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Background: The effects of α-trinositol (1D -myo-inositol-1,2,6-triphosphate, IP3) on burn-induced edema formation were investigated. Methods: Lymph flow (QL; μl/min) and lymph-to-plasma protein ratio (CL/CP) were monitored in groups of five to six dogs before and 4 hours after (1) a 5-second 100° C or 90° C foot paw scald; (2) IP3 (45 mg/kg intravenous bolus, then a 20 mg/kg/hr infusion) 30 minutes before or after 100° C scald, or 30 minutes after 90° C scald. Hind paw venous pressure was elevated and maintained by outflow restriction until reaching steady state QL and (CL/CP)min. Macromolecular reflection coefficient (1 – CL/CP) was measured. Fluid filtration coefficient (Kf; ml/min/mm Hg/100 gm) was calculated. Relative paw weight gain (%) was measured. Results: Compared with preburn values, scald uniformly produced significant increases in QL, CL/CP, and Kf. IP3 significantly (p < 0.02, ANOVA) reduced paw weight gain when given before, but not after, 100° C burn (41% ± 5% versus 18% ± 7% preburn IP3 and 31% ± 3% postburn IP3). Compared with 90° C burn animals, postburn treatment significantly (p < 0.017) attenuated 4-hour increases in QL (550 ± 87 versus 252 ± 29 μl/min), Kf (0.016 ± 00 versus 0.007 ± 00 μl/min/mm/Hg/100gm), and relative paw weight gain (28% ± 3% versus 12% ± 5%). Conclusions: α-Trinositol given after a 90° C scald blunted edema formation at the site of scald, likely through reduced transmembrane fluid flux. (Surgery 1998;123:36-45.)

We bring up to date our series of direct measurements of portal flow and pressure in patients with cirrhosis of the liver. In 153 patients the portal flow averaged 447 plus or minus 350 ml. Hg per minute and the portal pressure 28.5 plus or minus 4 mm. Hg (approximately 387 mm. H2O). Both quantities compare favorably with our previous measurements in smaller groups of patients. In 80 of our patients we had also measurements of pressure on the hepatic and splanchnic sides of a clamp occluding the portal vein. Nine of these patients had an hepatic occluded portal pressure higher than either or both the free portal pressure and the splanchnic occluded portal pressure. Of these nine patients with reversed pressure differences, two had stagnant portal flow and the remaining seven had forward flow into the liver measuring from 80 to 1,116 ml. Hg per minute.

"Venous" ulceration is usually ascribed to deep venous insufficiency. We record the cases of 20 patients with 23 ulcers without a history suggestive of deep vein disease who were found to have a normal deep venous system when evaluated by Doppler ultrasound, ambulatory venous pressures, and photoplethysmography. All had gross varicose veins present for many years (mean 24 years; range 10 to 35 years), and only 14 limbs had incompetent calf perforating veins. Effective treatment is facilitated by recognition of the relationship of varicose ulcer to superficial venous disease, usually incompetence of the saphenofemoral junction, with or without the presence of incompetent calf perforating veins.

Malnutrition is frequently associated with advanced cirrhosis. To investigate the role of portal hypertension in nutritional impairment, we developed an animal model to isolate and characterize the effects of chronic intestinal venous hypertension on intestinal nutrient absorption. We performed mesenteric arteriovenous anastomosis combined with portal vein banding in rats. Hepatic architecture and excretory function (bile flow and bile salt output) were unaltered, while severe and persistent intestinal venous hypertension was produced. We then measured in vivo absorption rates of three test nutrients (vitamin D3, valine, and tryptophan) and water. Vitamin D3 absorption was significantly impaired by intestinal congestion, while amino acid absorption was unaffected. Splanchnic hypertensive rats absorbed less water than controls. We conclude that chronic intestinal venous hypertension alone selectively impairs nutrient absorption.

