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.

scholarly journals Banti’s Syndrome Presenting as Hematemesis - A Case Report

2021 ◽  
Vol 10 (10) ◽  
pp. 749-751
Author(s):  
Aishwarya Ghule ◽  
Sourya Acharya ◽  
Samarth Shukla ◽  
Sunil Kumar ◽  
Parth Godhiwala
Keyword(s):  
Portal Hypertension ◽  
Portal Pressure ◽  
Normal Liver ◽  
Liver Function Tests ◽  
Massive Bleeding ◽  
Idiopathic Portal Hypertension ◽  
Hepatic Veins ◽  
Massive Splenomegaly ◽  
History Of ◽  
Banti's Syndrome

Massive splenomegaly presenting with hypersplenism, pancytopenia and portal hypertension, without any underlying known cause is known as Banti’s syndrome. There are various causes of splenomegaly. When all the known causes of portal hypertension are ruled out, it is termed as Banti’s syndrome. This syndrome was discovered by Guido Banti in 1882 and is named after him. Banti’s syndrome is also known as idiopathic portal hypertension or non-cirrhotic portal fibrosis.1 Banti’s syndrome is commonly found in India and Japan than in the West. 2 There is absence of any haematologic cause, primary hepatic cause or any tumour or mass lesion involving the spleen. Banti had stated that the primary organ involved was spleen and not the liver leading to secondary splenomegaly. Other features include normal liver function tests, varices seen in endoscopy, cytopenia of one or more cell lines, absence of cirrhosis, patent hepatic veins and elevated portal pressure with multiple collaterals. The complications include rupture of varices and massive bleeding. 3 We report a case of a 20-year-old male who presented to us with a history of fever for 7 days and one-episode of hematemesis on the day of admission. All known causes of hypersplenism were ruled out and he was diagnosed to have idiopathic massive splenomegaly with portal hypertension and hypersplenism.

Nanoliter-volume flow-through fluorometer

1982 ◽  
Vol 54 (4) ◽  
pp. 840-842 ◽  
Author(s):  
Gerald G. Vurek
Keyword(s):  
Volume Flow ◽  
Flow Through

Diameter, wall tension, and flow in mesenteric arterioles during autoregulation

1981 ◽  
Vol 241 (6) ◽  
pp. H829-H837 ◽  
Author(s):  
M. E. Burrows ◽  
P. C. Johnson
Keyword(s):  
Arterial Pressure ◽  
Average Diameter ◽  
Vessel Diameter ◽  
Flow Regulation ◽  
Blood Velocity ◽  
Volume Flow ◽  
Wall Tension ◽  
Pressure Data ◽  
Dependent Mechanism ◽  
Intravascular Pressure

The effect of arterial pressure on vessel diameter, blood velocity, and intravascular pressure was examined in cat mesenteric arterioles in the arterial pressure range of 120—40 mmHg. Circumferential wall tension and volume flow in individual vessels were calculated. Twenty-nine arterioles with an average diameter of 25.1 micrometers were studied. Twenty-six reactive vessels dilated by an average of 6.5 micrometers with arterial pressure reduction, whereas three nonreactive arterioles narrowed by an average of 5.9 micrometers. When pressure was reduced, circumferential wall tension in reactive arterioles tended to be maintained, whereas in nonreactive vessels tension decreased more than pressure. Data from 25 of 26 reactive arterioles were consistent with the hypothesis that regulation of wall tension accounts for the autoregulatory response; however, in 18 of these vessels a flow-dependent mechanism could also account for the response. Thus the hypothesis that wall tension is a controlled variable responsible for autoregulation is supported, but an important role for flow regulation in local control is also supported.

