[The mechanics of bile flow and its relation to the motor function of the gut].
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Biomedical subjects
Publications and source records attributed to O Aziz.
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The fluid content of circulating blood was followed continuously by conductometric measurement of large vein hematocrit in the alert rat. Arterial pressure was registered simultaneously. 2.5-23% of the determined blood volume was withdrawn rapidly and the changes of fluid content (delta v) calculated. Determinations of plasma protein showed that calculated delta v(delta vapp) may exceed true delta v due to transvascular fluid inflow by maximally 38%. A very fast phase of fluid inflow into the circulation (delta vfapp, within 1 min) was observed at the beginning, followed by a slow phase (delta vsapp), the magnitude of both being proportional to the concomitant arterial pressure drop (delta p). At delta p = 0, delta vfapp was 20% of the volume of blood withdrawn, total replacement (delta vfapp + delta vsapp = volume withdrawn) being complete in 60 min. At delta p = -20 mm Hg the figures were 40% and 20 min, respectively. Experiments on splenectomized animals showed essentially the same relations, excepting that delta vsapp may have been underestimated in normal rats. An arterial pressure rise after hemorrhage may attenuate complete replacement. The results are discussed in terms of capillary fluid conductivity. Thus CFC may be in the order of 0.029 ml/min x mm Hg x 100 g.
Short bursts of activity are accompanied by a sharp rise, then a sharp drop, followed facultatively by a tonic rise of pressure in the portal and mesenteric vein. Caval vein and abdominal pressure show only a monophasic rise during activity. The drop of portal pressure immediately after the activity peak can be shown to be passive, due to a fall in portal flow rate. The tonic rise after activity can be reproduced by single injections of catecholamines, noradrenalin being more effective than adrenalin. Systemic injections as against intramesenteric injections show, on the other hand, that adrenalin more effectively produces the postactivity pressure drop in the V. portae than noradrenalin. Raising venous pressures in the abdominal cavity by 15-40 mm H2O through acute introduction of air into the abdomen produces no change of venous hematocrit values. The results are discussed in connection with transvascular fluid shifts caused by activity and catecholamines. Portal vein pressure fluctuates with the same frequency, but with a phase displacement of 180 degrees, as Mayer waves.
A method for continuous plasmapheresis and refractometric determination of the protein concentration of blood circulating in the vascular system of the unanesthetized rat is presented. The method is applied to demonstrate very rapid transvascular fluid exchange during physical activity of the animal, noradrenalin infusions and hemorrhage. Changes of protein concentration are compared with concomitant changes of hematocrit in the hepatic portal vein and the v. cava inferior. Though both parameters invariably change in a parallel fashion, relative variations of protein concentration fall short of hot variations by 50%.
Single injections of noradenaline and adrenalineeeee were made into the v. cava of conscious rats during continuous registration of arterial blood pressure and conductivity (reciprocal hematocrit) in blood from different circulatory areas. The resulting hct and B.P. changes were compared with similar changes elicited by a 3-sec tactile stimulus. Two phases of hct response--the first due to local vascular reactions, the second due to a general vasodilatory reaction--can be distinguished. Whereas adrenalin and noradrenaline show differential effectivity in producing the local reactions (the former more potent as a precapillary vasoconstrictor, promoting hct drop due to fluid inflow in the portal and hepatic vein, the latter more so in the renal vein and the aorta), adrenalin is invariably more effective in producing the second phase dilatory reaction with fluid outflow (hct rise). In the v. cava close to the iliac bifurcation a greater hemoconcentrative potency of adrenalin can be demonstrated, but only by close injections into the aorta. Close injections into the portal vein make postcapillary hepatic reactions more sensitive to adrenalin manifest. The catecholamine dose equivalent to a 3-sec tactile stimulus in the rat is 80-120 ng.
Blood (3.4-13.5% of blood volume) was pumped in and out of the circulation of rats at different rates and period lengths during continuous measurements of blood conductivity (reciprocally related to hematocrit) and arterial pressure. Hct followed the same zig-zag course as the induced changes of blood volume in every case, indicating that fluid shifts (delta v) between interstitium and intravascular space closely follow blood volume changes. As the hct increase during reinfusion was not as great as the preceding decrease, hct dropped continuously during the 20-90 minutes of experimentation, so that a final volume increase (delta v) by about 4% was calculated, which was confirmed by a corresponding decrease of plasma protein concentration. Both final delta v and delta v during periodic volume change (delta % B.V.) were greater when arterial pressure dropped. delta v was directly related to delta % B.V. but not to its rate of change. Heart rate dropped slightly at the end of the reinfusion periods, whereas it rose to control at the end of the withdrawal periods. The results were regarded as evidence of blood volume regulation proportional to the absolute volume of blood lost in non-hypotensive hemorrhage.
A refractometric method was used for the continuous registration of plasma protein concentration in rats during and after 3 and 5 minutes of provoked activity. Simultaneous conductometric measurements of hematocrit (hct) showed that, although both invariably changing in the same direction, the relative change of protein concentration is always less than that of hct: plasma volume changes calculated from the former fall short of those calculated from hct by 34 +/- 23% during the hemoconcentrative period during activity and by 52 +/- 11% during the hemodilutory period after activity. The difference between these figures was significant, thus implying that fluid leaving the circulation during the filtration phase is less rich in protein than that entering it during the absorptive phase of microvascular adjustments. A kinetic analysis of the period after activity was made. The rate constants of fluid- and protein-flux were closely correlated. Both plasma volume and intravascular protein mass increased asymptotically to a new equilibrium 6% above control within 30 min after activity. It is suggested that the excess protein is mobilized from large parenchymatous organs, mainly the liver.
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