Myocutaneous flap ischemia: flow dynamics following venous and arterial obstruction.

To further clarify the pathogenesis of the poorer prognosis in skin flaps exposed to venous stasis compared with arterial insufficiency, a microsphere study was conducted in bilateral rectus abdominis island flaps in seven pigs. The relationship between capillary blood flow and arteriovenous (A-V) shunting was studied during progressive 1-hour intervals of arterial insufficiency and venous stasis and during 3 hours of reperfusion. Under controlled conditions, total blood flow was reduced from 100 percent to both 50 and 25 percent by application of an adjustable clamp on the artery supplying one flap and on the vein draining the contralateral flap. The relative distribution between A-V shunt flow and capillary blood flow was different in arterial insufficiency when compared with venous stasis at both the 50 percent and the 25 percent blood flow levels. In the arterial insufficiency flaps, the A-V shunt flow and capillary blood flow shared the total blood flow in the following percentages: 64/36 (at 100 percent total blood flow), 44/56 (at 50 percent total blood flow level), and 22/78 (at 25 percent total blood flow level). In the venous stasis flaps, the A-V shunt flow and the capillary blood flow shared the total blood flow in percentages of 70/30, 66/34, and 55/45, respectively. Hence, in arterial insufficiency flaps, capillary blood flow was spared by a relatively greater decline in A-V shunting compared with venous stasis flaps. Redistribution of capillary blood flow from subcutaneous tissue to muscle was observed, whereas blood flow was equally distributed throughout the length of the flaps at all flow levels.(ABSTRACT TRUNCATED AT 250 WORDS)     

Morphological changes in the spinal cord, its meninges and epidural structures in experimental disorders of blood flow in the venae cavae

The experiment has been carried out on 72 dogs. The dynamics of morphofunctional changes in the spinal cord, its meninges and in the epidural structures have been investigated when the epidural veins of the spinal canal are involved into the collateral blood stream after ligation of the anterior or posterior venae cavae. During the first 24 h after disturbance of the blood stream in the venae cavae, there appears venous stasis in the vessels of the epidural structures, of the spinal cord and its meninges, in neurons and glial elements hypoxia and acidosis appear. However, in connection with reconstruction of the collateralies, compensating the disturbed blood stream, by the end of the first week the phenomena of the venous stasis disappear. As the result of further reconstruction of the collateral bed, the epidural veins of the spinal canal become the main (short) bypass. During 3-5 months after occlusion of the venae cavae not only the ventral epidural veins of the spinal canal are gradually dilating, but the veins of the roots and meninges of the spinal cord, as well. The spinal cord edema develops, its volume increases by 10-18%, neural cells undergo severe morphological changes up to their death. The phenomena of a chronic venous congestion increase in their severity during 3 years, after that compensatory and restorative changes begin prevailing.     

Criteria for analysis of arterial and venous occlusion

To provide a better understanding of analysis of arterial (AO) and venous occlusion (VO) tracings, using a constant and nonpulsatile perfusion pressure system, we set up an isolated in situ dog lobe preparation perfused with autologous blood. Four signals were recorded: arterial pressure, arterial inflow rate, venous pressure, and venous outflow rate. The four signals were recorded into the memory of a computer. When flow into the lobe was abruptly stopped (AO), flow out of the lung continued unchanged for approximately 150 ms and then decreased slowly to zero. Likewise, when flow out of the lung was abruptly stopped (VO), the flow into the lung continued unchanged for approximately 130 ms and then decreased slowly to zero. A monoexponential curve was fitted to different stretches of data between 0.1 and 5 s postocclusion and extrapolated to the instant of occlusion (defined here as the instant when flow at the site of occlusion becomes zero). The results indicate that 1) the first 150 ms postocclusion should be avoided because of the oscillatory artifacts generated by the occlusion maneuver, 2) use of a long segment of postocclusion data (5 s) tends to underestimate the middle pressure gradient and overestimate the arterial and venous pressure gradients, and 3) the changes in segmental vascular resistance under different experimental conditions were found to be unaffected by the criteria of analysis. Analysis of the postocclusion (AO and VO) tracings was found to be most compatible with the double-occlusion capillary pressure by fitting a stretch of data between 0.2 and 2.5 s postocclusion and extrapolating back to the instant when flow becomes zero at the site of occlusion but no earlier.     

