Venous Outflow Pressure Research Articles

Detecting arterial and venous obstruction in flaps.

Island skin flaps based on the latissimus dorsi muscle were raised in domestic pigs. Flap circulation, maintained only by the vascular pedicle, was monitored by laser Doppler flowmetry, laser photometry, and transcutaneously measured carbon dioxide tension. Both arterial and venous occlusion were accompanied by very low laser Doppler flow values. In laser photometry, the backscattered intensity of light remained unchanged or was slightly increased during arterial occlusion. In response to venous occlusion, however, the light intensity decreased markedly. Transcutaneous carbon dioxide tension increased in both venous and arterial occlusion. When venous outflow pressure was raised incrementally, both the laser Doppler flow value and the total backscattered light intensity fell proportionately. Laser Doppler flowmetry might thus be useful clinically to detect decreased blood flow in transferred flaps, and laser photometry may determine if the decreased flow is related to the arterial or venous side.

Sympathetic stimulation and intestinal capillary fluid exchange.

Sympathetic nerve stimulation is generally considered not to alter intestinal capillary pressure or filtration rate because of appropriate adjustments in the pre-to-postcapillary resistance ratio. To directly assess this possibility, we measured lymph flow, capillary pressure, capillary filtration coefficient, and the transcapillary oncotic pressure gradient in the cat small intestine. Measurements were taken under control conditions and during the steady-state phase of periarterial nerve stimulation, i.e., following completion of the escape phase. Venous outflow pressure was held constant (0 mmHg) during the entire experiment. Nerve stimulation resulted in a significant reduction of lymph flow (by 65%), capillary filtration coefficient (by 75%), and capillary pressure (by 15%). Interstitial fluid pressure, calculated from the measured parameters in the Starling equation, was also reduced (from -0.74 to -2.53 mmHg) by nerve stimulation. The results of this study indicate that intestinal capillary pressure and capillary filtration rate are not "autoregulated" during sympathetic nerve stimulation. Capillary derecruitment appears to be largely responsible for the dramatic reduction in filtration rate associated with adrenergic stimulation.

Pulmonary hemodynamics and gas exchange properties during progressive edema.

In this investigation we have studied the effect of increments of pulmonary edema on pulmonary hemodynamics, and physiological and hemodynamic shunt in an isolated lung preparation. Hemodynamic shunt was defined by the slope of the relationship between pulmonary arterial and airway pressures; when the slope decreases, there is a greater degree of shunt. Cardiovascular changes were analyzed using a Starling resistor model of the pulmonary circulation where the effective downstream pressure to flow as seen from the pulmonary artery exceeds the pulmonary venous outflow pressure. This effective downstream pressure is referred to as the critical pressure (Pc), and at low lung inflation the locus of this critical pressure is in extra-alveolar vessels. With 3-4 h of progressive edema to an average of 185% initial lobe weight we found a progressive rise in pulmonary arterial pressure (Ppa) from 12.1 to 21.5 cmH2O. About one-third of this increase in Ppa resulted from an increased Pc and the remainder resulted from an increased resistance upstream from the locus of Pc. These results are consistent with the hypothesis that the interstitial accumulation of fluid creates enough of an increase in interstitial pressure to compress extra-alveolar vessels. There was no significant correlation between the amount of edema and the measured physiologic shunt, but the hemodynamic shunt showed a highly significant correlation. The hemodynamic shunt theoretically measures the extent of obstructed airways and may be a useful index of the degree of pulmonary edema.

Fluid shift across the placenta: III. Application of a computer model of passive placental transfer

Summary A small computer model (8 kbytes BASIC) is described that allows the simulation of passive transfer in a concurrent or counter-current flow placenta with constant arterial flow rates. Hydrostatic and colloid osmotic forces as well as diffusion may influence the transfer. Input to the model consists of run time, arterial flow rates and direction of flow, arterial concentrations, permeability, hydraulic conductance, reflection coefficient and venous outflow pressure. The effect of highly viscous colloidal solutions on hydrostatic pressure is considered. Output from the programme comprises distribution of concentrations, flow rates, hydrostatic and colloid osmotic pressures in 10 maternal and fetal compartments. The model is applied to study the effect of colloid osmotic pressure on transplacental bulk flow. If parameters are chosen to simulate the isolated guinea-pig placenta results are obtained which are in satisfactory agreement with experimental data.

