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Finger systolic blood pressure (FSP) was measured indirectly in normal subjects and patients with primary Raynaud phenomenon by applying a thin-walled plastic cuff around the finger and a strain gauge more distally to detect volume changes. Inducing a high vascular tone in one or more fingers by direct cooling or intra-arterial noradrenaline infusion caused a marked drop in FSP in the exposed fingers, but not in the non-exposed fingers of the same hand. The fact that the non-exposed fingers retained the normal (arm systolic) pressure level is taken to indicate that palmar arch blood pressure also remained normal. In the high vascular tone state, a large transmural pressure difference must apparently be established before the digital arteries are forced open. The lowered opening pressure constitutes a manifestation of the closure phenomenon of the digital arteries described in patients with vasospastic arterial disease. It implies an underestimation of palmar arch systolic pressure measured indirectly on the fingers. FSP measured under these circumstances may be taken as an estimate of the vascular tone, and can be employed in diagnosis and quantification of vasospastic disorders.

Overall transvascular escape rate of albumin [TERalb, i.e. the fraction of intravascular mass of albumin (IVMalb) passing to the extravascular space per unit time] was determined from the disappearance of i.v. injected radioiodinated serum albumin. Patients with tense ascites due to liver cirrhosis and pigs with posthepatic portal hypertension and intraperitoneally instilled fluid were studied before and after abdominal paracentesis in order to evaluate the effect of ascitic fluid hydrostatic pressure on the transvascular escape rate of albumin.TERalb of the ascitic patients (n = 6) were on average 7.8% IVMalb±h-1, which is somewhat higher but not significantly above normal (mean 5.6% IVMalb ± h-l). After paracentesis and removal of the ascitic fluid, TERalb rose significantly to an average of 11.9% IVMalb h-1 (P<0.05). The fraction of lVMalb passing into the peritoneal cavity was on average 0.21 and 0.38% IVMalb ±h - l before and after paracentesis, respectively (n = 4).In ascitic, posthepatic portal-hypertensive pigs (n = 6), TERalb averaged 15.1% IVMalb ±h - 1, a value not being significantly different from non-ascitic, normotensive controls (mean 16.1% IVMalb±h-l). After paracentesis, TERalb rose significantly to an average of 24.3% IVMalb±h - l.The increased albumin extravasation rate after removal of ascites is best explained by an increased sinusoidal-tissue pressure difference caused by a decreased hydrostatic fluid pressure in the liver interstitium (portal and sub-capsular spaces) due to the hydrostatic effect of the removed ascitic fluid.

Fractional peritoneal reabsorption rates (FPRR) were determined from the plasma activity after simultaneous intraperitoneal injection of 131 I-labelled serum albumin (a) and 125I-labelled immunoglobulin G-IgG (g) in eight patients with cirrhosis (+ ascites 6, -ascites 2) and in one patient with carcinomatous ascites. Trans-vascular escape rates of albumin (TERa) and IgG (TERg) were determined in the cirrhotic patients from the disappearance of simultaneously intravenously injected 131I-labeIled serum albumin and 125I-labelled IgG. Peritoneal space to plasma appearance times ranged 0.1-3.3 h, and the appearance times of albumin and IgG were almost identical. In patients with cirrhosis FPRRa and FPRRg were on average 1.27 and 1.21 % of intraperitoneal protein masses returning to plasma per hour, respectively. Mean FPRRa/FPRRa ratio was 0.95 and this value was not significantly different from unity, but significantly higher (P< 0.001) than the ratio between the free diffusion coefficients of IgG and albumin (0.6). The calculated ascitic fluid flow rate was on average 61 ml/h. TERa and TERg were on average 9.6 and 8.6% of intravascular protein masses per hour, mean TERg/TER, ratio was 0.95. Peritoneal space to plasma protein flux averaged 0.4% of the intravascular protein mass per hour. The results point to filtration (convective flux) as the main transport mechanism responsible for protein passage into the peritoneal cavity as well as for the protein passage (lymphatic drainage) back into the plasma. Pressure measurements during catheterization confirmed pressure differences essential for convective flux.

Transvascular escape rate of albumin [TERalb, i.e. the fraction of the intra-vascular mass of albumin (IVMalb) passing to the extravascular space per unit time] was determined from the disappearance of i. v. injected radioiodinated serum albumin in anaesthetized pigs during control conditions and during regional venous congestion in the infradiaphragmatic area. Balloon catheters were placed in the portal vein (infrahepatic portal congestion) and in the inferior vena cava above (suprahepatic caval congestion) and below (infrahepatic caval congestion) the outlets of the hepatic veins. TERalbwas on the average 13% 1VMalb.h−−lunder basal pressure conditions. TERalbrose significantly (P<0.01) during suprahepatic caval and infrahepatic portal congestion to an average of 29 and 19 % IVMalb* h−−l, respectively. TERalbwas positively correlated to the portal pressure (r = 0.75, P<0.001). Only a minor increment in TERalb was found during infrahepatic caval congestion. The hepatic share of the increased TERalbduring stasis above the hepatic veins was estimated to be threefold that of the extrahepatic splanchnic area. Our results point to filtration of protein, pre-dominantely through the lining of the sinusoids and perisinusoidal space of the liver into the interstitial space around the portal vessels and further into the lymphatics, as the main mechanism of the previously demonstrated marked increase in TERalbin patients with portal venous hypertension due to cirrhosis of the liver.

