Contribution of the large hepatic veins to postsinusoidal vascular resistance

1992 ◽  
Vol 262 (1) ◽  
pp. G14-G22 ◽  
Author(s):  
R. Maass-Moreno ◽  
C. F. Rothe
Keyword(s):  
Transition Point ◽  
Venous Pressure ◽  
Primary Site ◽  
The Other ◽  
Hepatic Veins ◽  
Pressure Gradients ◽  
Double Lumen ◽  
Pentobarbital Sodium ◽  
Anesthetized Dogs ◽  
Flow Through

We tested the hypothesis that the larger (greater than 2 mm ID) hepatic veins are the primary site of the portal-to-caval venous pressure gradient in the dog. Double-lumen catheters were inserted through the caval wall into hepatic veins of pentobarbital sodium-anesthetized dogs. One lumen opened at the end, and the other to the side. Each catheter was advanced until stopped and then it was withdrawn. The pressure at either port dropped from 87 +/- 31 to 13 +/- 11% of the portal-to-caval pressure difference as each moved past a transition point (TP). The location of the TP depended on the catheter diameter. Intraportal histamine or norepinephrine, 4 and 2.6 micrograms.min-1.kg body wt-1 respectively, augmented only the pressure measured upstream to the TP. A mathematical model of flow through a vessel with a catheter inside predicted a marked increase in resistance when the ratio of catheter OD to vessel ID exceeded approximately 0.6. Autopsy revealed ratios greater than 0.6 upstream to the TP. A hydraulic model confirmed that this effect caused the appearance of the TP. Given the depth (11.7 cm) at which near caval pressures could be found, even during histamine administration, we conclude that the major pressure gradients in the canine liver must lie upstream to the large hepatic veins.

Renal effects of prostaglandin inhibition during increases in renal venous pressure

1991 ◽  
Vol 260 (4) ◽  
pp. F525-F529 ◽  
Author(s):  
M. J. Fiksen-Olsen ◽  
J. C. Romero
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Filtration Rate ◽  
Venous Pressure ◽  
Interstitial Pressure ◽  
Pentobarbital Sodium ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Pressure Changes

The role of prostaglandins (PGs) in mediating the hemodynamic and natriuretic responses to increases in renal interstitial pressure (RIP) induced by altering renal venous pressure (RVP) from control (3.6 +/- 0.6) to 15 and 30 mmHg was examined before and after PG inhibition in pentobarbital sodium-anesthetized dogs. These elevations of RVP resulted in RIP increasing from control (6 +/- 1) to 11 +/- 1 and 23 +/- 2 mmHg, respectively, without altering mean arterial pressure (MAP), renal blood flow (RBF), and glomerular filtration rate (GFR). Sodium excretion increased only when RVP reached 30 mmHg. During the inhibition of PG synthesis, 15 mmHg RVP induced a 10% decrease in RBF, and 30 mmHg RVP induced a further 20% decrease in RBF and a 50% decrease in GFR. PG synthesis inhibition did not alter either the RIP or the sodium excretory response. In conclusion, the natriuresis associated with the RIP increases induced by increasing RVP appears to be independent of PG synthesis. PGs, however, appear to be important for the maintenance of RBF and GFR during increased RVP. These findings suggest that different mechanisms are involved in the hemodynamic and natriuretic responses to arterial vs. venous pressure changes.

Relationship between lymphatic and venous pressure in leg of dog

1959 ◽  
Vol 196 (3) ◽  
pp. 495-498 ◽  
Author(s):  
Aya Irisawa ◽  
Robert F. Rushmer
Keyword(s):  
Venous Pressure ◽  
The Other ◽  
A Value ◽  
Peripheral Venous Pressure ◽  
Anesthetized Dogs

In resting, anesthetized dogs the lymphatic pressure has a value close to, but a little below, peripheral venous pressure. Contrary to previous observations the lymphatic pressure in the resting hind leg is measurable and even small fluctuations in pressure can be detected with the techniques employed. Changes in peripheral lymphatic and venous pressures are neither simultaneous nor equal. Even large changes of pressure in one system were not reflected in the other. A definite rise in lymphatic pressure was observed during spontaneous muscle movements. Fluctuation in lymphatic pressure was recorded during normal and forced abdominal respiration.

A computational model-based study on the exchangeability of hepatic venous pressure gradients measured in multiple hepatic veins

2020 ◽  
Vol 84 ◽  
pp. 28-35
Author(s):  
Tianqi Wang ◽  
Fuyou Liang ◽  
Lei Li ◽  
Wen Zhang ◽  
Guangchuan Wang ◽  
...  
Keyword(s):  
Computational Model ◽  
Venous Pressure ◽  
Hepatic Veins ◽  
Pressure Gradients ◽  
Model Based

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.

