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.

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.

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.

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 coronary sinus occlusion on coronary pressure-flow relations

1980 ◽  
Vol 239 (1) ◽  
pp. H57-H64 ◽  
Author(s):  
R. F. Bellamy ◽  
H. S. Lowensohn ◽  
W. Ehrlich ◽  
R. W. Baer
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Coronary Sinus ◽  
Coronary Circulation ◽  
Reactive Hyperemia ◽  
Venous Pressure ◽  
Aortic Pressure ◽  
Pressure Flow ◽  
Coronary Pressure ◽  
The Relationship

We studied the effect of transient occlusion of the coronary sinus on the relationship between aortic pressure and circumflex coronary blood flow in open-chest anesthetized dog preparations during artificially prolonged diastoles. The coronary pressure-flow relation was linear, and flow stopped at an arterial pressure (Pf = 0) that always exceeded coronary venous pressure (Pcv). During reactive hyperemia, Pf = 0 was 31 mmHg when Pcv was 5 mmHg and increased to 52 mmHg when the coronary sinus was occluded (Pcv, 38 mmHg). Elevation of Pcv translated the coronary pressure-flow relation to a higher Pf = 0 without altering the slope of the relation. Pf = 0 increased by about two-thirds of the increase in Pcv. We found no evidence that there existed a level of Pcv below which changes in Pcv had no effect on the coronary pressure-flow relation. These data are not compatible with the existence of a vascular waterfall mechanism in the coronary circulation unless it is assumed that Pcv is one of the determinants of Pf = 0.

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.

Pulsatile Pressure and Flow in the Skeletal Muscle Microcirculation

1990 ◽  
Vol 112 (4) ◽  
pp. 437-443 ◽  
Author(s):  
Shou-Yan Lee ◽  
G. W. Schmid-Scho¨nbein
Keyword(s):  
Skeletal Muscle ◽  
Arterial Pressure ◽  
Time Course ◽  
Venous Pressure ◽  
Time Dependent ◽  
Physiological Importance ◽  
Pulsatile Pressure ◽  
Theoretical Predictions ◽  
Skeletal Muscle Microcirculation

Although blood flow in the microcirculation of the rat skeletal muscle has negligible inertia forces with very low Reynolds number and Womersley parameter, time-dependent pressure and flow variations can be observed. Such phenomena include, for example, arterial flow overshoot following a step arterial pressure, a gradual arterial pressure reduction for a step flow, or hysteresis between pressure and flow when a pulsatile pressure is applied. Arterial and venous flows do not follow the same time course during such transients. A theoretical analysis is presented for these phenomena using a microvessel with distensible viscoelastic walls and purely viscous flow subject to time variant arterial pressures. The results indicate that the vessel distensibility plays an important role in such time-dependent microvascular flow and the effects are of central physiological importance during normal muscle perfusion. In-vivo whole organ pressure-flow data in the dilated rat gracilis muscle agree in the time course with the theoretical predictions. Hemodynamic impedances of the skeletal muscle microcirculation are investigated for small arterial and venous pressure amplitudes superimposed on an initial steady flow and pressure drop along the vessel.

L-arginine analogues inhibit aldosterone secretion in rats

1995 ◽  
Vol 268 (5) ◽  
pp. R1137-R1142 ◽  
Author(s):  
J. C. Simmons ◽  
R. H. Freeman
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Methyl Ester ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Bilateral Nephrectomy ◽  
Aldosterone Secretion ◽  
Series Of Experiments

L-Arginine analogues, e.g., NG-nitro-L-arginine methyl ester (L-NAME), increase arterial pressure and suppress renin release in the rat. On the basis of these observations, it was hypothesized that L-arginine analogues also would attenuate aldosterone secretion. This hypothesis was tested in anesthetized rats treated with L-NAME or NG-nitro-L-arginine (L-NNA, 185 mumol/kg ip). The aldosterone secretion rate, plasma renin activity, and adrenal blood flow were attenuated in rats treated with L-NAME and L-NNA compared with control animals. Similar experiments were performed in anephric rats to examine the effects of L-NAME on aldosterone secretion independent of the circulating reninangiotensin system. The administration of L-NAME reduced adrenal blood flow but failed to reduce aldosterone secretion in these anephric rats. Bilateral nephrectomy reduced plasma renin activity essentially to undetectable levels in these animals. In a third series of experiments, two groups of anephric rats were infused with angiotensin II (3 micrograms/kg body wt iv) to provide a stimulus for aldosterone secretion. Aldosterone secretion and adrenal blood flow were markedly reduced in angiotensin II-infused rats pretreated with L-NAME compared with the control anephric animals infused with angiotensin II. Overall these results suggest that L-arginine analogues attenuate aldosterone secretion by inhibiting the adrenal steroidogenic effects of endogenous or exogenous angiotensin II and/or by reducing plasma levels of renin/angiotensin.

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.

Mesenteric Blood Flow as Influenced by Progressive Hypercapnia

1956 ◽  
Vol 184 (2) ◽  
pp. 275-281 ◽  
Author(s):  
Eugene W. Brickner ◽  
E. Grant Dowds ◽  
Bruce Willitts ◽  
Ewald E. Selkurt
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Oxygen Content ◽  
Vascular Resistance ◽  
Pulse Pressure ◽  
Venous Pressure ◽  
Mesenteric Blood Flow ◽  
Initial Tendency ◽  
Elevated Heart Rate

The influence of hypercapnia on mesenteric blood flow was studied in dogs subjected to progressive increments in CO2 content of inspired air produced by rebreathing from a large spirometer. Oxygen content was maintained above 21 volumes %. Although some animals showed an initial tendency for mesenteric blood flow to decrease and arterial pressure to increase in the range 0–5 volumes % of CO2, the usual hemodynamic change in the range 5–16 volumes % was an increase in mesenteric blood flow resulting from decrease in intestinal vascular resistance, accompanied by a decline in arterial pressure. Portal venous pressure was progressively elevated. Heart rate slowed in association with an increase in pulse pressure. The observations suggest that in higher ranges of hypercapnia, CO2 has a direct dilating action on the mesenteric vasculature.

Corrigenda for vol. 80, Cover legend

1996 ◽  
Vol 80 (6) ◽  
pp. 2254-2254
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Network Topology ◽  
Pulmonary Circulation ◽  
Pressure Flow ◽  
Pulsatile Pressure ◽  
Volume Relationship ◽  
Pressure Volume Relationship ◽  
Pulse Waves

Cover legend: In the cover legend for the March and April issues, the starting sentence "Pulsatile pressure-volume relationship..." should read instead "Pulsatile pressure-flow relationship..." Cover legend is reprinted below. Cover: Pulsatile pressure-flow relationship, input impedance, encodes network topology, geometry, and design via reflected pulse waves from distributed branching sites in the pulmonary circulation. Network design is a system property conferring a susceptibility to modulate the amplitude of wall shear stress in vessles with the distribution of blood flow. (From Bennett et al. J. Appl. Physiol. 80: 1033-1056, 1996)

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