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.

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.

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.

Portal venous infusions of L-glutamine in anaesthetized dogs do not influence renal function

1992 ◽  
Vol 70 (10) ◽  
pp. 1432-1435
Author(s):  
Mortimer Levy
Keyword(s):  
Wistar Rats ◽  
Femoral Vein ◽  
Venous Pressure ◽  
Renal Perfusion ◽  
Portal Venous Pressure ◽  
Portal System ◽  
Similar Data ◽  
Free Base ◽  
Hepatorenal Reflex ◽  
Intraportal Infusion

It has been reported that the intraportal infusion of glutamine in Munich–Wistar rats will cause depression of renal perfusion and the urinary excretion of salt and water. We have attempted to reproduce these findings in anaesthetized dogs. L-Glutamine was infused at doses between 120 and 150 μmol/min into the portal vein and femoral vein of anaesthetized dogs. No effect was observed on portal venous pressure, blood pressure, or kidney function. Similar data were obtained with D-glutamine. Liver biopsy revealed no abnormalities. When 1.5–3 μg histamine (free base) was infused into the portal system, portal venous pressure rose from 15.2 ± 0.33 to 24.8 ± 0.40 cmH2O (p < 0.05) (1 cmH2O = 98.1 Pa). Glutamine infusions do not appear to initiate hepatorenal reflexes in dogs as they have been reported to do in rats.Key words: liver, portal hypertension, hepatorenal reflex.

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.

Effect of Propranolol on Hepatic Blood Flow in Normal and Portal Hypertensive Rats

1982 ◽  
Vol 63 (1) ◽  
pp. 29-32 ◽  
Author(s):  
P. Hillon ◽  
L. Blanchet ◽  
D. Lebrec
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Hepatic Blood Flow ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Portal Vein Stenosis ◽  
Vein Stenosis

1. The effects of propranolol on heart rate, arterial pressure, portal venous pressure and fractional hepatic blood flow were studied in rats with hepatic artery ligature or with portal vein stenosis, and in sham-operated rats. The effect of propranolol on cardiac output was also studied in normal rats. 2. In rats with hepatic artery ligature or with portal vein stenosis, and in sham-operated rats, propranolol decreased heart rate and portal venous pressure significantly and did not alter arterial pressure. Propranolol decreased fractional hepatic blood flow significantly in rats with hepatic artery ligature, but did not change hepatic blood flow in rats with portal vein stenosis or in sham-operated rats. 3. We conclude therefore that: (a) propranolol decreases portal venous pressure in rats; (b) this decrease in portal venous pressure results in a reduction in portal blood flow which is related, in part, to a reduction in cardiac output; (c) propranolol does not alter hepatic blood flow in normal rats or in rats with portal hypertension.

scholarly journals Vascular Involvements in Cholangiocarcinoma: Tips and Tricks

Cancers ◽  
2021 ◽  
Vol 13 (15) ◽  
pp. 3735
Author(s):  
Roberta Angelico ◽  
Bruno Sensi ◽  
Alessandro Parente ◽  
Leandro Siragusa ◽  
Carlo Gazia ◽  
...  
Keyword(s):  
Portal Vein ◽  
Hepatic Artery ◽  
Vena Cava ◽  
High Volume ◽  
Vascular Reconstruction ◽  
Ex Situ ◽  
Vascular Involvement ◽  
Hepatic Veins ◽  
Hepatic Artery Resection ◽  
Artery Resection

Cholangiocarcinoma (CCA) is an aggressive malignancy of the biliary tract. To date, surgical treatment remains the only hope for definitive cure of CCA patients. Involvement of major vascular structures was traditionally considered a contraindication for resection. Nowadays, selected cases of CCA with vascular involvement can be successfully approached. Intrahepatic CCA often involves the major hepatic veins or the inferior vena cava and might necessitate complete vascular exclusion, in situ hypothermic perfusion, ex situ surgery and reconstruction with autologous, heterologous or synthetic grafts. Hilar CCA more frequently involves the portal vein and hepatic artery. Resection and reconstruction of the portal vein is now considered a relatively safe and beneficial technique, and it is accepted as a standard option either with direct anastomosis or jump grafts. However, hepatic artery resection remains controversial; despite accumulating positive reports, the procedure remains technically challenging with increased rates of morbidity. When arterial reconstruction is not possible, arterio-portal shunting may offer salvage, while sometimes an efficient collateral system could bypass the need for arterial reconstructions. Keys to achieve success are represented by accurate selection of patients in high-volume referral centres, adequate technical skills and eclectic knowledge of the various possibilities for vascular reconstruction.