Previous studies have shown that decreasing blood flow in the superior mesenteric artery (SMA) by the infusion of intra-arterial vasopressin into or partial mechanical obstruction of the SMA by a balloon catheter (partial balloon obstruction) causes similar alterations in splanchnic hemodynamics, but divergent changes in systemic hemodynamics. The effects of these two methods of reducing SMA blood flow were compared in each of six anesthetized normal dogs. Vasopressin and partial balloon obstruction induce similar reductions in portal pressure (-54 +/- 12% vs. -46 +/- 11%), wedge hepatic vein pressure (-54 +/- 13% vs. -53 +/- 18%), and portal venous flow (-34 +/- 7% vs. -37 +/- 7%). Significantly different effects between intra-arterial vasopressin and partial balloon obstruction were observed, however, in cardiac output (a decrease of -24 +/- 5% vs. an increase of +12 +/- 4%) (P less than 0.001), heart rate (-8 +/- 3% vs. 0) (P less than 0.05), and systemic vascular resistance (+36 +/- 8% vs. -2 +/- 2%) (P less than 0.005), respectively. These results indicate that the two procedures are equally effective in reducing portal venous pressure and blood flow. Partial balloon obstruction, however, does not induce the potentially deleterious systemic hemodynamic effects seen with vasopressin infusion. In fact, some of the changes observed with partial balloon obstruction, especially the increase in cardiac output, are considered to be beneficial. In an additional five dogs, partial balloon obstruction was maintained for 5 hours. Throughout, the reduction in portal venous pressure (hepatic venous wedge minus hepatic venous free pressure) was maintained at less than half of the baseline levels (4.75 +/- 0.43 vs. 2.25 +/- 0.32 mm Hg), and the mean arterial pressure at baseline values. All of the dogs survived and were well at 1 week after the prolonged partial obstruction. No abnormalities were observed in the anatomical or histological studies of the small intestine. This study suggests that partial balloon obstruction of the SMA has theoretical therapeutic advantages over intra-arterial vasopressin for reducing portal venous pressure.

Peripheral postcapillary venous pressure (PCVP) and mixed venous oxygen saturation (SvO2 or PASO2) have been shown to be sensitive indicators of volume status and appear to reflect the adequacy of peripheral perfusion during controlled bleeding. This study demonstrates that in an open-chest dog model with controlled venous return, PCVP is closely and linearly (r2 = 0.6) correlated with cardiac output (CO). Furthermore, oxygen saturation as measured in the central venous system (CVSO2) and peripheral vein PVSO2) were found to be closely and linearly related to PASO2 (r = 0.72 to 0.99 and 0.91 to 0.98, respectively). Thus PCVP, CVSO2, and PVSO2 represent easily and safely obtainable parameters that closely reflect major physiologic variables. During resuscitation after controlled hemorrhage, the PCVP and PVSO2 accurately reflected the restoration of blood volume and were as good as CO and central saturations. Central venous and pulmonary wedge pressures both poorly reflected the return to full volume repletion (P less than 0.01). Thus, PCVP and PVSO2 seem to be reliable indices of volume status and perfusion and do not require invasive, central monitoring.

The formation of a temporary distal arteriovenous fistula (dAVF) has been used clinically to palliate patients with symptomatic venous hypertension. This study tested the efficacy of a temporary dAVF for the treatment of venous hypertension in an experimental model. Twenty-four New Zealand white rabbits were divided into two experimental groups. Group I rabbits (n = 12) underwent standardized ligation of the iliac and femoral venous systems. Group II rabbits (n = 12) underwent standardized ligation of the iliac and femoral venous systems with the formation of a temporary dAVF. Venous obstruction was documented with venography, and venous hypertension was documented with femoral venous pressure measurements. Venous pressure, resistance, blood flow, vein circumference, vein cross-sectional area, vein wall thickness, and venography were compared between four rabbits from each group at 2, 4, and 8 weeks. The effect of differences in baseline venous pressures was eliminated by subtracting the venous pressure in the unobstructed rabbit limb from the pressure in the obstructed rabbit leg. Group II rabbits had a lower standardized venous pressure (4.4 +/- 2.2 versus 9.5 +/- 4.2 mm Hg, p less than 0.01) and venous outflow resistance (0.16 +/- 0.08 versus 0.36 +/- 0.18, p less than 0.05) than did group I rabbits. Group II rabbits also had a larger superficial femoral vein circumference (3.46 +/- 0.67 versus 2.57 +/- 0.08 mm, p less than 0.05) and cross-sectional area (0.66 +/- 0.31 versus 0.31 +/- 0.09 mm2, p less than 0.01) than did group I rabbits. The improvement persisted throughout the 6-week study, which suggested an improved venous outflow.