Pancreatic circulation: intrinsic regulation.

The purpose of the present study was to characterize the intrinsic mechanisms involved in the regulation of blood flow and oxygenation in the totally isolated, perfused canine pancreas. Arterial pressure, venous outflow pressure, blood flow, arteriovenous oxygen difference, and capillary filtration coefficient were measured during graded arterial pressure reductions and venous pressure elevation. Reductions in arterial pressure caused pancreatic blood flow and vascular resistance to decrease, whereas venous pressure elevation resulted in a decreased blood flow and increased vascular resistance. The reductions in blood flow produced by arterial and venous pressure alterations were associated with increases in oxygen extraction and capillary filtration coefficient. During the same pressure perturbations, oxygen uptake remained constant between blood flows of 40-100 ml.min-1.100 g-1, yet decreased progressively as blood flow was reduced below 40 ml.min-1.100 g-1. Arterial occlusion resulted in a postocclusive reactive hyperemia, the magnitude of which was related to the duration of occlusion. The findings of this study suggest that intrinsic regulation of pancreatic blood flow can be attributed to both metabolic and myogenic mechanisms. Resistance and exchange vessels both appear to play a role in the regulation of oxygen delivery to the pancreatic parenchyma.

Relation between intestinal blood flow and oxygen uptake

In autoperfused and pump-perfused preparations of canine ileum, arterial pressure, venous outflow pressure, blood flow, and arteriovenous oxygen difference were measured while blood flow was altered either mechanically or by graded intra-arterial infusions of isoproterenol, adenosine, or 2,4-dinitrophenol. In pump-perfused preparations, mechanical alterations in blood flow resulted in opposite changes in arteriovenous oxygen difference, so that ileal oxygen uptake was independent of blood flow over the range of 30-140 ml.min-1.100 g-1. Only at flow rates below 30 ml.min-1.100 g-1 was oxygen uptake dependent on blood flow. Isoproterenol, adenosine, and dinitrophenol produced dose-dependent increases in blood flow under free-flow conditions and decreases in perfusion pressure under constant-flow conditions. Ileal oxygen uptake was not affected by isoproterenol, decreased by adenosine, and increased by dinitrophenol. The effects of these drugs on intestinal oxygen uptake are in accord with their effects on oxygen consumption in vitro. These results suggest that vasodilators will not alter intestinal oxygen uptake in autoperfused preparations in which oxygen uptake is independent of blood flow, unless they exert an effect on oxidative metabolism.

Postprandial intestinal hyperemia: role of bile salts in the ileum

In an autoperfused dog ileum preparation, artificial pressure, venous outflow pressure, blood flow, and arteriovenous oxygen difference were measured while bile and bile salt solutions, at physiological concentrations, were placed in the lumen. Intraluminal placement of endogenous bile, synthetic bile, or bile salt solutions increased ileal blood flow (99 +/- 10, 94 +/- 20, and 104 +/- 17%, respectively) and oxygen uptake (30 +/- 5, 36 +/- 9, and 28 +/- 5%, respectively). Endogenous bile pretreated with cholestyramine, a bile salt-sequestering resin, did not alter ileal blood flow, yet increased ileal oxygen uptake by 11 +/- 3%, a response similar to that observed while Tyrode's solution (the vehicle) was in the lumen. Intra-arterial infusion of bile salts increased ileal blood flow in a dose-dependent manner, while not significantly altering ileal oxygen uptake. The results of the present study indicate that bile salts play an important role in the functional (postprandial) hyperemia in the ileum by 1) directly dilating the ileal vasculature and 2) enhancing ileal metabolism during their active absorption.

Effect of luminal distension on intestinal transcapillary fluid exchange.

