Hepatic arterial and portal venous pressure-flow relationships in isolated, perfused liver

1962 ◽  
Vol 202 (6) ◽  
pp. 1090-1094 ◽  
Author(s):  
Robert E. Condon ◽  
Niles D. Chapman ◽  
Lloyd M. Nyhus ◽  
Henry N. Harkins
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Portal Vein ◽  
Venous Pressure ◽  
Perfused Liver ◽  
Perfusion Rate ◽  
Flow Curves ◽  
Pressure Flow ◽  
Pressure Axis ◽  
Blood Pressure Responses

Blood pressure responses to alteration in blood flow were studied in the completely isolated, excised liver of the calf during perfusion of the hepatic artery or portal vein. The pressure-flow curves in both of the afferent vessels of the liver are curvilinear, with concavity toward the pressure axis. Resistance increases progressively with increases in perfusion rate; resistance increases are proportionately of greater magnitude than the increases in blood flow demonstrating autoregulation in both hepatic arterial and portal venous systems. The autoregulatory nature of pressure-flow responses is not affected by prolonged perfusion or marked acidosis.

Effect of portal hypertension on splenic blood flow, intrasplenic extravasation and systemic blood pressure

2003 ◽  
Vol 284 (6) ◽  
pp. R1580-R1585 ◽  
Author(s):  
Susan Kaufman ◽  
Jody Levasseur
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Venous Pressure ◽  
Splenic Vein ◽  
Systemic Blood Pressure ◽  
Portal Venous Pressure ◽  
Systemic Blood ◽  
Fluid Extravasation

We have previously shown that intrasplenic fluid extravasation is important in controlling blood volume. We proposed that, because the splenic vein flows in the portal vein, portal hypertension would increase splenic venous pressure and thus increase intrasplenic microvascular pressure and fluid extravasation. Given that the rat spleen has no capacity to store/release blood, intrasplenic fluid extravasation can be estimated by measuring the difference between splenic arterial inflow and venous outflow. In anesthetized rats, partial ligation of the portal vein rostral to the junction with the splenic vein caused portal venous pressure to rise from 4.5 ± 0.5 to 12.0 ± 0.9 mmHg ( n = 6); there was no change in portal venous pressure downstream of the ligation, although blood flow in the liver fell. Splenic arterial flow did not change, but the arteriovenous flow differential increased from 0.8 ± 0.3 to 1.2 ± 0.1 ml/min ( n = 6), and splenic venous hematocrit rose. Mean arterial pressure fell (101 ± 5.5 to 95 ± 4 mmHg). Splenic afferent nerve activity increased (5.6 ± 0.9 to 16.2 ± 0.7 spikes/s, n = 5). Contrary to our hypothesis, partial ligation of the portal vein caudal to the junction with the splenic vein (same increase in portal venous pressure but no increase in splenic venous pressure) also caused the splenic arteriovenous flow differential to increase (0.6 ± 0.1 to 1.0 ± 0.2 ml/min; n = 8). The increase in intrasplenic fluid efflux and the fall in mean arterial pressure after rostral portal vein ligation were abolished by splenic denervation. We propose there to be an intestinal/hepatic/splenic reflex pathway, through which is mediated the changes in intrasplenic extravasation and systemic blood pressure observed during portal hypertension.

Quantitative study of intramyocardial compression in the fibrillating heart

1979 ◽  
Vol 237 (2) ◽  
pp. H191-H196 ◽  
Author(s):  
J. M. Downey ◽  
R. W. Chagrasulis ◽  
V. Hemphill
Keyword(s):  
Blood Flow ◽  
Left Ventricle ◽  
Coronary Blood Flow ◽  
Quantitative Study ◽  
Coronary Arteries ◽  
Venous Pressure ◽  
Beating Heart ◽  
Flow Curves ◽  
Pressure Flow ◽  
Zero Flow