The substitute "valve" operation with use of a silicone tendon designed to produce a valvelike mechanism in the popliteal veins of 29 patients with 31 postphlebitic limbs caused by reflux in the deep veins is described. The results have been assessed by measurements, taken during ambulation, of venous pressure before operation, 1 week after operation, and 1 year after operation and by phlebography. In 29 limbs there was clinical improvement associated with improvement in the venous pressure assessed during ambulation and phlebographic evidence of a functioning substitute valve.

The consequences of occlusion of a major upper extremity vein were evaluated in eight patients with effort thrombosis, ten with thrombosis secondary to intimal injury, six with extrinsic compression, and one hypercoagulable patient, all of whom were followed for an average of 4 years. Twenty-two patients had venography, which confirmed the diagnosis but often failed to define the proximal extent of obstruction. Thirteen patients had noninvasive hemodynamic studies which did not corroborate chronic morbidity, but which were valuable in assessing the effect os specific therapy. Twelve patients were treated with anticoagulants, and six had operative removal or bypass of the obstruction. Three patients had pulmonary emboli; two embolized while on anticoagulants and both died. Swelling, pain, prominent veins, and easy fatigability of the affected extremity were the late sequelae of occlusion. Chronic morbidity was more dependent on etiology than on initial treatment. Thrombosis secondary to intimal injury caused no persistent symptoms, whether treated with anticoagulants or not. Effort thrombosis was intermediate: three fourths complained that their affected arm tired easily and half had prominent veins or persistent swelling. All of those with obstruction secondary to extrinsic compression had easy fatigability. The majority also had concomitant swelling, pain, and prominent collaterals. Operative treatment produced objective improvement in venous outflow but often was unsuccessful in relieving symptoms, particularly in patients with obstruction from extrinsic compression.

Peripheral postcapillary venous pressure (PCVP) appears to be an indicator of peripheral perfusion (cutaneous blood flow) in the experimental animal. Eighteen male mongrel dogs under balanced anesthesia were subjected to either slow, continuous hemorrhage 0.65 ml/kg/min) or plasma expansion with dextran 40 (0.80 ml/kg/min) over a period of 1 hour. Peripheral PCVP, cental venous pressure arterial pressure, cardiac output (CO), mixed venous oxygen saturation, pulmonary arterial pressure, and pulmonary wedge pressure were monitored on a continuous basis. The only parameter that consistently gave a predictable measure of the degree of induced volume change without requiring pulmonary arterial catheterization was PCVP. PCVP showed a close correlation with CO (r = 0.96).

We estimated ambulatory venous pressure (AVP) noninvasively with a new technique of quantitative photoplethysmography (PPG). Postural changes of hydrostatic pressure permitted in vivo calibration of the PPG. We recorded quantitative PPG and AVP in 14 normal subjects and 14 patients with postthrombotic chronic venous insufficiency. The results were contrasted with qualitative PPG recordings on 41 consecutive patients with chronic venous insufficiency. All but one of the latter patients demonstrated a decrement in skin blood content with exercise of the calf muscle, and shortened recovery time ws the only significant indicator of venous disease. Quantitative PPG correlated closely with AVP with respect to both estimated drop in superficial venous pressure (r = 0.97, P less than 0.001) and recovery time (r = 0.98, P less than 0.001). PPG estimates of intravenous pressure in normal and postthrombosis patients, 42 +/- 10 and 62 +/- 18 mm Hg, respectively, agreed with AVP measurements, 39 +/- 9 and 61 +/- 18 mm Hg, respectively. Quantitative PPG may prove to be an accurate estimate of AVP in patients with suspected chronic venous insufficiency.