The direct effects of luminal distension pressure on intestinal transcapillary fluid exchange were studied in isolated autoperfused cat ileum preparations. Intestinal lymph flow, lymphatic pressure, lymph-to-plasma protein concentration ratio (L/P), blood flow, and perfusion pressures were allowed to reach a steady state at different luminal distension pressures (0-40 mmHg). Luminal distension was induced using a nonabsorbable silicone solution, thereby eliminating an influence of net water absorption. At a venous outflow pressure of 0 mmHg, lymph flow and lymphatic pressure increased, whereas blood flow and L/P decreased as luminal pressure was increased. The relationship between lymph flow, blood flow, and venous pressure was acquired at luminal pressures of 0 and 20 mmHg. When luminal pressure was 0, lymph flow increased and blood flow decreased progressively with venous pressure elevation; however, when luminal pressure was 20 mmHg, lymph flow and blood flow were unaffected until pressure exceeded 20 mmHg. The results of this study indicate that luminal pressure elevation enhances transcapillary fluid exchange and imposes a "waterfall" effect on the intestinal vasculature.

Effect of local arterial hypotension on cat intestinal capillary permeability

The effects of local arterial hypotension on lymph flow, lymphatic protein flux, and capillary permeability were analyzed in an isolated vascularly perfused cat ileum preparation. Reductions in perfusion pressure to 30–40 mmHg (60 min) resulted in a lowering of lymph flow and an increase in the lymph to plasma protein concentration ratio. Release of the partial arterial occlusion caused lymph flow and lymph to plasma protein concentration ratio to increase above their control values. Venous outflow pressure was then increased in 10 mmHg increments to 30 mmHg. The capillary osmotic reflection coefficient was estimated from the relationship between lymph to plasma protein concentration ratio and lymph flow. Values of the osmotic reflection coefficient for total proteins and individual protein fractions were significantly lower than control values. The results of this study indicate that 1 hr of regional ischemia significantly increases the permeability of intestinal capillaries. The increased capillary permeability accounts, at least in part, for the enhanced capillary filtration and interstitial fluid accumulation which occurs in the posthypotensive small intestine.

Intrinsic control of colonic blood flow and oxygenation.

In a denervated autoperfused dog colon preparation, arterial perfusion pressure, venous outflow pressure, blood flow, and arteriovenous O2 difference were measured during graded arterial pressure alterations, arterial occlusion, venous pressure elevation, venous occlusion, and local intra-arterial infusion of adenosine. As perfusion pressure was reduced from 100 to 30 mmHg, colonic blood flow decreased and arteriovenous O2 difference increased. Although blood flow was not autoregulated O2 delivery was maintained within 10% of control between 70 to 100 mmHg and then decreased with further reduction in perfusion pressure. Arterial occlusion (15, 30, and 60 s) resulted in a postocclusion reactive hyperemia; the magnitude of the hyperemia was directly related to the duration of occlusion. Venous occlusion resulted in a postocclusion reactive hypoemia. Elevation of venous pressure from 0 to 20 mmHg increased vascular resistance, O2 extraction, and the capillary filtration coefficient, but decreased O2 delivery. Infusion of adenosine decreased vascular resistance and O2 extraction, but increased O2 delivery. These data suggest that both metabolic and myogenic mechanisms are involved in the control of colonic blood flow and oxygenation.

Permeability of intestinal capillaries to endogenous macromolecules.

Steady-state lymphatic and plasma protein concentration (CL and CP) and lymph flows were analyzed in an autoperfused cat ileum preparation at venous outflow pressures of 0, 10, 20, and 30 mmHg. Albumin and nine endogenous protein fractions were analyzed in lymph and plasma by polyacrylamide gradient gel electrophoresis. The osmotic reflection coefficient (sigma d = 1--CL/CP when CL/CP is no longer influenced by capillary filtration rate. The sigma d values acquired increased as the molecular radius of the protein fraction increased. Permeability-surface area products were estimated for the various protein fractions by applying the acquired data to the Kedem-Katchalsky protein flux equation. A comparison of the permeability-surface area products at various venous pressures suggests a reduction in capillary surface area as venous pressure is increased to 20 and 30 mmHg. The results suggest that intestinal capillaries selectively restrict macromolecules to a greater degree than the continuous type of capillaries of many other organs.