Vascular adaptation to 4 wk of deconditioning by unilateral lower limb suspension

Physical inactivity or deconditioning is an independent risk factor for atherosclerosis and cardiovascular disease. In contrast to exercise, the vascular changes that occur as a result of deconditioning have not been characterized. We used 4 wk of unilateral lower limb suspension (ULLS) to study arterial and venous adaptations to deconditioning. In contrast to previous studies, this model is not confounded by denervation or microgravity. Seven healthy subjects participated in the study. Arterial and venous characteristics of the legs were assessed by echo Doppler ultrasound and venous occlusion plethysmography. The diameter of the common and superficial femoral artery decreased by 12% after 4 wk of ULLS. Baseline calf blood flow, as measured by plethysmography, decreased from 2.1 +/- 0.2 to 1.6 +/- 0.2 ml.min(-1).dl tissue(-1). Both arterial diameter and calf blood flow returned to baseline values after 4 wk of recovery. There was no indication of a decrease in flow-mediated dilation of the superficial femoral artery after ULLS deconditioning. This means that functional adaptations to inactivity are not simply the inverse of adaptations to exercise. The venous pressure-volume curve is shifted downward after ULLS, without any effect on compliance. In conclusion, deconditioning by 4 wk of ULLS causes significant changes in both the arterial and the venous system.     

Immediate exercise hyperemia in humans is contraction intensity dependent: evidence for rapid vasodilation.

We tested the hypothesis that rapid vasodilation proportional to contraction intensity contributes to the immediate (first cardiac cycle after initial contraction) exercise hyperemia. Ten healthy subjects performed single 1-s isometric forearm contractions at 5, 10, 15, 20, 30, 50, and 70% maximal voluntary contraction intensity (MVC) in arm above heart (AH) and below heart (BH) positions. Forearm blood flow (FBF; brachial artery mean blood velocity, Doppler ultrasound), mean arterial pressure (arterial tonometry), and heart rate (electrocardiogram) were measured beat by beat. Venous emptying (measured with a forearm strain gauge) was already maximized at 5% MVC, indicating that increases in contraction intensity did not further empty the forearm veins. Immediate increases in FBF were linearly proportional to contraction intensity from 5 to 70% MVC in AH (slope = 4.4 +/- 0.5%DeltaFBF/%MVC). In BH, the immediate increase in FBF demonstrated a curvilinear relationship with increasing contraction intensity and was greater than AH at 15, 20, 30, and 50% MVC (P < 0.05). Peak changes in FBF were greater in BH vs. AH from 10 to 50% MVC, even when venous refilling was complete (P < 0.05). These data support the existence of a rapid-acting vasodilatory mechanism(s) at the onset of human forearm exercise.     

Effect of hypoxia on pulmonary blood flow-segmental vascular resistance relationship in perfused cat lungs

To investigate the effect of alveolar hypoxia onthe pulmonary blood flow-segmental vascular resistance relationship, wedetermined the longitudinal distribution of vascular resistance whileincreasing blood flow during hyperoxia or hypoxia in perfused catlungs. We measured microvascular pressures by the micropipetteservo-null method, partitioned the pulmonary vessels into threesegments [i.e., arterial (from main pulmonary artery to 30- to50-µm arterioles), venous (from 30- to 50-µm venules to leftatrium), and microvascular (between arterioles and venules)segments] and calculated segmental vascular resistance. Duringhyperoxia, total resistance decreased with increased blood flow becauseof a reduction of microvascular resistance. In contrast, duringhypoxia, not only microvascular resistance but also arterial resistancedecreased with increase of blood flow while venous resistance remainedunchanged. The reduction of arterial resistance was presumably causedby arterial distension induced by an elevated arterial pressure duringhypoxia. We conclude that, during hypoxia, both microvessels andarteries >50 µm in diameter play a role in preventing furtherincreases in total pulmonary vascular resistance with increased bloodflow.

     

Differential effects of venous stasis and arterial insufficiency on tissue oxygenation in myocutaneous island flaps: an experimental study in pigs.