Effect of small doses of 5-hydroxytryptamine (serotonin) on pulmonary circulation in the closed-chest dog

1959 ◽  
Vol 197 (5) ◽  
pp. 963-967 ◽  
Author(s):  
John T. Shepherd ◽  
David E. Donald ◽  
Erland Linder ◽  
H. J. C. Swan
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Blood Flow ◽  
Pulmonary Veins ◽  
Pulmonary Vessels ◽  
Isolated Perfused Lung ◽  
Small Doses ◽  
Perfused Lung ◽  
Anesthetized Dogs ◽  
Flow Through ◽  
The Difference

5-Hydroxytryptamine (serotonin) was infused into anesthetized dogs at a rate of 20 µg/kg/min. In nine sets of observations on three dogs the increase in the difference of pressure between the pulmonary artery and the left atrium, which averaged 55%, consistently exceeded the increase in pulmonary blood flow, which averaged 16%. 5-HT therefore is a potent constrictor of pulmonary vessels, even in small concentrations. No changes in the pulmonary-artery wedge and pulmonary-vein pressures were detected during the infusions of 5-HT, nor was there any change in the volume of blood between the pulmonary artery and the root of the aorta. With this dose of 5-HT the principal site of the increased resistance to flow through the lungs appeared to be in the precapillary vessels. In the isolated perfused lung, moderate constriction of pulmonary veins also was produced by large doses of 5-HT.

Interaction of right and left carotid sinus baroreflexes in the dog

1986 ◽  
Vol 250 (1) ◽  
pp. H96-H107 ◽  
Author(s):  
A. S. Greene ◽  
M. J. Brunner ◽  
A. A. Shoukas
Keyword(s):  
Heart Rate ◽  
Tidal Volume ◽  
Carotid Sinus ◽  
The Other ◽  
Reflex Response ◽  
Pentobarbital Sodium ◽  
Simultaneous Excitation ◽  
Carotid Sinus Baroreflex ◽  
The Right ◽  
Sinus Pressure

Carotid sinus reflex interactions were studied in 10 dogs anesthetized with pentobarbital sodium. The right and left carotid sinus regions were isolated and perfused at controlled pressures. Pressure in the right and left carotid sinuses were independently varied, and the resulting steady-state reflex changes in arterial pressure, heart rate, respiratory frequency, tidal volume, and total ventilation were measured. Reflex changes when carotid sinus pressure was changed on one side were strongly influenced by pressure in the contralateral carotid sinus (P less than 0.05). Right carotid sinus gain was found to be 0.628 +/- 0.058 at a left carotid sinus pressure of 50 mmHg and 0.148 +/- 0.027 when left carotid sinus pressure was 200 mmHg. Similar results were found for left carotid sinus gain. Suppression was also found for heart rate, respiratory rate, tidal volume, and total ventilation. The hypothesis that rapid resetting of one carotid sinus baroreflex might influence responses from the other side was also tested. Although ipsilateral resetting was consistently observed, no contralateral component of the resetting was detected. An additional inhibitory summation between the right and left carotid sinuses was found such that simultaneous excitation of both receptors resulted in a smaller reflex response than did the sum of individual responses. Sympathetic denervation of the carotid sinus region had no effect.

scholarly journals Blood Perfusion of the Kidney of Lophius Piscatorius L.

1953 ◽  
Vol 32 (2) ◽  
pp. 329-336 ◽  
Author(s):  
L. Brull ◽  
E. Nizet ◽  
E. B. Verney
Keyword(s):  
Blood Flow ◽  
Critical Level ◽  
Perfusion Pressure ◽  
Blood Perfusion ◽  
Urine Flow ◽  
The Other ◽  
Protein Nitrogen ◽  
Other Hand ◽  
Flow Through

Lophius kidneys perfused with the heparinized blood (venous) of the fish secrete urine in which total non-protein nitrogen is concentrated, magnesium highly concentrated, and chloride only slightly so or not at all. Oxygenation of the blood, or lowering the temperature of the perfusate from c. 20° to c. 5° C. does not appear to influence secretion. The blood flow through the kidneys increases with the perfusion pressure, the increase often becoming disproportionately large. The urine flow, on the other hand, above a certain critical level is largely independent of changes in perfusion pressure.

scholarly journals The structure and dynamics of patch-clamped membranes: a study using differential interference contrast light microscopy.