Volume of the capillary exchange vessels measured with a gravimetric method in rat hindquarters

To measure the volume of the true exchange vessels, i.e., that of the “functional” capillaries, in rat skeletal muscle, two parallel-coupled hindquarter vascular beds were perfused at a constant flow with oxygenated plasma substitute. Continuous recordings were performed of changes in the total weight of the two preparations, caused by sudden arterial occlusion in one, thus doubling the flow to the other while venous drainage was left open in both. Venous outflow pressure was kept constant, usually at a level where the veins remained well distended. After a rapid and small change in total weight, reflecting the balance between vascular distension and recoil in the two circuits, the subsequent weight change showed a continuous increase, but after a distinct delay. From this delay, caused by transient absorption into the semistagnant capillary contents of the arterially occluded vascular bed, the absorbed fluid amount, Q, was calculated. Functional capillary volume, V c, was then calculated from the following equation (see text for derivation): V c= Q ln [ π c π c−P c+P v ] where π c, P c, and P v represent effective plasma colloid osmotic pressure, equivalent capillary pressure, and venous outflow pressure during isogravimetric conditions. This functional capillary volume, which thus includes permeable venular sections, amounted to 0.55–0.60% of the tissue weight, varying slightly with the prevailing P c, and corresponding to 10–15% of the total volume of the regional vascular bed. Capillary density in skeletal muscle was also deduced from these data and from known microvascular diameters, giving a value of 450–500/mm 2, which is in fair agreement with morphological data. The physiological significance of measuring the functional capillary volume by this method is discussed.

Control of the microcirculation in the hind limb skeletal muscle vascular bed of the possum (Trichosurus vulpecula)

1. Sympathetic stimulation of the hind limb vasculature of the possum produced a reduction in the limb blood flow and the limb volume. 2. At supramaximal frequencies, the responses of both capacitance and resistance vessels was reduced in both the possum ( Trichosurus vulpecula) and the cat ( Felis catus). 3. Capillary filtration coefficients for the possum were different when estimated by increasing the venous outflow pressure (0.043 ± 0.008 SD) from those estimated by decreasing the venous outflow pressure (0.067 ± 0.022 SD). Either value was significantly greater than that recorded by Mellander (1960) for the cat (0.02−0.03).

Vascular capacitance of dog intestine using mean transit time of indicator.

Changes in vascular volume of dog jejunum caused by norepinephrine, isoproterenol, or acetylcholine at constant=flow perfusion, were compared to changes in volume caused by changes in blood flow or venous pressure. Vascular volume was measured by indicator dilution mean transit time, using a step input of indocyanine green (125 microgram/min). Venous pressure was held at 10 mmHg; control arterial pressure was about 110 mmHg. At a control flow of 521 ml/min.kg of tissue, the vascular volume was 104 +/- 14 (SD) ml/kg of tissue. Reducing flow by 75 percent caused the volume to decrease by 29 percent (--31 ml/kg); maximal norepinephrine infusion at constant flow and venous pressure decreased the vascular volume by 24 percent, and a 10-mmHg reduction in venous outflow pressure caused a 25 percent (--27 ml/kg) reduction. On the other hand, isoproterenol (100 microgram/liter) at constant flow caused a 245 percent increase in conductance and only a 12 percent increase in vascular volume. Thus, active venoconstriction, changes in venous pressure, or changes in flow independently may cause changes in vascular volume of the intestine. Active smooth muscle changes in the venous capacitance vessels are not necessarily correlated with changes in the arterial resistance vessels.

Interaction of capillary and tissue forces in the cat small intestine.