Non-invasive methods in the assessment of portal hypertension severity

2021 ◽  
Vol 75 (2) ◽  
pp. 125-133
Author(s):  
Soňa Franková ◽  
Jan Šperl
Keyword(s):  
Portal Hypertension ◽  
Liver Fibrosis ◽  
Shear Wave ◽  
Transient Elastography ◽  
Venous Pressure ◽  
Liver Stiffness ◽  
Invasive Technique ◽  
Hepatic Veins ◽  
Oesophageal Varices ◽  
Non Invasive

Portal hypertension represents a wide spectrum of complications of chronic liver diseases and may present by ascites, oesophageal varices, splenomegaly, hypersplenism, hepatorenal and hepatopulmonary syndrome or portopulmonary hypertension. Portal hypertension and its severity predicts the patient‘s prognosis: as an invasive technique, the portosystemic gradient (HPVG – hepatic venous pressure gradient) measurement by hepatic veins catheterisation has remained the gold standard of its assessment. A reliable, non-invasive method to assess the severity of portal hypertension is of paramount importance; the patients with clinically significant portal hypertension have a high risk of variceal bleeding and higher mortality. Recently, non-invasive methods enabling the assessment of liver stiffness have been introduced into clinical practice in hepatology. Not only may these methods substitute for liver biopsy, but they may also be used to assess the degree of liver fibrosis and predict the severity of portal hypertension. Nowadays, we can use the quantitative elastography (transient elastography, point shear-wave elastrography, 2D-shear-wave elastography) or magnetic resonance imaging. We may also assess the severity of portal hypertension based on the non-invasive markers of liver fibrosis (i.e. ELF test) or estimate clinically signifi cant portal hypertension using composite scores (LSPS – liver spleen stiff ness score), based on liver stiffness value, spleen diameter and platelet count. Spleen stiffness measurement is a new method that needs further prospective studies. The review describes current possibilities of the non-invasive assessment of portal hypertension and its severity.

Reflex effects of hepatic baroreceptors on renal and cardiac sympathetic nerve activity

1980 ◽  
Vol 238 (5) ◽  
pp. R390-R394 ◽  
Author(s):  
D. R. Kostreva ◽  
A. Castaner ◽  
J. P. Kampine
Keyword(s):  
Sympathetic Nerve Activity ◽  
Carotid Sinus ◽  
Venous Pressure ◽  
Vena Cava ◽  
Systemic Blood Pressure ◽  
Nerve Activity ◽  
Efferent Nerve ◽  
Cardiac Sympathetic Nerve Activity ◽  
Cervical Vagotomy ◽  
Hepatic Nerves

The reflex effects of hepatic low-pressure baroreceptors on renal and cardiopulmonary sympathetic efferent nerve activity were studied in mongrel dogs anesthetized with pentobarbital sodium. Systemic blood pressure, central venous pressure, hepatic, renal, and portal venous pressures were all measured during occlusion of the thoracic vena cava above the diaphragm, below the liver, and during occlusion of the portal vein. Renal and cardiopulmonary sympathetic efferent nerve activity was continuously recorded along with the hepatic efferent nerve activity during the caval occlusions. Hepatic baroreceptor excitation resulted in marked increases in hepatic afferent nerve activity and reflex increases in renal and cardiopulmonary sympathetic efferent nerve activity without a change in heart rate. Section of the anterior hepatic nerves eliminated the reflex increase in renal efferent nerve activity, but did not eliminate the increase in cardiopulmonary sympathetic efferent nerve activity. Carotid sinus denervation, bilateral cervical vagotomy, and phrenectomy did not alter the reflex responses to hepatic baroreceptor excitation. These hepatorenal and hepatocardiopulmonary reflexes may be important reflex mechanisms that are activated during congestive heart failure and cirrhosis of the liver.

Portal venous pressure in “pipestem” fibrosis of the liver due to schistosomiasis

1959 ◽  
Vol 27 (5) ◽  
pp. 807-810 ◽  
Author(s):  
Arthur H. Aufses ◽  
Fenton Schaffner ◽  
William S. Rosenthal ◽  
Bernard E. Herman
Keyword(s):  
Venous Pressure ◽  
Portal Venous Pressure
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