Effect of Narcotic Agents and of Bleeding on Systemic and Renal Haemodynamics in Healthy and CCl4-treated Cirrhotic Rats

1997 ◽  
Vol 93 (6) ◽  
pp. 549-556 ◽  
Author(s):  
G. Van Roey ◽  
P. Lijnen ◽  
R. Verbesselt ◽  
A. Verbruggen ◽  
J. Fevery
Keyword(s):  
Arterial Pressure ◽  
Plasma Volume ◽  
Renal Plasma Flow ◽  
Portal Pressure ◽  
Plasma Renin ◽  
Repeated Measurements ◽  
Peripheral Vasodilatation ◽  
Profound Hypotension ◽  
Awake Rat ◽  
Related Mortality

1. The haemodynamic effects of different narcotic agents have been tested in healthy rats and in rats with cirrhosis. 2. Pentobarbital suppresses the sympathetic nervous system. Susceptibility to ketamine is unpredictable, leading to both insufficient pain relief and narcosis related mortality. The combination diazepam—fluanisone induces profound hypotension. After insertion of catheters, awake, freely moving rats are stable and not distressed. This allows repeated measurements after manipulation. Moreover, procedure-related mortality is low and rats have a better stress response. 3. In the awake animal, arterial pressure is 126 ± 10 for healthy animals, and 111 ± 16 and 102 ± 10 mmHg for cirrhotic animals without and with ascites, respectively (P = 0.018). The respective values for portal pressure are 6.9 ± 1.4, 11.6 ± 2.5 and 16.2 ± 2.9 mmHg (P = 0.0001). After a bleeding, arterial pressure is better preserved than portal pressure in the three groups (P < 0.0001). Plasma volume in cirrhotic rats exceeds that of healthy rats. Plasma renin activity, aldosterone and catecholamines do not differ between the groups studied. In cirrhotic rats with and without ascites, glomerular filtration rate tends to be higher (P = 0.12), renal plasma flow is elevated (P = 0.001) and nitration fraction is lower (P = 0.002) than in healthy rats. 4. In conclusion, haemodynamic experiments in the cirrhotic rat should be performed in the awake rat. Arterial hypotension, impaired filtration fraction, enlarged plasma volume and portal hypertension are present in cirrhosis before the development of ascites. This can as well be explained by splanchnic pooling of blood, as by peripheral vasodilatation. The decrease in portal pressure with preserved arterial pressure after a bleeding protects cirrhotic rats from ongoing variceal bleeding.

Effect of thioridazine and chlorpromazine on rat liver hemodynamics

1960 ◽  
Vol 199 (5) ◽  
pp. 793-796 ◽  
Author(s):  
Gabriel L. Plaa ◽  
Edwin C. McGough ◽  
Gerry J. Blacker ◽  
James M. Fujimoto
Keyword(s):  
Mean Arterial Pressure ◽  
Marked Decrease ◽  
Portal Pressure ◽  
Liver Ischemia ◽  
Phenothiazine Derivatives ◽  
Perfusate Flow ◽  
Flow Through ◽  
Liver Hemodynamics ◽  
Rat Livers ◽  
Higher Doses

Evidence is presented which indicates that two phenothiazine derivatives—thiroidazine and chlorpromazine— increase hepatic vascular resistance in isolated perfused rat livers. These substances produce the following: a) a decrease in perfusate flow through the organ, b) an increase in portal pressure and c) a decrease in organ weight. These effects were demonstrated with doses as low as 4 mg but were quantitatively more pronounced and of longer duration with higher doses. Tachyphylaxis did not occur. The effects could be blocked with sodium nitrite. Both phenothiazines were found to produce liver ischemia in anesthetized, laparotomized rats. Thioridazine was found to raise portal pressure in anesthetized, laparotomized cats in spite of a marked decrease in mean arterial pressure.

Splanchnic blood flow in the monkey during hemorrhagic shock

1965 ◽  
Vol 208 (2) ◽  
pp. 265-269 ◽  
Author(s):  
Francis L. Abel ◽  
John A. Waldhausen ◽  
Ewald E. Selkurt
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Portal Vein ◽  
Hemorrhagic Shock ◽  
Hepatic Vein ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Mesenteric Arteries ◽  
Splanchnic Blood Flow

Blood flow in the celiac and superior mesenteric arteries was measured in nine Macaca monkeys during a standardized hemorrhagic shock procedure. Simultaneous pressures were obtained from the hepatic vein, portal vein, and aorta. Each animal was bled rapidly to an arterial pressure of 40 mm Hg and maintained at this level until 30% of the bled volume had spontaneously reinfused. The remaining blood was then rapidly reinfused and the animal observed until death. The results show a lack of overshoot of venous pressure on reinfusion, grossly pale intestines with some microscopic congestive changes, and a decrease in splanchnic conductance throughout the postinfusion period. Hepatic venous pressure exceeded portal pressure in six of the nine animals during the period of hemorrhage. The results are interpreted as indicative of insignificant splanchnic pooling during hemorrhagic shock in this animal.