The supply, consumption, and tissue tension of oxygen were studied in experimental bilateral myocutaneous island flaps in five control pigs and in eight pigs during progressive 1-hour intervals of flap ischemia. Progressive ischemia was obtained by partial to complete clamping of the artery in one flap, producing arterial insufficiency, and simultaneous clamping of the vein in the other flap, producing venous stasis. Blood flow was reduced to 50, 25, and 0 percent of baseline. In the arterial insufficiency flaps, the oxygen tension in subcutaneous tissue, muscle, and venous outflow was significantly reduced once blood flow was reduced to 50 percent of baseline. Oxygen consumption during partial vessel occlusion was lower in the venous stasis flaps than in the arterial insufficiency flaps when blood flow was reduced to 25 percent of baseline, suggesting either that cellular metabolism is reduced in the venous stasis flaps or that the oxygen which is delivered is unavailable for the cells. Increased presence of tissue fluid in the venous stasis flap inhibits the diffusion of oxygen through the interstitial tissue, and this may explain the lower oxygen consumption. During 3 hours of reperfusion, increased blood flow was observed in the arterial insufficiency flaps, whereas blood flow in the venous stasis flaps was sluggish. The arterial insufficiency flaps recovered more rapidly than the venous stasis flaps during the first hour of reperfusion, judged by the rate of increase in oxygen tension and the higher venous oxygen tension. Oxygen tension increased more rapidly in muscle than in subcutaneous tissue.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparative effects of vasodilator drugs on flow distribution and venous return

Systemic vascular effects of hydralazine, prazosin, captopril, and nifedipine were studied in 115 anesthetized dogs. Blood flow (Q) and right atrial pressure (Pra) were independently controlled by a right heart bypass. Transient changes in central blood volume after an acute reduction in Pra at a constant Q showed that blood was draining from two vascular compartments with different time constants, one fast and the other slow. At three dose levels producing comparable reductions in systemic arterial pressure (30-40% at the highest dose), these drugs had different effects on flow distribution and venous return. Hydralazine and prazosin had parallel and balanced effects on arterial resistance of the two vascular compartments, and flow distribution was unaltered. Captopril preferentially reduced arterial resistance of the compartment with a slow time constant for venous return (-26 +/- 6%, -30 +/- 6%, -50 +/- 5% at 0.02, 0.10, and 0.50 mg X kg-1 X h-1, respectively; means +/- SEM) without altering arterial resistance of the fast time-constant compartment. Blood flow to the slow time-constant compartment was increased 43 +/- 14% at the highest dose, and central blood volume was reduced 108 +/- 15 mL. In contrast, nifedipine had a balanced effect on arterial resistance with the lowest dose (0.025 mg/kg) but caused a preferential reduction in arterial resistance of the fast time-constant compartment at higher doses (-38 +/- 4% and -55 +/- 2% at 0.05 and 0.10 mg/kg, respectively). Blood flow to the slow time-constant compartment was reduced 36 +/- 5% at the highest dose of nifedipine, and central blood volume was increased 66 +/- 12 mL. Total systemic venous compliance was unaltered or slightly reduced by each of the four drugs. These results add further evidence to the hypothesis that peripheral blood flow distribution is a major determinant of venous return to the heart.     

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

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.     

Oxygen limitation of thermal tolerance in cod, Gadus morhua L., studied by magnetic resonance imaging and on-line venous oxygen monitoring

The hypothesis of an oxygen-limited thermal tolerance due to restrictions in cardiovascular performance at extreme temperatures was tested in Atlantic cod, Gadus morhua (North Sea). Heart rate, changes in arterial and venous blood flow, and venous oxygen tensions were determined during an acute temperature change to define pejus ("getting worse") temperatures that border the thermal optimum range. An exponential increase in heart rate occurred between 2 and 16 degrees C (Q(10) = 2.38 +/- 0.35). Thermal sensitivity was reduced beyond 16 degrees C when cardiac arrhythmia became visible. Flow-weighted magnetic resonance imaging (MRI) measurements of temperature-dependent blood flow revealed no exponential but a hyperbolic increase of blood flow with a moderate linear increase at temperatures >4 degrees C. Therefore, temperature-dependent heart rate increments are not mirrored by similar increments in blood flow. Venous Po(2) (Pv(O(2))), which reflects the quality of oxygen supply to the heart of cod (no coronary circulation present), followed an inverse U-shaped curve with highest Pv(O(2)) levels at 5.0 +/- 0.2 degrees C. Thermal limitation of circulatory performance in cod set in below 2 degrees C and beyond 7 degrees C, respectively, characterized by decreased Pv(O(2)). Further warming led to a sharp drop in Pv(O(2)) beyond 16.1 +/- 1.2 degrees C in accordance with the onset of cardiac arrhythmia and, likely, the critical temperature. In conclusion, progressive cooling or warming brings cod from a temperature range of optimum cardiac performance into a pejus range, when aerobic scope falls before critical temperatures are reached. These patterns might cause a shift in the geographical distribution of cod with global warming.     