We measured steady state capillary hydrostatic pressure (P c,i), plasma and lymph protein concentrations, lymph and blood flow, and capillary filtration coefficients in an in situ loop of cat small intestine at venous outflow pressures (PV) of 0, 5, 10, 15, 20, 25, and 30 mm Hg. The data were used to calculate colloid osmotic pressure of lymph and plasma, interstitial fluid pressure (Pt), pre- and postcapillary resistances, and a tissue pressure-volume curve of the intestinal interstitium. When PV was elevated from 0 to 30 mm Hg, lymph protein concentration decreased from 3.8 to 1.9 g/100 ml (representing a change in colloid osmotic pressure of 6.2 mm Hg), lymph flow increased 7-fold (or an equivalent imbalance in Starling forces of 4.3 mm Hg), and the calculated PT increased from 1.8 to +5.3. Because lymph flow draining the loop decreased during the determination of Pc, i at venous pressures between 15 and 30 mm Hg, the corresponding calculated PT may be in error by 1-2 mm Hg. The tissue pressure-volume relationship calculated from the data indicates that the intestinal interstitial volume expands nonlinearly and this expansion is characterized by two distinctly different compliant components: (1) tissue compliance is low at PV between 0 and 15 mm Hg (0.4 ml/mm Hg), and (2) at PV greater than 15 mm Hg the tissue compliance is relatively high (4 ml/mm Hg). We found that when PV was elevated from 0 to 15 mm Hg, increases in PT are the major tissue adjustments that oppose the increased filtration pressures. Furthermore, at Pv of 20-30 mm Hg, tissue protein concentration decreases, lymph flow relative to the filtration coefficient (deltaP DROP) increases and, to a much lesser extent, PT increases. Finally, the combination of these changes in tissue force at high filtration pressures represent a maximum tissue edema "safety factor" of 10 mm Hg; further increases in filtration pressures result in large volume movements into the intestinal lumen.

Digoxin induced intestinal vasoconstriction. The effects of proximal arterial stenosis and glucagon administration.

Previous studies have been shown that intravenous cardiac glycosides produce mesenteric vasoconstriction (MVC). The possibility that this might critically compromise blood flow in patients with mesenteric vascular disease was suggested. To evaluate whether MVC occurs with intravenous cardiac glycosides in the presence of proximal mesenteric artery stenosis, blood flow in the superior mesenteric artery (SMA) of thirteen dogs was measured with a Doppler flowmeter. The SMA was constricted and pressures were measured in the aorta, SMA, and superior mesenteric vein. Superior mesenteric vascular resistance (SMVR) was calculated by dividing the pressure difference between the SMA and superior mesenteric vein by the total blood flow to the superior mesenteric vasculature and was reported as mm Hg/cc-min. Blood flow was measured simultaneously by a drop rate meter in the vein of a surgically isolated intestinal segment supplied by a single arterial arcade. Venous outflow pressure from this segment was also monitored, which allowed calculation of isolated gut segment resistance (IGSR) in mm Hg/cc-min per 100 g gut. Stenosis of the SMA produced pressure gradients of 10 to 75 mm Hg and decreased resting blood flow by as much as 82%. Digoxin produced an increase in both SMVR and IGSR throughout the 30 to 120 minute period of the study in thirteen dogs despite the presence of severe grades of SMA stenosis. There was no relationship between the degree of proximal SMA stenosis and the magnitude of resistance change due to digoxin. To determine if this MVC was reversible, glucagon was administered to eleven dogs 30 to 60 minutes after digoxin and completely overcame the constriction. Thus, digoxin produced MVC in the presence of proximal SMA stenosis. This MVC was pharmacologically reversible. These data suggest that intravenous digoxin might contribute to intestinal ischemia in patients with preexisting vascular disease.

Influence of adenosine and lowered cerebral blood flow on the cerebrovascular efefct of theophylline

The responses of brain vessels to theophylline infused intra-arterially was evaluated. The experiments were performed on isolated canine brains perfused by donor dogs. Thus secondary effects due to theophyline were eliminated. Arterial pO 2, pCO 2, pH and brain temperature were kept constant. Cerebral vascular resistance (CVR) was calculated from total venous outflow and cerebral perfusion pressure. A 2 mg doses of theophylline per brain was given at normal cerebral perfusion pressure (about 81 mm Hg), at lowered perfusion pressure (about 37 mm Hg), and during and adenosine infusion lasting 10 min (10 −7 mol/min). At normal pressure theophylline showed a significant 15% decrease of CVR, but at lowered perfusion pressure a significant 19% increase occured. During infusion of adenosine, which decreased CVR by 23%, theophylline again increased CVR by 20% thus demonstrating an edonosine-theophylline antagonism. From our results, it is suggested that adenosine could be involved in the vasodilatation of cerebral vessels in the hypoxic brain.