Nielsen, P. E., Levin Nielsen, S., Holstein, P., Löönsmann Poulsen, H., Hart Hansen, E. & Lassen, N. A. Intra-Arterial Infusion of Prostaglandin E1in Normal Subjects and Patients with Peripheral Arterial Disease. Scand. J. clin. Lab. Invest. 36, 633––640, 1976.Acute vasodilatation was produced by infusion of prostaglandin E1(PGE1) in the femoral artery in 6 patients with occlusive arterial disease of the legs and in 3 normal subjects. The effect on blood flow and on blood pressure was measured at different segments of the leg with the strain gauge technique, isotope clearance technique, and photoelectric technique. Skin temperature was measured at different levels by using thermocouples. The blood pressure on the legs decreased at all segments during vasodilatation as well in patients as in controls. The blood flow increased in all segments in normal controls. In patients the blood flow increased proximally in the legs. Distally, however, no increase could be demonstrated. As a good effect of PGE1on ischaemic rest pains has been reported, mechanisms other than vasodilatation should probably be considered.

Simultaneous measurement during 24 h of mean arterial blood pressure (MABP) and forefoot subcutaneous adipose tissue blood flow (SBF) was undertaken in eight patients (15 feet) with different degrees of arterial insufficiency. The recordings were undertaken with the patients in the supine position only. The MABP decreased by 19±9 from awake to asleep independently of symptomatology. In two limbs with normal circulation, SBF decreased by 8±7. In five limbs with arterial insufficiency but no rest pain SBF decreased by 16±8, and in eight limbs with ischaemic nocturnal rest pain, SBF was reduced by 32±12 during sleep. It is concluded that nocturnal hypotension is the major aethiological factor for the symptom ischaemic nocturnal rest pain.

Transvascular escape rate of albumin (TERalb, i.e. the fraction of intravascular mass of albumin (IVMalb) passing to (or during steady state returning from) the extravascular space per unit time) was determined from the initial disappearance rate of i.v. injected radioiodinated serum albumin in anaesthetized pigs during control conditions and during diuretic medication (furosemide i.v. 20 mg15 min, total 160–200 mg). During diuretic medication TERalb(mean 17.1 IVMalb· h-1, range 11.5–21, n 6) increased significantly above the control period (mean 12.3 IVMalb· h-1, range 9.5–16.5, P<0.05). Pressures in artery, right atrium, hepatic and portal veins did not change significantly from control to diuretic period. TERalbequals the lymphatic return rate of albumin provided the transport mechanisms are filtrative-convective (i.e. no local back transport). Additional measurements in five pigs with proteins of different molecular size confirmed a dominating filtrative-convective transport. The increased TERalbduring diuretic medication is best explained by an increased lymph drainage, which may decrease interstitial fluid pressure and thereby increase the transmural capillary pressure difference being essential for a filtrative-convective transvascular albumin transport. Increased lymph drainage may contribute to the therapeutic effect of diuretic treatment in oedema and ascites.

Nielsen, P. E., Levin Nielsen, S., Holstein, P., Lönsmann Poulsen, H., Hart Hansen, E. & Lassen, N. A. Intra-Arterial Infusion of Prostaglandin E1 in Normal Subjects and Patients with Peripheral Arterial Disease. Scand. J. clin. Lab. Invest. 36, 633-640, 1976.Acute vasodilatation was produced by infusion of prostaglandin E1 (PGE1) in the femoral artery in 6 patients with occlusive arterial disease of the legs and in 3 normal subjects. The effect on blood flow and on blood pressure was measured at different segments of the leg with the strain gauge technique, isotope clearance technique, and photoelectric technique. Skin temperature was measured at different levels by using thermocouples. The blood pressure on the legs decreased at all segments during vasodilatation as well in patients as in controls. The blood flow increased in all segments in normal controls. In patients the blood flow increased proximally in the legs. Distally, however, no increase could be demonstrated. As a good effect of PGE1 on ischaemic rest pains has been reported, mechanisms other than vasodilatation should probably be considered.