Extravascular compression inhibits coronary blood flow in fibrillating hearts. Pressure-flow curves from spontaneously fibrillating hearts whose coronary arteries were maximally dilated were examined to see whether this inhibition involves a vascular waterfall mechanism as has been found in the beating heart. Waterfall behavior is indicated when pressure-flow curves are linear and experience a zero-flow intercept at pressures greater than venous pressure. Regional pressure-flow curves revealed a zero flow intercept of 28.4 mmHg for the inner quarter of the left ventricle, indicating that compression is quite high in that region. A zero-pressure intercept of only 15.1 was found at the outer quarter, which was not significantly different from venous pressure. We conclude that the spontaneously fibrillating heart experiences a gradient of compression falling from 28 mmHg at the subendocardium to near zero at the subepicardium.

Effect of pulsatile pressure and metabolic rate on intestinal autoregulation

1982 ◽  
Vol 242 (5) ◽  
pp. H769-H775 ◽  
Author(s):  
A. P. Shepherd ◽  
G. L. Riedel
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Metabolic Rate ◽  
Venous Pressure ◽  
Systematic Effect ◽  
Flow Curves ◽  
Pressure Flow ◽  
Pulsatile Pressure ◽  
Series Of Experiments ◽  
Pressure Autoregulation

In the intestine, raising venous pressure elicits a precapillary vasoconstriction that has been ascribed to a myogenic mechanism. Such myogenic responses occur more frequently and have a greater magnitude if arterial pressure is pulsatile. This laboratory reported that the ability of the gut to autoregulate blood flow in response to perfusion pressure manipulations is enhanced if metabolic rate is stimulated by transportable intraluminal solutes. Since both myogenic and metabolic mechanisms may participate in local control, we attempted to delineate the relative contributions the two mechanisms make to autoregulation. In one set of experiments, pulse pressures of 20 and 40 mmHg evoked a slight but statistically significant vasoconstriction. In a second series of experiments, pressure-flow curves were determined in isolated canine small bowel. The ability of the gut to autoregulate was compared at pulse pressures of 0, 20, and 40 mmHg and at basal and elevated metabolic rates. Altering pulse pressure had no systematic effect on the ability of the intestine to autoregulate blood flow. In contrast, increasing metabolic rate consistently enhanced autoregulation at each of the pulse pressures studied. Therefore, these results indicate that although a myogenic mechanism may best account for the response to elevated venous pressure, autoregulation as expressed in pressure-flow curves is more strongly influenced by the prevailing metabolic rate than by stretch stimuli such as arterial pressure pulsations.

Pressure-flow relations of diaphragm and vital organs with nitroprusside-induced vasodilatation

1986 ◽  
Vol 61 (2) ◽  
pp. 409-416 ◽  
Author(s):  
S. Magder
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Venous Pressure ◽  
Maximal Conductance ◽  
Pressure Flow ◽  
Anesthetized Dogs ◽  
Phrenic Nerves ◽  
The Mean ◽  
Spontaneously Breathing ◽  
The Brain

We determined maximal conductance in the diaphragm and other vital organs in 14 anesthetized dogs, weighing 22.8 +/- 4.2 kg, which were given maximal vasodilating doses of nitroprusside (mean dose 13.9 +/- 4.3 micrograms X kg-1 X min-1) and the blood pressure was lowered in stages by hemorrhage. Blood flow in the diaphragm, brain, heart, kidney, gut, and quadriceps was measured with radiolabeled microspheres. To ensure maximal vasodilatation of diaphragmatic vessels, we stimulated the phrenic nerves to produce diaphragmatic contractions at 0.3 Hz. The mean cardiac output was 2.13 +/- 0.42 l/min (thermodilution) before nitroprusside and 4.68 +/- 1.45 after (P less than 0.001). Nitroprusside failed to break the autoregulation of the brain. Pressure-flow relations (P-F) in other regions were linear (r = 0.70 +/- 0.03, P less than 0.001) and blood pressure at zero flow (X-intercept) was always greater than venous pressure (diaphragm = 11, kidney = 19, heart = 8, gut = 8, quadriceps = 32 mmHg). The flow to the diaphragm (Qdi) could be predicted by Qdi (ml X min-1 X g-1) = [(3.13 +/- 0.56) X Pa X 10(-2)] -0.52 (r = 0.71), where Pa is mean arterial pressure. The maximal vascular conductance (i.e., slope of the P-F relation) of the diaphragm was 27% of the conductance in the kidney, 87% of the value in the gut, and 42% of that in the heart. In conclusion the maximal diaphragmatic blood flow at a given blood pressure is much larger when the muscle is stimulated than is observed in spontaneously breathing animals.