A 10-year-old girl had bilateral, symmetrical swelling of the lower extremities, which had been present since the age of 1 year. Noninvasive vascular laboratory measurements of the ambulatory venous pressure, venous recovery time, and maximum venous outflow revealed profound bilateral lower extremity venous valvular incompetence. Duplex imaging of the veins of the lower extremities demonstrated no evidence of thrombosis, and no venous valves could be imaged. On phlebography, the patient was found to have no venous valves in the superficial and deep systems of the leg. We conclude that congenital absence of the venous valves of the lower extremities is almost certainly underdiagnosed and that the vascular laboratory can accurately and easily differentiate between lymphedema and venous valvular imcompetence. Such differentiation may have therapeutic implications.

Twelve limbs in nine patients undergoing venous valve transposition in treatment of severe chronic deep venous insufficiency are the subject of this report. Hemodynamic measurements including venous pressure studies, photoplethysmography, directional venous Doppler assessment, and impedance plethysmography were done pre- and postoperatively in each case, as was ascending and descending venography. The surgical technique is described in detail and diagrams illustrate general features of the reconstruction. The results show that a functioning valve in the deep venous system of the lower extremity may reverse pre-operative pathophysiology. This preliminary view of the operation indicates that it may have great promise in the field of direct venous reconstruction.

To investigate the possible anatomic and hemodynamic reasons for the variability in response to surgery for venous insufficiency (a 50% ulcer recurrence rate following ligation of incompetent perforating veins), we performed phlebography and venous pressure measurements in 109 legs of 77 patients and in 30 healthy volunteers. Patients were divided into five groups: saphenofemoral incompetence alone (group 1), saphenopopliteal incompetence (group 2), incompetent lower leg communicating veins alone (group 3), calf communicating veins and saphenous incompetence (group 4), and postthrombotic limbs (group 5). Patients in groups 1 through 4 had phlebographically normal deep veins. As compared to the normal controls (68%), preoperative pressure measurements revealed a significantly smaller pressure fall during exercise (deltaVPex) in all groups, which was the least marked in groups 3 (26%) and 5 (17%). These latter two groups failed to increase their pressure fall with thigh tourniquet. deltaVPex 3 months after operation demonstrated normalization in groups 1, 2, and 4 (52%, 57% and 59% respectively). Groups 3 and 5 improved little following surgical ligation. Whenever saphenous vein incompetence coexists with lower leg communicating vein incompetence, the former appears to be the dominant cause of the pressure abnormalities. Based on venous pressure measurements and phlebography, patients with normal deep veins and who increase their deltaVPex with a thigh tourniquet should respond favourably to orthodox surgical ligation of the saphenofemoral or saphenopopliteal junction. By contrast, if no change in deltaVPex is noted in patients with incompetent perforating veins and the deep veins look abnormal on the phlebogram, then ligation of the incompetent communicating veins would appear to be associated with a high recurrence rate.

This is a report of an experiment wherein a calf had its natural heart replaced with an artificial heart and survived for 18 days and 20 hours. All measured physiologic parameters remained normal until the fourteenth day. Thereafter a gradual persistent rise in venous pressure and signs of a decreased cardiac output occurred. However, the animal outwardly appeared normal until the eighteenth day. During the nineteenth day it became comatose and was killed. At autopsy large thrombi were found in both atria, impairing ventricular filling, resulting in venous congestion and diminished cardiac output. This extended survival time and our ability to understand and eliminate the problems associated with artificial heart implantation give support to our hope that artificial hearts for man will be possible in the not too distant future.

