The Central Nervous System ◽  
Infusion Of Norepinephrine

Hemodynamic relationships between flows, pressures, and blood volume have been examined in the denervated liver of cats anesthetized with pentobarbital. Portal and hepatic lobar venous pressures, portal and total hepatic flows, and hepatic blood volume were recorded when portal flow was varied from 0 to 240 ml X min-1 X 100 g liver-1 and when hepatic outflow pressure was varied from 0 to 9.5 mmHg, before, during, and after intravenous infusion of norepinephrine (2 micrograms X min-1 X kg body wt-1). Portal pressure was 1-2 mmHg higher than lobar venous pressure and 8-9 mmHg higher than inferior vena caval pressure, showing that the major site of resistance in the portal circuit was in the large hepatic veins. Intrahepatic pressure was linearly related to total hepatic flow, and norepinephrine increased the intercept but not the slope of this relationship. Hepatic blood volume was linearly related to intrahepatic pressure with a calculated compliance of 2.5-3.0 ml X mmHg-1 X 100 g liver-1 and a calculated unstressed volume at zero pressure of 10-15 ml/100 g liver. Norepinephrine did not significantly change vascular compliance but caused a marked reduction of 15-20 ml/100 g liver in calculated unstressed volume. Thus norepinephrine reduced hepatic blood volume by 15-20 ml/100 g liver at any given intrahepatic pressure. It is concluded that venoconstriction in the hepatic bed occurs by a decrease in unstressed volume with little change in compliance. Unstressed volume represents a true blood volume reserve, independent of passive influences, which can be mobilized by the central nervous system.

Localization of intrahepatic portal vascular resistance

1986 ◽  
Vol 251 (3) ◽  
pp. G375-G381 ◽  
Author(s):  
W. W. Lautt ◽  
C. V. Greenway ◽  
D. J. Legare ◽  
H. Weisman
Keyword(s):  
Pressure Drop ◽  
Portal Vein ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Vena Cava ◽  
Sympathetic Nerves ◽  
Hepatic Veins ◽  
Pressure Changes ◽  
Stimulation Of ◽  
Anesthetized Cat

The pressure drop from the portal vein to the vena cava occurs primarily across a postsinusoidal site localized to a narrow segment (less than 0.5 cm) of hepatic veins (roughly 1.5 mm diam) in the anesthetized cat. Portal venous pressure (PVP = 8.9 +/- 0.3 mmHg) and lobar hepatic venous pressure (LVP = 8.7 +/- 0.4 mmHg) are insignificantly different, and pressure changes imposed from the presinusoidal or postsinusoidal side are equally transmitted to both pressure sites. Several types of experiments were done to validate the LVP measurement. The portal vein, hepatic sinusoids, and hepatic veins proximal to the resistance site are all under a similar pressure. Previously reported calculations of hepatic vascular resistance are in error because of incorrect assumptions of sinusoidal pressure and localization of the portal resistance site as presinusoidal. Stimulation of hepatic sympathetic nerves for 3 min caused LVP and PVP to increase equally, showing that the increased "portal" resistance is postsinusoidal across the same region of the hepatic veins that was previously localized as the site of resistance in the basal state.

Active hepatic capacitance responses to neural and humoral stimuli in dogs

1982 ◽  
Vol 242 (6) ◽  
pp. H1000-H1009 ◽  
Author(s):  
T. D. Bennett ◽  
C. L. MacAnespie ◽  
C. F. Rothe
Keyword(s):  
Blood Volume ◽  
Nerve Stimulation ◽  
Venous Pressure ◽  
Constant Flow ◽  
Arterial Infusion ◽  
Hepatic Arterial Flow ◽  
Fluid Filtration ◽  
Control Value ◽  
Flow Perfusion ◽  
Hepatic Vasculature

Active changes in hepatic capacitance were studied in pump-perfused dog livers during hepatic nerve stimulation or during intrahepatic arterial infusion of histamine (0.01-1 mg/l) or epinephrine (0.05 mg/l). Hepatic nerve stimulation at 5 pulses/s (pps) reduced hepatic blood volume by 76 +/- 39 (SD) ml/kg tissue and decreased the apparent hepatic compliance 36% from a control value of 25.6 +/- 9.3 ml.kg-1.mmHg-1, with constant flow perfusion. With a constant hepatic arterial pressure, 5 pps stimulation decreased hepatic arterial flow to 16% of control; the volume expelled was 91 +/- 33 ml/kg. Epinephrine caused hepatic artery constriction, the active expulsion of 71 ml/kg of blood, and a decrease of about 30% in hepatic compliance. Histamine dramatically reduced the hepatic vascular compliance, decreased the portal venous conductance, increased hepatic arterial conductance, and caused the apparent hepatic blood volume to double. Increased hepatic venous pressure, hepatic nerve stimulation, epinephrine, and, especially, histamine caused a significant filtration of fluid from the hepatic vasculature. We conclude that significant active capacitance changes and transsinusoidal fluid filtration can be induced in the canine liver by neural and hormonal stimuli.