Effect of sympathectomy on arterial and venous changes in renal hypertensive rats

1981 ◽  
Vol 241 (3) ◽  
pp. H449-H454
Author(s):  
G. Simon
Keyword(s):  
Arterial Pressure ◽  
Structural Changes ◽  
Venous Pressure ◽  
Vena Cava ◽  
Hypertensive Rats ◽  
Flow Curves ◽  
Pressure Flow ◽  
Pressure Axis ◽  
Arteries And Veins ◽  
Renal Hypertensive Rats

Arterial pressure-flow and venous pressure-volume relationships were measured at maximal vasodilatation in the denervated pump-perfused hindquarters of four groups of rats: 1) neonatally sympathectomized (guanethidine-injected and adrenal-demedullated), one-kidney, one-clip hypertensive (n = 9); 2) sympathectomized, sham-operated, unilaterally nephrectomized control (n = 10); 3) sham-sympathectomized, one-kidney, one-clip hypertensive (n = 8); and 4) sham-sympathectomized, sham-operated, unilaterally nephrectomized control (n = 9). Dry defatted weight of anatomically defined segments of the aorta and vena cava in the four groups of rats also was measured. Significant rises in arterial pressure developed in sympathectomized rats after clipping of the renal artery and contralateral nephrectomy. Arterial pressure-flow curves were shifted toward the pressure axis (P less than 0.01) in clipped rats whether sympathectomized or not. In sympathectomized clipped rats, there was also a shift of the venous pressure-volume curves toward the pressure axis (P less than 0.05). The same degree of hypertrophy of the aorta was found in sympathectomized and sham-sympathectomized clipped rats. The findings indicate that in renal hypertensive rats structural changes of both large arteries and veins may develop in the absence of an intact sympathoadrenergic system.

Effect of hypoxic hypoxia on systemic vasculature

1984 ◽  
Vol 56 (5) ◽  
pp. 1403-1410 ◽  
Author(s):  
J. Malo ◽  
H. Goldberg ◽  
R. Graham ◽  
H. Unruh ◽  
C. Skoog
Keyword(s):  
Arterial Pressure ◽  
Inferior Vena ◽  
Superior Vena ◽  
Venous Pressure ◽  
Vena Cava ◽  
Venous Drainage ◽  
Hypoxic Hypoxia ◽  
Venous Compliance ◽  
Flow Curves ◽  
Pressure Flow

Effects of hypoxic hypoxia (HH) on cardiac output (CO), CO distribution, arterial and venous pressure-flow curves, vascular compliance, vascular time constant (tau), and resistance to venous return (RVR) were evaluated on six dogs. The vascular bed was isolated into four compartments depending on venous drainage: superior vena cava (SVC), splanchnic, renal and adrenal, and the remainder of the inferior vena cava (IVC). Low arterial O2 content and PO2 produced a threefold increase in CO at the same mean arterial pressure and a significant redistribution of CO to the SVC. Arterial pressure-flow curves decreased their slope (i.e., flow resistance) by a factor of two in the IVC and renal beds and by a factor of three in the splanchnic and SVC beds. Venous pressure-flow curves for the animal also decreased their slope significantly. HH causes a twofold increase in venous compliance and in mean venous pressure; tau did not change, but RVR halved. Seventy percent of the CO increase is explained by the increase in mean venous pressure and 30% by the reduction in RVR.