1990 ◽  
Vol 111 (2) ◽  
pp. 599-606 ◽  
Author(s):  
M Sokabe ◽  
F Sachs
Keyword(s):  
Cell Surface ◽  
Transmural Pressure ◽  
Positive Pressure ◽  
Radius Of Curvature ◽  
Pressure Gradients ◽  
Structure And Motion ◽  
Excised Patches ◽  
Glass Interface ◽  
Pipette Tip ◽  
Flow Through

We have developed techniques for micromanipulation under high power video microscopy. We have used these to study the structure and motion of patch-clamped membranes when driven by pressure steps. Patch-clamped membranes do not consist of just a membrane, but rather a plug of membrane-covered cytoplasm. There are organelles and vesicles within the cytoplasm in the pipette tip of both cell-attached and excised patches. The cytoplasm is capable of active contraction normal to the plane of the membrane. With suction applied before seal formation, vesicles may be swept from the cell surface by shear stress generated from the flow of saline over the cell surface. In this case, patch recordings are made from membrane that was not originally present under the tip. The vesicles may break, or fuse and break, to form the gigasealed patch. Patch membranes adhere strongly to the wall of the pipette so that at zero transmural pressure the membranes tend to be normal to the wall. With transmural pressure gradients, the membranes generally become spherical; the radius of curvature decreasing with increasing pressure. Some patches have nonuniform curvature demonstrating that forces normal to the membrane may be significant. Membranes often do not respond quickly to changes in pipette pressure, probably because viscoelastic cytoplasm reduces the rate of flow through the tip of the pipette. Inside-out patches may be peeled from the walls of the pipette, and even everted (with positive pressure), without losing the seal. This suggests that the gigaseal is a distributed property of the membrane-glass interface.

Intrapleural fluid movements described by a porous flow model

1992 ◽  
Vol 73 (6) ◽  
pp. 2511-2516 ◽  
Author(s):  
G. Miserocchi ◽  
D. Venturoli ◽  
D. Negrini ◽  
M. C. Gilardi ◽  
R. Bellina
Keyword(s):  
Porous Medium ◽  
Gamma Camera ◽  
Flow Model ◽  
Pleural Space ◽  
Interstitial Tissue ◽  
Hydraulic Pressure ◽  
Pressure Gradients ◽  
Hydraulic Radius ◽  
Porous Flow ◽  
Anesthetized Dogs

We injected technetium-labeled albumin (at a concentration similar to that of the pleural fluid) in the costal region of anesthetized dogs (n = 13) either breathing spontaneously or apneic. The decay rate of labeled activity at the injection site was studied with a gamma camera placed either in the anteroposterior (AP) or laterolateral (LL) projection. In breathing animals (respiratory frequency approximately 10 cycles/min), 10 min after the injection the activity decreased by approximately 50% on AP and approximately 20% on LL imaging; in apneic animals the corresponding decrease in activity was reduced to approximately 15 and approximately 3%, respectively. We considered label translocation from AP and LL imaging as a result of bulk flows of liquid along the costomediastinal and gravity-dependent direction, respectively. We related intrapleural flows to the hydraulic pressure gradients existing along these two directions and to the geometry of the pleural space. The pleural space was considered as a porous medium partially occupied by the mesh of microvilli protruding from mesothelial cells. Solution of the Kozeny-Carman equation for the observed flow velocities and pressure gradients yielded a mean hydraulic radius of the pathways followed by the liquid ranging from 2 to 4 microns. The hydraulic resistivity of the pleural space was estimated at approximately 8.5 x 10(5) dyn.s.cm-4, five orders of magnitude lower than that of interstitial tissue.

scholarly journals AN EXPERIMENTAL STUDY INTO THE CAUSE OF THE INCREASED PORTAL PRESSURE IN PORTAL CIRRHOSIS

1907 ◽  
Vol 9 (1) ◽  
pp. 93-104 ◽  
Author(s):  
Frederick C. Herrick
Keyword(s):  
Arterial Pressure ◽  
Portal Pressure ◽  
Normal Liver ◽  
Volume Flow ◽  
Cirrhotic Liver ◽  
Return Flow ◽  
Hepatic Veins ◽  
Portal Cirrhosis ◽  
Arterial Inflow ◽  
Flow Through

1. In the liver of portal cirrhosis there is a far freer communication between the arterial and portal currents than in the normal liver. 2. Factors contributing to the increased portal pressure in portal cirrhosis are (1) the direct communication of the arterial pressure to the portal vessels through dilated capillaries, (2) the larger volume-flow of the hepatic artery in proportion to the portal flow in cirrhosis as compared to that in the normal liver. 3. A portal cirrhotic liver gives passage to an amount of portal fluid proportionate to .its weight. There is no obstruction to the portal vessels from fibrosis in the large portal cirrhotic liver. 4. From an arterial inflow there is a free return flow through the portal as well as through the hepatic veins in both normal and cirrhotic livers. 5. From a portal inflow the return is through the hepatic vein only. The Gad's theory of valves and the arterial capillary network account for this fact. 6. The portal pressure has a decided influence on the arterial volume-flow and vice versa. This influence is more marked in the cirrhotic than in the normal liver. 7. The communication of the arterial pressure to the portal pressure is an important factor in an explanation of the increased portal pressure in portal cirrhosis.

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