Impedance plethysmography (IPG) is an attractive diagnostic method for evaluating deep vein thrombosis in the pregnant patient because it is noninvasive and it avoids x-ray or radionuclide exposure. However, the accurate diagnosis of deep venous thrombosis by IPG in pregnant patients might be altered by the normal physiologic and anatomic changes that occur during pregnancy. We evaluated 50 healthy women by IPG throughout their pregnancies and during their nonpregnant state. We found that venous capacitance during pregnancy increases 50% over venous capacitance during the non pregnant state. Most of this change occurs during early pregnancy because of a decrease in venous tone caused by rising levels of progesterone and estradiol. During the third trimester of pregnancy venous outflow is diminished compared to outflow during early pregnancy. Venous obstruction by the gravid uterus and fetal head engaging in the pelvis are factors that contribute to this finding. The IPG results in four patients with ileofemoral thrombosis and in three with postpartum pulmonary emboli are also reported. IPG may be utilized as an accurate diagnostic technique in the pregnant woman if the physiologic and anatomic alterations of pregnancy, which are reflected as significant changes in venous capacitance and outflow on IPG testing, are considered.

Blood flow and pressures around a canine femoral arteriovenous fistula, constructed from an autogenous carotid artery, were measured to determine the pressure-flow relationships within the fistula, as well as to determine the presence or absence of retrograde flow in the distal artery and vein. The findings indicate that retrograde arterial flow occurs only when the proximal femoral artery is occluded and, even then, the contribution to fistula flow is small and well below control femoral arterial flow. Retrograde distal venous flow is negligible. Pressure within the fistula is high at the arterial end but is rapidly dissipated across the loop fistula to equal systemic venous pressure on the venous side. Modest distal venous hypertension accompanies this type of fistula. For these reasons, a loop-type, arteriovenous fistula is preferable to other types of fistulas for most clinical surgical indications.

In an attempt to develop a noninvasive test to assess objectively the magnitude of venous valvular dysfunction in pathologic states, photoplethysmography (PPG) was compared to venous pressure in the saphenous vein at the ankle. Simultaneous venous pressure and PPG recordings were taken before, during, and after exercise with subjects in the sitting position. In a total of 338 paired measurements in 24 normal, 25 postphlebitic, and 14 varicose limbs, PPG and venous pressure tracings appeared to be identical; data points had a correlation coefficient of great significance (r = 0.898). Postexercise recovery times clearly separated the normal from the postphlebitic limbs. Varicose limbs were assessed accurately regarding results of proposed surgery using an above-knee tourniquet. It appears that the PPG evaluation provides information comparable to venous pressure studies and does so more quickly and noninvasively. The test holds promise in measuring results of direct venous reconstructive surgery as well as in venectomy procedures.

Clinical studies demonstrating the effectiveness of the Kim-Ray Greenfield vena caval filter in the management of pulmonary emboli have stimulated efforts to accurately define this filter's capability to entrap sized emboli and maintain caval patency. Twenty-three dogs had filters inserted and positioned distal to the renal veins. Radiopaque emboli measuring 2 to 5 mm were introduced via the femoral vein. Cineradiography allowed direct observation of emboli capture and filter flow dynamics. Probability of entrapment was found to be related to (1) emboli size, (2) depth of filling of the conical-shaped filter by prior entrapment of emboli, and (3) absence of distal venous hypertension. The geometric design of the filter, which allows progressive vertical filling while maintaining circumferential blood flow, is thought to be responsible for entrapment of emboli and avoidance of venous thrombosis and hypertension.

Measurements of calf volume changes during treadmill ambulation were taken using mercury-in-Silastic (silicone rubber) strain gauges for noninvasive study of venous function in patients with chronic venous disease. Seventy-four limbs were evaluated: 24 with postphlebitic changes, 26 with superficial varicosities, and 24 normal. Calf volume changes as measured by mercury-in-Silastic strain-gauge plethysmography (MISSGP) during ambulation correlated well (r = 0.8) with simultaneously obtained direct venous pressure measurements. The refill time as measured by MISSGP also correlated with the pressure restoration time (r = 0.8). Patients with moderate-to-severe obstructive patterns as shown by contrast venography were found to decrease their calf volume with MISSGP significantly less (P less than 0.001) than did those patients with minimal or no obstruction of venous outflow as depicted by venography. MISSGP is shown to be a useful method of quantitatively evaluating the efficiency of the calf venous pump, the degree of reflux, and the severity of venous obstruction.

