Effect Of Venous Pressure Research Articles

Effect of Venous Pressure on Fractional Flow Reserve and Index of Microcirculatory Resistance in Patients with Stable Chest Pain Syndromes

Effect of Venous Pressure on Fractional Flow Reserve and Index of Microcirculatory Resistance in Patients with Stable Chest Pain Syndromes

Effects of venous pressure and posture on skin capillary perfusion.

Various vasoconstriction mechanisms after a change in posture are involved in controlling skin blood flow and capillary transmural pressure to maintain adequate transcapillary exchange. The role of venous orthostatic pressure in the regulation of capillary nutritive perfusion, however, is less clear. We investigated capillary perfusion in 30 healthy subjects using intravital capillary microscopy of the big toenail-fold. Measurements were made in the supine and the sitting positions before and after incremental elevation of venous resistance, and thus the pre- to post-capillary pressure difference, by inflating a cuff around the ankle. On dependency, median capillary density rose (P < 0.0001), whereas red blood cell perfusion decreased (P < 0.0001). Cuff inflation of 30-60 mmHg in the supine position induced similar phenomena. Repeatedly, the same capillaries were found to be recruited after an increase in transmural pressure. We conclude that post-capillary pressure appears to be an important factor in the regulation of capillary perfusion, because an increase in venous resistance mimics the effects of dependency. The findings in this study support the theory of 'minimum perfusion pressure' for each capillary to be perfused with erythrocytes.

Lymph flow in sheep with rapid cardiac ventricular pacing

Increases in systemic venous pressure (Pv) associated with heart failure cause an increase in microvascular fluid filtration into the tissue spaces. By removing this excess filtrate from the tissues, lymphatic vessels help to prevent edema. However, the lymphatics drain into systemic veins and an increase in Pv may interfere with lymphatic flow. To test this, we cannulated caudal mediastinal node efferent lymphatics in sheep. We used rapid cardiac ventricular pacing (240-275 beats/min) to cause heart failure for 4-7 days. Each day we determined the lymph flow rate two ways. First, we adjusted the lymph cannula height so that the pressure at the outflow end of the lymphatic was zero. After we determined the lymph flow with zero outflow pressure, we raised the cannula so that outflow pressure was equal to the actual venous pressure. We quantitated the effect of venous pressure on lymph flow rate by comparing the flow rate with outflow pressure = Pv to the flow rate with zero out low pressure. At baseline, Pv = 5.0 +/- 2.5 (SD) cmH2O and we found no difference in the two lymph flow rates. Pacing caused Pv and both lymph flow rates to increase significantly. However for Pv < 15 cmH2O, we found little difference in the two lymph flow rates. Thus increases in Pv to 15 cmH2O at the outflow to the lymphatics had little effect on lymph flow. By comparison, Pv > 15 cmH2O slowed lymph flow by 55 +/- 29% relative to the lymph flow rate with zero outflow pressure. Thus Pv values > 15 cmH2O interfere with lymph flow from the sheep caudal mediastinal lymph node.

Effects of venous pressure on coronary circulation and intramyocardial fluid mechanics.

This investigation examined the interaction between right heart pressure (RHP), coronary perfusion pressure (CPP), intramyocardial tissue pressure (IMP), and coronary flow mechanics, including partitioning of coronary effluent in the isolated Krebs-Henseleit perfused rabbit heart. The major new finding was a parallel shift in the IMP-inflow relationship to a higher tissue pressure level in response to an increase in RHP. Accompanying the rise in RHP from 0 to 15 and 25 mmHg, IMP at zero coronary inflow in the beating (and arrested) heart increased from 5.8 +/- 1.0 (7.7 +/- 1.2) to 16.3 +/- 1.2 (17.9 +/- 1.3) and 28.6 +/- 1.7 (26.4 +/- 2.0) mmHg, respectively. A concomitant parallel shift in the CPP-inflow relation to higher pressures was consistently observed. The fraction of total coronary flow drained by the right heart was not constant. A higher partition of coronary outflow to the left heart (7.8 +/- 3.8, 34.3 +/- 3.0, and 47.9 +/- 4.3%, respectively) accompanied the increase in RHP. Intramyocardial partitioning of coronary outflow pathways mediates the effects of venous pressure modulation on coronary circulation. The interaction between coronary venous pressure and the extravascular environment modifies the effective back pressure to arterial inflow.