Flow through zone 1 lungs utilizes alveolar corner vessels

1991 ◽  
Vol 70 (4) ◽  
pp. 1518-1523 ◽  
Author(s):  
W. J. Lamm ◽  
K. R. Kirk ◽  
W. L. Hanson ◽  
W. W. Wagner ◽  
R. K. Albert
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Left Lung ◽  
Lateral Position ◽  
Double Lumen Endotracheal Tube ◽  
Mean Pulmonary Arterial Pressure ◽  
Flow Through ◽  
Pulmonary Arterial ◽  
Isolated Lungs

We have previously observed flows equivalent to 15% of the resting cardiac output of rabbits occurring through isolated lungs that were completely in zone 1. To distinguish between alveolar corner vessels and alveolar septal vessels as a possible zone 1 pathway, we made in vivo microscopic observations of the subpleural alveolar capillaries in five anesthetized dogs. Videomicroscopic recordings were made via a transparent thoracic window with the animal in the right lateral position. From recordings of the uppermost surface of the left lung, alveolar septal and corner vessels were classified depending on whether they were located within or between alveoli, respectively. Observations were made with various levels of positive end-expiratory pressure (PEEP) applied only to the left lung via a double-lumen endotracheal tube. Consistent with convention, flow through septal vessels stopped when PEEP was raised to the mean pulmonary arterial pressure (the zone 1-zone 2 border). However, flow through alveolar corner vessels continued until PEEP was 8-16 cmH2O greater than mean pulmonary arterial pressure (8-16 cm into zone 1). These direct observations support the idea that alveolar corner vessels rather than patent septal vessels provide the pathway for blood flow under zone 1 conditions.

A High Performance PFB System for Utility Application

1987 ◽  
Author(s):  
Paul A. Berman ◽  
Jeffrey A. Hynds
Keyword(s):  
Power System ◽  
High Performance ◽  
State Of The Art ◽  
Combustion Products ◽  
Volume Flow ◽  
Power Cycle ◽  
Turbine Inlet ◽  
Alkali Vapors ◽  
Fluid Bed ◽  
Flow Through

In the traditional pressurized fluid bed (PFB) power system, the PFB is located in the highest pressure portion of the power cycle, Figure 1. This results in the smallest volume flow through the PFB, but also requires the combustion products to flow through the entire expansion train. This is not expected to be a major problem when the PFB temperature is limited to 1600°F for effective sulfur capture and to avoid alkali vapors in the products of combustion. However, when topping combustion is added ahead of the turbine so as to reach state-of-the-art turbine inlet temperatures, a major risk for turbine corrosion and fouling develops.

scholarly journals Detection of cirrhosis through ultrasound imaging by intensity difference technique

2019 ◽  
Vol 2019 (1) ◽  
Author(s):  
Karan Aggarwal ◽  
Manjit Singh Bhamrah ◽  
Hardeep Singh Ryait
Keyword(s):  
High Performance ◽  
Research Work ◽  
Region Of Interest ◽  
Normal Liver ◽  
Cirrhotic Liver ◽  
Intensity Difference ◽  
Non Invasive ◽  
The Us ◽  
The Difference ◽  
Two Parameters

Abstract Cirrhosis is a liver disease that is considered to be among the most common diseases in healthcare. Due to its non-invasive nature, ultrasound (US) imaging is a widely accepted technology for the diagnosis of this disease. This research work proposed a method for discriminating the cirrhotic liver from normal liver through US images. The liver US images were obtained from the radiologist. The radiologist also specified the region of interest (ROI) from these images, and then the proposed method was applied to it. Two parameters were extracted from the US images through differences in intensity of neighboring pixels. Then, these parameters can be used to train a classifier by which cirrhotic region of test patient can be detected. A 2-D array was created by the difference in intensity of the neighboring pixels. From this array, two parameters were calculated. The decision was taken by checking these parameters. The validation of the proposed tool was done on 80 images of cirrhotic and 30 images of normal liver, and classification accuracy of 98.18% was achieved. The result was also verified by the radiologist. The results verified its possibility and applicability for high-performance cirrhotic liver discrimination.

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