الفهرس 
acknowledgmentOnly 14 pages are availabe for public view
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Abstract
’he hydratOict study of the problem of portal hyper-
nsion by means of an ”In Vitro” model is not so easy
cause of the difficulty of construction of an ideal
draulic model representing all the characteristics of
e portal tract and representing all the IN Vivo parameters
, the hepato-portal circulations
iat’ difficulties result f romt
Lack of definite informations about the portal tract and
the hepatoportal circulation in man and experimental
animal3 on respect to their definite anatomical and
physiological properties*
Qualitative evaluation of the circulatory physiology of the liver and other splanchnic viscera has proved extremely difficult owing to the inadequacies of the methods avail¬able, to uncertainties arising from species differences and to the lack of data obtained simultaneously to provide information regarding the behaviour of the remainder of the circulatory system. Measurement of the cardiac out¬put and the arterial blood pressure are required to determine whether changes in the hepatic hemodynamics are produced by local vasomotor activity or by passive changes in response to alterations in the perfusing pressure.
- As alterations in the vascular dimensions and elastic
properties and in the hemodynamic patterns arise primarily
from the varied inter play of vasoconstriction, closure
or collapse of vessels and rearrangement of the vascular pathways, also additional extraneous factors extravital have modifying , integrating and directive influence. Among the latter it is necessary to consider neural mechanisms, humoral agents and external physical agents that are imposed by abdominal muscular contractions, tissue tension, gravity, respiration,, .vito.
All these factors can not be represented in an In Vitro model by which one obtain quantitative hydraulic study of the portal tract.
- Also due to lack of certain equipments and materials
which are necessary for manufacturing an exact dynamic
simulator, a geometric model was manufactured with
pressures and flow rate correlating with the normal
standard values as obtained from our materials and from
the standard literature. That model was used to give a
qualitative description of the portal hemodynamics,
Prom all the mentioned study one can conclude the following: 1- Anatomically, the portal tract has no constent structure i normal to all materials especially in respect to its smaller vessels.
Measurements obtained In the dissection of 20 cadavers in respect to the angles, lengths and diameters of the arteries and vein3 of the portal system was presented.
2- Using direct tension test, the veins of the portal tract proved to have a limited distensibiiity , and that of the portal vein is less than that of the splenic and superior mesentric veins•
i
4- By application of Reynold’s principle on the flow of
blood in all the vessels of the hepatoportal tract one find that the flow is typical laminar non rotational flow I.e. viscous flow.
5- from the experiments done on the geometric model represent¬
ing the portal tract one can deduce that:
a- The pressure in the portal vein and its tributaries
is raised by»
- Increase in the splenic venous flow.
- Increase in the portal venous resistance.
- Increase in the post sinusoidal resistance.
- Back pressure on the portal circulation distal to the liver.
The development of portosystemic collaterals compensates for the obstruction and alleviate the rise of the pressure in the portal tract.
H- The pressure in the portal vein and its tributaries can be decreased by:
- Closure of the hepatic artery.
- Closure of the splenic artery,
- Closure of the superior mesentric artery. Although complete closure of the superior mesentric artery decreases the portal vein pressure more than closure of the splenic and hepatic arteries yet when the hepatic flow is decreased by a certain value through any of the three arteries the DROP in the pressure of the portal vein is more in case of the
[ hepatic artery then splenic artery then the superior I mesentric artery.
I c- The hepatic blood flow ia reduced by:
I - Closure of any of the supplying arteries.
I - Increase of the resistances inside the liver presinusoidal
I or post sinusoidal.
I - Back pressure on the hepatic ciraulation.
I d- Hepatic blood flow is raised by:
I - Reduction of the arterial resistance in any of the
I drained splanchnic beds,
I e- The development of collaterals not only alleviates the I increase in the portal pressure but also affects the ■ pressure gradient in the portal tract so that in severe
presinusoidal or post sinusoidal obstruction the vein from which the collateral flow is established ’rca \Vifc least pressure.
F- The pressure in any vein of the portal tract depends on: 1- Rate of flow through that bein i.e. the pressure varies directly with the rate of flow through that vessel.
2- The anatomical pathway of the vein more angles equals more pressure*
3- Position of collateral circulation,
g- With developing portosystemic collaterals, the post-ainusoidal resistance has a higher effect than that of the presinusoidal resistance in raising the portal vein pressure the reverse is correct when the collaterals circulation is not established.