Effect of venous pressure on hepatic microcirculation and lymph flow

Effect of venous pressure on hepatic microcirculation and lymph flow

Quantitative ultrastructural morphometry of blood capillary endothelium in skeletal muscle: Effect of venous pressure

Rat hindquarter preparations were perfused with a plasma substitute for 20 min at high venous pressure (+10 cm H 2O; HVP rats) or low venous pressure (−4 cm H 2O; LVP rats). Perfusion-fixed specimens for electron microscopy were obtained from the rectus femoris, biceps femoris, tibialis anterior, and gastrocnemius (medial head) muscles. Endothelial thickness and frequency of plasmalemmal vesicles (luminal, abluminal, and free vesicles) were assessed on randomly selected capillaries. Mean endothelial thickness was: HVP, 0.26 μm; LVP, 0.28 μm ( P < 0.02). In both groups the abluminal vesicles outnumbered the luminal ones ( P < 0.01), by 35% (LVP) and by 8% (HVP). This difference in abluminal vesicle excess was significant ( P < 0.01). There were no statistically demonstrable differences between the groups in luminal or free vesicle counts per unit luminal surface area or in total vesicle count per unit cytoplasmic volume. The depletion of abluminal vesicles in HVP rats conformed quantitatively with a concept of vesicle membrane incorporation into the plasmalemma proper at pressure-induced capillary dilatation. Provided that the vesicular turnover rate does not change with pressure, the net effect of the reduction in size of the abluminal vesicle population could be an augmented vesicle-bound transendothelial transport of macromolecules from the capillaries to the interstitium. The study indicates that vesicular transport should be regarded as a balance, influenced by hemodynamics, between two separate transport processes in the respective directions.

Transcapillary protein leakage and fluid movement: Effect of venous pressure

The effect of elevating venous pressure ( ΔP v) on the transcapillary escape of albumin ( Q T) in control and papverinized gracilis muscles perfused at constant flow was determined by means of direct monitoring of the rate of accumulation of tissue 125I-labeled albumin radioactivity. Simultaneously, transcapillary fluid movement (FM) was assessed volumetrically. Under control isovolumetric conditions, Q T = 2.25 mg/min · 100 g. In addition to causing an FM of 0.03 ml/min · 100 g · mm Hg, increasing P v enhanced Q T by 0.06 mg/min · 100 g · mm Hg. Papverinization itself decreased Q T to 2.0 mg/min · 100 g and affected FM only slightly. However, the superposition of P v elevation caused a FM of 0.008 ml/min · 100 g · mm Hg and resulted in Q T increasing by 0.29 mg/min · 100 g · mm Hg. The results of this study indicate that Q T is sensitive to changes in microvascular hemodynamics, and thus changes in microvascular pressure may affect FM in two ways, first by increasing the transcapillary pressure gradient and second by augmenting Q T which may superimpose an oncotic adjunct to FM.

EFFECT OF VENOUS PRESSURE ON MEAN CAPILLARY PRESSURE AND VASCULAR RESISTANCE IN THE INTESTINE.

Elevation of venous pressure in the intestine increases capillary pressure by amounts that average 62% of the venous pressure increment. The relation may be expressed as P c = 9.7 + 0.62 P v , where P c represents the mean capillary pressure and P v represents venous pressure (both expressed in mm Hg). The increase of capillary pressure is less than expected for a rigid system and less than reported for skeletal muscle. This attenuation of the effect of increments of venous pressure on capillary blood pressure is due to precapillary constriction and postcapillary dilation, with the latter playing the dominant role. Measurement of resistance in a segment of the venous vasculature confirmed this and also demonstrated that most of the reduction of resistance occurs in venous vessels with diameters greater than 0.5 mm.

The effect of venous pressure on oxygen availability in cerebral tissue.

The effect of venous pressure on oxygen availability in cerebral tissue.

The effect of venous pressure on the oxygen content of venous blood in the deep forearm veins.

The effect of venous pressure on the oxygen content of venous blood in the deep forearm veins.

Effect of Venous Pressure on Volume Pulsation

In a previous study it was noted that, with ligation of the main venous outlet from the lower extremity of the dog, a marked reduction in peripheral pulse volume occurred.1 The present observations were made to throw some light on the mechanism of these changes.In 14 dogs the volume of pulsations in the hind foot was determined by adapting a specially constructed cellulose-acetate cup to the sensitive plethysmograph of Turner.2 All observations were conducted under ether anesthesia and the operative procedure, consisting of isolation and ligation with silk of the femoral vein at the level of Poupart's ligament, was performed aseptically. Direct venous pressure determinations3 were made in the saphenous vein at heart level before and after the ligation during the continuous determination of pulse volume. All observations were conducted under controlled atmospheric conditions, temperature 75 °F and humidity 50%.Observations were made on 2 groups of dogs: (1) 6 animals with intact sympathetic innervation, an...

The Effect of Venous Pressure on the Pulse

The Effect of Venous Pressure on the Pulse