Splanchnic vascular capacitance and positive end-expiratory pressure in dogs

1991 ◽  
Vol 70 (2) ◽  
pp. 818-824 ◽  
Author(s):  
C. Risoe ◽  
C. Hall ◽  
O. A. Smiseth
Keyword(s):  
Blood Volume ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Central Blood Volume ◽  
Positive End Expiratory Pressure ◽  
Splenic Volume ◽  
Vascular Volume ◽  
Vascular Capacitance ◽  
Anesthetized Dogs ◽  
Blood Volumes

We have investigated the effect of positive end-expiratory pressure ventilation (PEEP) on regional splanchnic vascular capacitance. In 12 anesthetized dogs hepatic and splenic blood volumes were assessed by sonomicrometry. Vascular pressure-diameter curves were defined by obstructing hepatic outflow. With 10 and 15 cmH2O PEEP portal venous pressure increased 3.1 +/- 0.3 and 5.1 +/- 0.4 mmHg (P less than 0.001) while hepatic venous pressure increased 4.9 +/- 0.4 and 7.3 +/- 0.4 mmHg (P less than 0.001), respectively. Hepatic blood volume increased (P less than 0.01) 3.8 +/- 0.9 and 6.3 +/- 1.4 ml/kg body wt while splenic volume decreased (P less than 0.01) 0.8 +/- 0.2 and 1.3 +/- 0.2 ml/kg body wt. The changes were similar with closed abdomen. The slope of the hepatic vascular pressure-diameter curves decreased with PEEP (P less than 0.01), possibly reflecting reduced vascular compliance. There was an increase (P less than 0.01) in unstressed hepatic vascular volume. The slope of the splenic pressure-diameter curves was unchanged, but there was a significant (P less than 0.05) decrease in unstressed diameter during PEEP. In conclusion, hepatic blood volume increased during PEEP. This was mainly a reflection of passive distension due to elevated venous pressures. The spleen expelled blood and thus prevented a further reduction in central blood volume.

Effect of raised portal venous pressure and postocclusive hyperemia on superior mesenteric arterial resistance in control and adenosine receptor blocked state in cats

1986 ◽  
Vol 64 (10) ◽  
pp. 1296-1301 ◽  
Author(s):  
W. Wayne Lautt
Keyword(s):  
Arterial Pressure ◽  
Adenosine Receptor ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Systemic Blood Pressure ◽  
Portal Venous Pressure ◽  
Arterial Perfusion ◽  
Resistance Vessels ◽  
Adenosine Antagonist ◽  
Adenosine Antagonism

Superior mesenteric arterial (SMA) blood flow was measured in pentobarbital-anesthetized cats using a noncannulating electromagnetic flowprobe. The selective adenosine antagonist 8-phenyltheophylline (8-PT) antagonized the dilator effect of infused adenosine but not isoproterenol. The vasodilation in response to reduced arterial perfusion pressure (autoregulation) was blocked by the adenosine receptor blockade, which also reduced the degree of postocclusive (1 min) hyperemia by one-half to two-thirds. The remainder of the hyperemia may have been due partially to adenosine, since exogenous adenosine still produced a small vasodilation (26%), so effects of endogenous adenosine could also still be expected to exert a small effect. Myogenic effects appear unlikely to be the mechanism of the small remaining hyperemia, since venous pressure increments within physiologically relevant ranges did not cause altered SMA conductance, and arterial dilation in response to large decreases in arterial pressure could be blocked by adenosine antagonism. Portal pressure was increased using hepatic nerve stimulation (8 Hz) to raise pressure from 7.0 to 12.4 mmHg (1 mmHg = 133.3 Pa). The small vasoconstriction seen in the SMA was due to the rise in systemic blood pressure, since prevention of a rise in SMA pressure prevented the response and 8-PT blocked the response (previously shown to block arterial pressure–flow autoregulation). An equal rise in PVP imposed by partial occlusion of the portal vein did not lead to changes in SMA vascular conductance. Thus, we conclude that within physiologically relevant ranges of arterial and portal venous pressure, the SMA does not show myogenic responses of the resistance vessels.

Effect of histamine, norepinephrine, and nerves on vascular pressures in dog liver

1987 ◽  
Vol 252 (4) ◽  
pp. G472-G478 ◽  
Author(s):  
W. W. Lautt ◽  
D. J. Legare
Keyword(s):  
Pressure Drop ◽  
Hepatic Artery ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Hepatic Veins ◽  
Small Doses ◽  
Hepatic Nerves ◽  
Dog Liver ◽  
Control State ◽  
Intraportal Infusion