Blood flow measurement from plethysmographic pulse waves without venous occlusion

An air plethysmograph with a sensitive phototransducer was constructed so that plethysmographic volume-change pulsations could be displayed in detail without using venous occlusion. Software was developed to allow analysis of the pulses using a modification of the backward extrapolation technique. This allowed calculation of the forward arterial blood flow and noninvasive derivation of the resting arterial flow waveform. There is good reproducibility of the technique, with 8% variability between pairs of measurements at rest and 4% variability after hand exercise. Direct comparison made with blood flows measured by venous occlusion plethysmography showed good average agreement. The mean blood flow for venous occlusion (rest and exercise) was 0.76 +/- 0.07 mL/beat (mean +/- SEM), and the mean blood flow for backward extrapolation (rest and exercise) was 0.74 +/- 0.09 mL/beat (mean +/- SEM). This corresponds to 3.86 +/- 0.36 mL/min/100 mL and 3.76 +/- 0.46 mL/min/100 mL, respectively. Important assumptions when using this method are that venous return is constant and that forward arterial flow is over before the end of the cardiac cycle.     

Increased vascular resistance in paralyzed legs after spinal cord injury is reversible by training.

The purpose of the present study was to determine the effect of a spinal cord injury (SCI) on resting vascular resistance in paralyzed legs in humans. To accomplish this goal, we measured blood pressure and resting flow above and below the lesion (by using venous occlusion plethysmography) in 11 patients with SCI and in 10 healthy controls (C). Relative vascular resistance was calculated as mean arterial pressure in millimeters of mercury divided by the arterial blood flow in milliliters per minute per 100 milliliters of tissue. Arterial blood flow in the sympathetically deprived and paralyzed legs of SCI was significantly lower than leg blood flow in C. Because mean arterial pressure showed no differences between both groups, leg vascular resistance in SCI was significantly higher than in C. Within the SCI group, arterial blood flow was significantly higher and vascular resistance significantly lower in the arms than in the legs. To distinguish between the effect of loss of central neural control vs. deconditioning, a group of nine SCI patients was trained for 6 wk and showed a 30% increase in leg blood flow with unchanged blood pressure levels, indicating a marked reduction in vascular resistance. In conclusion, vascular resistance is increased in the paralyzed legs of individuals with SCI and is reversible by training.     

Hemodynamic effects of blood loss during a passive response to a stressor in the conscious rabbit

In the conscious rabbit, exposure to an air jet stressor increases arterial pressure, heart rate, and cardiac output. During hemorrhage, air jet exposure extends the blood loss necessary to produce hypotension. It is possible that this enhanced defense of arterial pressure is a general characteristic of stressors. However, some stressors such as oscillation (OSC), although they increase arterial pressure, do not change heart rate or cardiac output. The cardiovascular changes during OSC resemble those seen during freezing behavior. In the present study, our hypothesis was that, unlike air jet, OSC would not affect defense of arterial blood pressure during blood loss. Male New Zealand White rabbits were chronically prepared with arterial and venous catheters and Doppler flow probes. We removed venous blood until mean arterial pressure decreased to 40 mmHg. We repeated the experiment in each rabbit on separate days in the presence and absence (SHAM) of OSC. Compared with SHAM, OSC increased arterial pressure 14 +/- 1 mmHg, central venous pressure 3.3 +/- 0.4 mmHg, and hindquarter blood flow 34 +/- 4% while decreasing mesenteric conductance 32 +/- 3% and not changing heart rate or cardiac output. During normotensive hemorrhage, OSC enhanced hindquarter and renal vasoconstriction. Contrary to our hypothesis, OSC (23.5 +/- 0.6 ml/kg) increased the blood loss necessary to produce hypotension compared with SHAM (16.8 +/- 0.6 ml/kg). In nine rabbits, OSC prevented hypotension even after a blood loss of 27 ml/kg. Thus a stressful stimulus that resulted in cardiovascular changes similar to those seen during freezing behavior enhanced defense of arterial pressure during hemorrhage.     