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.

Effect of stimulation of hepatic nerves on hepatic O2 uptake and blood flow

1977 ◽  
Vol 232 (6) ◽  
pp. H652-H656
Author(s):  
W. W. Lautt
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Oxygen Uptake ◽  
Portal Vein ◽  
Hepatic Artery ◽  
Venous Blood ◽  
Neurogenic Vasoconstriction ◽  
Pressure Changes ◽  
Hepatic Nerves ◽  
Stimulation Of

Acute denervation of the liver did not result in changes of oxygen uptake or hemodynamics in the intact liver of the cat. Stimulation of the hepatic nerves resulted in a marked reduction of vascular conductance of the hepatic artery and portal vein (intrahepatic) resulting in almost complete cessation of arterial flow and increased portal blood pressure. The hepatic artery showed a more complete escape from the neurogenic vasoconstriction than did the portal vein. During the stable "escape phase" oxygen delivery was 86% of control, but hepatic extraction of oxygen increased so that oxygen uptake was not altered from control values. The return of oxygen consumption to normal during nerve stimulation suggests that redistribution of hepatic blood flow did not occur. In spite of arterial and portal venous blood pressure changes and changes in gut conductance, oxygen extraction of the gut did not change.

Perfusion rates of brain, intestine and heart under conditions of total body perfusion

1961 ◽  
Vol 200 (3) ◽  
pp. 551-556 ◽  
Author(s):  
John A. Johnson ◽  
Vincent Gott ◽  
Frederick Welland
Keyword(s):  
The Body ◽  
Tissue Analysis ◽  
Heart Ventricle ◽  
Perfusion Rate ◽  
Flow Curves ◽  
Local Flow ◽  
Pressure Flow ◽  
Total Body ◽  
The Brain

The perfusion rates of the brain, intestine and heart ventricle were studied under conditions of total body perfusion. The perfusion rates were estimated by using antipyrine and D2O as reference substances. Local flow was determined from arterial curves and tissue analysis. When the total body perfusion rate was varied between 20 and 80 cc/kg/min., it was found at each rate that the perfusion rate of these organs was over three times that of the body as a whole. At the lowest flows these three organs were favored even more. Tables of perfusion rates at various sites in the brain and intestine are given. Pressure-flow curves for the brain, intestine and heart are given.

Further evidence for the unimportance of renal autoregulation

1961 ◽  
Vol 201 (3) ◽  
pp. 495-498 ◽  
Author(s):  
Jimmy B. Langston ◽  
Arthur C. Guyton ◽  
C. C. Hull ◽  
G. G. Armstrong
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Circulation ◽  
Pressure Flow ◽  
Renal Autoregulation ◽  
Blood Flows ◽  
Mild Degree ◽  
Pressure Axis ◽  
Pressure Flow Study ◽  
Flow Study

Previous experiments from this laboratory indicated that normal kidneys may not have significant intrinsic ability to autoregulate their blood flow when renal arterial pressure is varied. However, in these earlier studies, the renal blood flow was less than that generally accepted as normal, and there was a possibility that the renal circulation had not been completely isolated. This could have resulted in extrarenal blood flow during the pressure-flow study. In the present experiments, renal blood flows were in the normal range at all pressure levels. This difference was achieved by rendering the animals areflex prior to the laparotomy. The pressure-flow relationship was studied under these conditions, and the resulting curves were slightly concave to the pressure axis in the lower pressure range, indicating only a mild degree of autoregulation, approximately the same degree as that found in other tissues. However, the renal blood flow still increased rapidly with each increase in perfusion pressure even in the range of so-called autoregulation. It was also shown that all the blood that passed through the perfusion system also passed through the kidney, eliminating the possibility of extrarenal blood flow.

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