In the control state, lobar venous pressure (LVP) measured proximal to a hepatic venous sphincter in dog liver (9.9 +/- 0.3 mmHg) is insignificantly different from portal venous pressure (PVP = 9.9 +/- 0.3 mmHg). Essentially all of the pressure drop occurs across the hepatic veins. Intraportal infusion of histamine constricts the hepatic venous sphincter and leads to similar elevations of LVP and PVP, indicating that all of the rise in PVP (except at small doses = 1 microgram X kg-1. min-1) can be accounted for by hepatic venous sphincter constriction. Norepinephrine at doses from 0.25 to 1.25 micrograms X kg-1. min-1 (intraportal) caused both hepatic venous sphincter constriction and constriction proximal to hepatic venous sphincters to roughly equal proportions, with approximately 44% of the rise in PVP due to hepatic sphincter constriction. Hepatic nerves activated both resistance sites, with 90% of the rise in PVP due to hepatic venous constriction at 2 Hz stimulation. By 4 Hz stimulation, the postsinusoidal sphincters were nearly maximally activated, but the “presinusoidal” resistance continued to increase until, at 10 Hz, the hepatic venous sphincter component accounted for only 59% of the rise in PVP. The proportion of PVP rise accounted for by hepatic venous sphincter resistance was not significantly altered by prior occlusion of the hepatic artery.

Hepatic venular pressures of rats, dogs, and rabbits

1991 ◽  
Vol 261 (3) ◽  
pp. G539-G547 ◽  
Author(s):  
H. G. Bohlen ◽  
R. Maass-Moreno ◽  
C. F. Rothe
Keyword(s):  
Inferior Vena Cava ◽  
Portal Vein ◽  
Inferior Vena ◽  
Venous Pressure ◽  
Vena Cava ◽  
Portal Venous Flow ◽  
Venous Flow ◽  
Norepinephrine Infusion ◽  
Venous Resistance ◽  
Venous Vasculature

We tested the hypotheses that the hepatic venule pressures (Phv), just downstream from the hepatic sinusoids, are closely similar (less than 2 mmHg) either to the portal venous pressure (Ppv), indicating a high hepatic venous resistance, or to the inferior vena cava (Pivc) pressure, indicating a high portal-sinusoidal venous resistance, as reported by previous investigators. A micropipette servo-null pressure measurement technique was used with rats, dogs, and rabbits. Phv, referred to the anatomic level of the vena cava, averaged 5.1 +/- 1.0, 6.4 +/- 1.1, and 5.4 +/- 1.0 (SD) mmHg in the rats, puppies, and rabbits, respectively. Ppv averaged 8.0 +/- 1.4, 10.8 +/- 2.2, and 7.4 +/- 1.5 mmHg, respectively. Norepinephrine infusion into the portal vein (1-5 micrograms.min-1.kg-1) caused Ppv to increase and the portal venous flow to decrease but did not significantly affect Phv. The hepatic venous circuit contributed 44 +/- 17% (rats) and 31 +/- 26% (dogs) of the total liver venous vascular resistance under control conditions. We conclude that the portal and sinusoidal vasculatures are the dominant, but not exclusive, resistance sites of the liver venous vasculature both at rest and during norepinephrine-induced vasoconstriction.

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

2004 ◽  
Vol 286 (1) ◽  
pp. H121-H130 ◽  
Author(s):  
Chiaki Kamikado ◽  
Toshishige Shibamoto ◽  
Minoru Hongo ◽  
Shozo Koyama
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Venous Pressure ◽  
Regression Line ◽  
Venous Occlusion ◽  
Portal Venous Pressure ◽  
Venous Resistance ◽  
Four Levels ◽  
Rat Livers ◽  
Line Analysis

We studied the effects of blood hematocrit (Hct), blood flow, or norepinephrine on segmental vascular resistances in isolated portally perfused rat livers. Total portal hepatic venous resistance ( Rt) was assigned to the portal ( Rpv), sinusoidal ( Rsinus), and hepatic venous ( Rhv) resistances using the portal occlusion (Ppo) and the hepatic venous occlusion (Phvo) pressures that were obtained during occlusion of the respective line. Four levels of Hct (30%, 20%, 10%, and 0%) were studied. Rpv comprises 44% of Rt, 37% of Rsinus, and 19% of Rhv in livers perfused at 30% Hct and portal venous pressure of 9.1 cmH2O. As Hct increased at a given blood flow, all three segmental vascular resistances of Rpv, Rsinus, and Rhv increased at flow >15 ml/min. As blood flow increased at a given Hct, only Rsinus increased without changes in Rpv or Rhv. Norepinephrine increased predominantly Rpv, and, to a smaller extent, Rsinus, but it did not affect Rhv. Finally, we estimated Ppo and Phvo from the double occlusion maneuver, which occluded simultaneously both the portal and hepatic venous lines. The regression line analysis revealed that Ppo and Phvo were identical with those measured by double occlusion. In conclusion, changes in blood Hct affect all three segmental vascular resistances, whereas changes in blood flow affect Rsinus, but not Rpv or Rhv. Norepinephrine increases mainly presinusoidal resistance. Ppo and Phvo can be obtained by the double occlusion method in isolated perfused rat livers.

Sign in / Sign up

Export Citation Format

Share Document