Pulsatile pressure and flow in the 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.     

Erythrocyte deformability and segmental pulmonary vascular resistance: osmolarity and heat treatment

The site and nature of change in resistance to blood flow in canine left lung lobe preparation after changes in blood viscosity were assessed by using the arterial and venous occlusion (AVO) technique and the vascular pressure-flow relationship. Blood viscosity was changed by erythrocyte (RBC) shrinkage and swelling with hypertonic and hypotonic NaCl solutions and by RBC membrane rigidification with heat treatment (49 degrees C for 1 h). The results show that although all three methods of changing blood viscosity increased the pulmonary vascular resistance (PVR) by 15-50%, the site and nature of the change in PVR were different in each case. The AVO data showed that the increase in PVR with heat treatment of RBC's was due entirely (100%) to increased resistance of the middle microvascular segment, whereas deviation from normal osmolarity potentiated the resistance in arterial, middle, and venous segments. By examining the effect of osmolarity in plasma-perfused lobes, it was possible to separate the increase in PVR due to changes in RBC deformability from those due to other factors. The increase in arterial and venous resistances with hypertonic solution was attributed in part (approximately 50%) to factors other than RBC's; however, the increase in middle resistance was entirely due to RBC crenation. The increase in arterial and venous resistances with hypotonic solutions was small and was apparently caused by factors other than RBC swelling, whereas the increase in middle resistance was partially (approximately 50%) due to RBC swelling and partially to other factors (e.g., endothelial cell hydration).(ABSTRACT TRUNCATED AT 250 WORDS)     

Species differences in the reflex effects of lingual afferent nerve stimulation on lip blood flow and arterial pressure

We evoked changes in lower lip blood flow and systemic arterial blood pressure by electrically stimulating the central cut end of the lingual nerve in artificially ventilated, urethane-anesthetized, cervically vago-sympathectomized cats, rats, rabbits, and guinea pig. The systemic arterial blood pressure changes were species-dependent: increases in rat, consistent decreases in rabbit and guinea pig, and variable among individuals in cat. In cat and rabbit, lip blood flow increases, which occurred only ipsilaterally to the stimulated nerve and showed no statistically significant correlation with the systemic arterial blood pressure changes. In rat, the ipsilateral lip blood flow increase was markedly greater than the contralateral one, and although there was a significant correlation between each of them and the systemic arterial blood pressure changes, the ipsilateral increase presumably included an active vasodilatation. In guinea pig, lip blood flow decreased on both sides in proportion to the systemic arterial blood pressure reductions. Thus, species variability exists in the sympathetic-mediated systemic arterial blood pressure changes and parasympathetic-mediated lip blood flow responses themselves, and in the relationship between them.Abbreviations a.u. arbitary units - LBF lip blood flow - LN lingual nerve - SABP systemic arterial blood pressure - SP substance P - Vsp trigeminal spinal nucleusCommunicated by I.D. Hume     

Obstetric epidural analgesia and postural hypotension.

Supine and erect arterial pressures were measured daily for six to seven days after delivery in 100 patients, of whom 50 had received epidural analgesia. There was no difference in the magnitude of postural hypotension between the epidural and control groups on any day after delivery, although in both groups the hypotension was greater during the first two days due almost entirely to changes in systolic arterial pressure. The incidence of dizziness on standing was similar in both groups (9%). Thus postural hypotension is no more common in women who have received epidural analgesia than in others. All patients should be helped out of bed after delivery, and any patient who experiences dizziness should have her blood pressure measured until the dizziness disappears.     

O2 metabolism of the sheep diaphragm during flow resistive loaded breathing

To determine whether O2 availability limited diaphragmatic performance, we subjected unanesthetized sheep to severe (n = 11) and moderate (n = 3) inspiratory flow resistive loads and studied the phrenic venous effluent. We measured transdiaphragmatic pressure (Pdi), systemic arterial and phrenic venous blood gas tensions, and lactate and pyruvate concentrations. In four sheep with severe loads, we measured O2 saturation (SO2), O2 content, and hemoglobin. We found that with severe loads Pdi increased to 74.7 +/- 6.0 cmH2O by 40 min of loading, remained stable for 20-30 more min, then slowly decreased. In every sheep, arterial PCO2 increased when Pdi decreased. With moderate loads Pdi increased to and maintained levels of 40-55 cmH2O. With both loads, venous PO2, SO2, and O2 content decreased initially and then increased, so that the arteriovenous difference in O2 content decreased as loading continued. Hemoglobin increased slowly in three of four sheep. There were no appreciable changes in arterial or venous lactate and pyruvate during loading or recovery. We conclude that the changes in venous PO2, SO2, and O2 content may be the result of changes in hemoglobin, blood flow to the diaphragm, or limitation of O2 diffusion. Our data do not support the hypothesis that in sheep subjected to inspiratory flow resistive loads O2 availability limits diaphragmatic performance.     