The effects of 10 and 15 cm H2O positive end-expiratory pressure (PEEP) on portal vein flow (PVF), superior mesenteric artery flow (SMAF), and cardiac output (CO) were studied. Portal vein pressure (PVP) and the intraluminal pressure gradient between portal vein and intrathoracic inferior vena cava (PVP-CVP) were also measured. PEEP caused a fall in CO and SMAF, and the fall in each was proportionately the same. PVF also fell and a linear correlation between PVF and SMAF during PEEP was observed. Although PVP increased relative to atmosphere, no increase in transmural PVP and no change in PVP-CVP gradient was observed with PEEP. These data suggest that the major effect of PEEP on portal hemodynamics is a reduction in portal flow secondary to the reduction of arterial inflow into the gut. These hemodynamic changes do not appear to be the result of an increase in resistance to protal flow at the liver but rather the result of PEEP reducing cardiac output.

We investigated the cuff-occluded rate of rise of peripheral venous pressure (CORRP)--a new, nearly noninvasive peripheral hemodynamic monitoring parameter--in dogs subjected to hemorrhage and resuscitation. Twelve adult mongrel dogs under general anesthesia were subjected to hemorrhage of 30% of their estimated total blood volume (TBV) for 30 minutes; after this time the extracted blood was reinfused. Arterial pressure (AP), central venous pressure (CVP), pulmonary arterial pressure (PAP), cardiac output (CO), pulmonary venous pressure (PWP), heart rate, and CORRP were continuously monitored. A "clinically significant change" (CSC) in CORRP and CO was defined as a change that exceeded two standard deviations from the mean of five baseline measurements made before the onset of hemorrhage, whereas a CSC in PWP or CVP was conservatively defined as a change that exceeded 2 mm Hg from the average of five baseline measurements, and a CSC in PAP and AP was defined as a change that exceeded 3 mm Hg and 5 mm Hg, respectively from the average of the baseline measurements. There was no consistent change in heart rate during hemorrhage. Thus defined, a CSC in CORRP occurred after an average extraction of 9.2% +/- 4.7% TBV, whereas a CSC was not seen until an average loss of 16.5% +/- 8.1% TBV for AP, 21% +/- 13% TBV for PWP, 15.5% +/- 7% TBV for PAP, and 35% +/- 3% TBV for CVP. These average blood losses are all significantly different from the average blood loss required to effect a CSC in CORRP. The blood loss required to effect a CSC in CO averaged 9.7% +/- 6%. We conclude that in these anesthetized dogs, CORRP detected blood loss earlier than other commonly used hemodynamic parameters, including several invasive parameters such as CVP, PAP, and PWP; CORRP and CO were equivalent in their ability to detect early stages of blood loss.

Nine patients with chronic iliac vein obstruction and venous claudication were investigated. Intramuscular pressure was measured in the anterior tibial and the deep posterior compartments in both legs at rest and during exercise. The pressures were significantly higher in the leg with iliac vein obstruction (39 +/- 10 mm Hg) than in the contralateral leg (26 +/- 12 mm Hg) at rest as well as during exercise (60 +/- 16 mm Hg and 41 +/- 15 mm Hg, respectively) in the deep posterior compartment. Similar changes were observed in the anterior tibial compartment. Muscle water content was higher (P less than 0.01) in the obstructed leg and contributes to the explanation for the high intramuscular pressure in this leg. Muscle blood flow, adenosine triphosphate, phosphocreatine, and lactate were determined in the gastrocnemius muscles at rest and at exercise. Muscle blood flow, measured with the 133xenon clearance technique, was lower in the obstructed leg (17.5 ml/min, 100 gm) than in the control leg (28.1 ml/min, 100 gm) during exercise. Lactate increased more (P less than 0.05) in the obstructed leg. It is suggested that pain in venous claudication is caused by the high intramuscular pressure, and therefore fasciotomy may be useful in the treatment of this disorder.