Raised intracranial pressure and cerebral blood flow. 3. Venous outflow tract pressures and vascular resistances in experimental intracranial hypertension.

Pressure changes within the venous outflow tract from the brain were studied in anaesthetized baboons. Segmental vascular resistance changes were also calculated and the results correlated with the changes in cerebral blood flow, measured by the (133)Xenon clearance method. Three different methods were used to raise intracranial pressure: cisterna magna infusion, a supratentorial subdural balloon, and an infratentorial subdural balloon. A close correlation was found between the cortical vein pressure and intracranial pressure with all methods of raising intracranial pressure: the overall correlation coefficient was 0·98. In the majority of animals sagittal sinus pressure showed little change through a wide range of intracranial pressure. In three of the six animals in the cisterna magna infusion group, however, sagittal sinus pressure increased to levels approaching the intracranial pressure during the later stages of intracranial hypertension. Jugular venous pressure showed little change with increasing intracranial pressure. The relationship between cerebral prefusion pressure and cerebral blood flow differed according to the method of increasing intracranial pressure. This was due to differing patterns of change in prevenous vascular resistance as venous resistance increased progressively with increasing pressure in all three groups. The present results confirm, therefore, the validity of the current definition of cerebral perfusion pressure-that is, cerebral perfusion pressure is equal to mean arterial pressure minus mean intracranial pressure-by demonstrating that intracranial pressure does represent the effective cerebral venous outflow pressure.

Sympathetic vasodilatation, kallikrein release and adrenergic receptors in the cat submandibular salivary gland.

AbstractThe adrenergic receptors involved in secretion of kallikrein and the vasodilatation occurring subsequent to sympathetic nerve stimulation have been studied in the cat submandibular salivary gland. Measurements were made of kallikrein content in glandular homogenate and of venous outflow and glandular perfusion pressure. Isoprenaline failed to cause secretion of kallikrein in contrast to sympathetic nerve stimulation and close arterial injections of noradrenaline. Nerve stimulation and noradrenaline reduced the amount of kallikrein in the glands by 60 and 50 per cent, respectively. The α‐blocking agent Regitin® inhibited completely the secretion of kallikrein induced by nerve stimulation, while adrenergic β‐blockade had no inhibitory effect on enzyme secretion. In this gland, therefore, the secretion of kallikrein is mediated entirely through activation of adrenergic α‐receptors.The β‐blocking agent propranolol reduced the nerve induced vasodilatation by about 40 per cent. This sympathetic vasodilator response was present, but markedly reduced, after pretreatment with Regitin,® which abolished kallikrein secretion and the vasoconstrictor phase of the nerve‐induced vascular response. This study and an earlier report (Gautvik, Kriz and Lund‐Larsen 1972 a) suggest that β‐adrenergic receptors in the glandular vessels, as well as ®aL‐adrenergic receptors involved in the secretion of kallikrein, play a role in the vasodilatation observed in this gland subsequent to sympathetic nerve stimulation.

Static and dynamic pressure-volume relations of the veins in the cat hind leg (author's transl)

In the artificially perfused hind legs of cats in vivo (chloralose anaesthesia) the distensibility characteristics of veins were investigated under conditions of different modes of pressure changes along the venous system. A dynamic pressure-volume relationship was obtained by a continuous change of venous outflow pressure. A static pressure-volume relationship was obtained by incremental variation of hydrostatic venous inflow or outflow pressure, respectively. Venous inflow pressure was varied by alteration of blood flow. Venous outflow pressure was changed by raising the level of the outflow orifice of the venous circuit. The static pressure-volume curve which occured with venous outflow elevation showed a sigmoid shape. The compliance was greatest at a pressure range of 8 to 28 mm Hg. It was smaller at the lower and higher pressure. The reduction in venous compliance was due to collaps phenomena and resistance changes or a decrease in vascular elasticity, respectively. The volume changes which occured with elevation of blood flow were greatest at the lower flow values. Dynamic changes of venous outflow pressure resulted in hysteresis loops. The width of the loop depended on vascular viscosity, venous resistance and transcapillary fluid transfer. On the contrary, nearly the whole area between the ascending limb of the dynamic and the static pressure volume curves was due to the viscosity.