Splenic baroreceptors control splenic afferent nerve activity

Stenosis of either the portal or splenic vein increases splenic afferent nerve activity (SANA), which, through the splenorenal reflex, reduces renal blood flow. Because these maneuvers not only raise splenic venous pressure but also reduce splenic venous outflow, the question remained as to whether it is increased intrasplenic postcapillary pressure and/or reduced intrasplenic blood flow, which stimulates SANA. In anesthetized rats, we measured the changes in SANA in response to partial occlusion of either the splenic artery or vein. Splenic venous and arterial pressures and flows were simultaneously monitored. Splenic vein occlusion increased splenic venous pressure (9.5 +/- 0.5 to 22.9 +/- 0.8 mmHg, n = 6), reduced splenic arterial blood flow (1.7 +/- 0.1 to 0.9 +/- 0.1 ml/min, n = 6) and splenic venous blood flow (1.3 +/- 0.1 to 0.6 +/- 0.1 ml/min, n = 6), and increased SANA (1.7 +/- 0.4 to 2.2 +/- 0.5 spikes/s, n = 6). During splenic artery occlusion, we matched the reduction in either splenic arterial blood flow (1.7 +/- 0.1 to 0.7 +/- 0.05, n = 6) or splenic venous blood flow (1.2 +/- 0.1 to 0.5 +/- 0.04, n = 5) with that seen during splenic vein occlusion. In neither case was there any change in either splenic venous pressure (-0.4 +/- 0.9 mmHg, n = 6 and +0.1 +/- 0.3 mmHg, n = 5) or SANA (-0.11 +/- 0.15 spikes/s, n = 6 and -0.05 +/- 0.08 spikes/s, n = 5), respectively. Furthermore, there was a linear relationship between SANA and splenic venous pressure (r = 0.619, P = 0.008, n = 17). There was no such relationship with splenic venous (r = 0.371, P = 0.236, n = 12) or arterial (r = 0.275, P = 0.413, n = 11) blood flow. We conclude that it is splenic venous pressure, not flow, which stimulates splenic afferent nerve activity and activates the splenorenal reflex in portal and splenic venous hypertension.     

Pulmonary vascular compliance and viscoelasticity

When dog lung lobes were perfused at constant arterial inflow rate, occlusion of the venous outflow (VO) produced a rapid jump in venous pressure (Pv) followed by a slower rise in both arterial pressure (Pa) and Pv. During the slow rise Pa(t) and Pv(t) tended to converge and become concave upward as the volume of blood in the lungs increased. We compared the dynamic vascular volume vs. pressure curves obtained after VO with the static volume vs. pressure curves obtained by dye dilution. The slope of the static curve (the static compliance, Cst) was always larger than the slope of the dynamic curve (the dynamic compliance, Cdyn). In addition, the Cdyn decreased with increasing blood flow rate. When venous occlusion (VO) was followed after a short time interval by arterial occlusion (AO) such that the lobe was isovolumic, both Pa and Pv fell with time to a level that was below either pressure at the instant of AO. In an attempt to explain these observations a compartmental model was constructed in which the hemodynamic resistance and vascular compliance were volume dependent and the vessel walls were viscoelastic. These features of the model could account for the convergence and upward concavity of the Pa and Pv curves after VO and the pressure relaxation in the isovolumic state after AO, respectively. According to the model analysis, the difference between Cst and Cdyn and the flow dependence of Cdyn are due to wall viscosity and volume dependence of compliance, respectively. Model analysis also suggested ways of evaluating changes in the viscoelasticity of the lobar vascular bed. Hypoxic vasoconstriction that increased total vascular resistance also decreased Cst and Cdyn and appeared to increase the vessel wall viscosity.