Hirai, M., Nielsen, S. L. & Lassen, N. A. Blood Pressure Measurement of All Five Fingers by Strain Gauge Plethysmography. Scand. J. din. Lab. Invest. 36, 627––632, 1976.The aim of the present paper was to study the methodological problems involved in measuring systolic blood pressure in all five fingers by the strain gauge technique. In 24 normal subjects, blood pressure at the proximal phalanx of finger I and both at the proximal and the intermediate phalanx of the other fingers was measured using a 24-mm-wide cuff. Blood pressure at the proximal phalanx was higher than that at the intermediate phalanx in all fingers except finger V. The difference of blood pressure values corresponded well with circumference of the finger. In 15 normal subjects, blood pressure at the proximal phalanx was compared in fingers I, III, IV, and V, using 16, 20, 24 and 27 mm wide cuffs. Finger blood pressure was closest to arm systolic blood pressure when a 24-mm or 27-mm-wide cuff was used in fingers I, III, and IV, and with a 20-mm-wide cuff in finger V. As the standard deviation of the mean values was larger with the 27-mm-wide cuff than with the 24-mm-wide cuff, the 24-mm-wide cuff was considered to be most suitable for clinical use in fingers I, II, III, and IV. By using the 20-mm-wide cuff in finger V and the 24-mm-wide cuff in the other fingers, normal value of finger blood pressure was determined for both proximal and intermediate phalanxes.

Minimal vascular resistance (MVR) was determined in a paralysed cutaneous vascular bed at the dorsum of the foot in diabetic patients. Twelve long-term insulin-dependent diabetic (IDDM) patients with and nine short-term IDDM patients without nephropathy and retinopathy and eight control subjects were investigated. The vascular bed was paralysed by local injection of histamine. Skin perfusion pressure was varied by applying graded external counter pressure over the investigated area. Skin blood flow was measured by the local 99mTc wash-out technique before, during and after three to five step-wise increases of external counter pressure. The MVR was calculated from the reciprocal of the slope of the relationship between blood flow and applied pressure. The MVR was significantly increased in diabetic patients with (mean: 9.3 mmHg ml-1·100 g·min) and without nephropathy and retinopathy (8.5 mmHg ml-1·100 g·min) compared with non-diabetic subjects (5.2 mmHg ml-1·100 g·min) (p<0.001 and p<0.005, respectively). Diabetic microangiopathy (increased hyalinusis of the basement membranes in the terminal arterioles) was found in skin biopsies in nine of the 12 long-term IDDM patients and in four of the nine short-term IDDM patients, but not in the control subjects. Multiple regression analysis demonstrated a highly significant direct association between MVR and degree of diabetic microangiopathy in the same skin area (p<0.0002). A less significant direct association between MVR and arm diastolic blood pressure (p<0.05) and blood glucose concentration (p<0.05) was also found. Our results indicate, that terminal arteriolar hyalinosis is the main determinant of the increased minimal vascular resistance in skin in short- and long-term IDDM patients.

The function of the local nervous veno-arteriolar reflex regulation of blood flow in subcutaneous tissue of the lower leg was studied in diabetic patients. The material comprised 11 long-term insulin-dependent diabetic (IDDM) patients with retinopathy and nephropathy and eight short-term IDDM patients without retinopathy or nephropathy and 11 non-diabetic subjects. The diabetic patients had no or a slight to moderate degree of peripheral autonomic and sensoric neuropathy. Blood flow was measured by the local 133Xe wash-out technique. Blood flow was determined before, during and after an approximately 40 mmHg increase in venous transmural pressure, induced by lowering the lower leg 50 cm below heart level. During lowering of the leg, the subcutaneous blood flow decreased to the same level in long-term IDDM patients (mean: 46), short-term IDDM patients (53) and control subjects (53). There was no association between the relative local blood flow during lowering and the degree of terminal arteriolar hyalinosis studied in skin biopsies from the same tissue area. Our results suggest that terminal arteriolar hyalinosis does not interfere with the local sympathetic-mediated veno-arteriolar reflex regulation of blood flow. Moreover, the vasoconstriction mediated by the veno-arteriolar reflex probably occurs in the larger arterioles (>50–100 μm) or small arteries.

The transcapillary escape rate of albumin (TERalb), i.e. the fraction of intravascular mass of albumin that passes to the extravascular space per unit time, was determined from the disappearance of intravenously injected 125I-labelled human serum albumin during the first 60 min after injection in nine patients with cirrhosis of the liver. Six of the patients had ascites. The wedged hepatic venous pressure or splenic pulp pressure ranged from 20 to 30 mmHg, mean 26 mmHg. Plasma albumin concentration was low, but plasma volume was slightly enlarged, and thus the intravascular mass of albumin was only moderately reduced. The transcapillary escape rate of albumin was significantly elevated in all the cirrhotics, mean 10.2%/h, range 8.8 to 12.3%/h, in comparison to values for twenty-eight normal subjects 5.4%/h, range 3.5-7.2%/h. Our results can best be explained by increased filtration out of the vessels in the portal system, due to the increased portal venous pressure. The increased TERalb probably contributes to the formation of oedema and ascitic fluid.

Transvascular escape rates of albumin and immunoglobulin-G, IgG (TERalb and TERIgG, i.e. the fractions of intravascular mass of albumin and IgG passing to the extravascular space per unit time) were determined simultaneously from the disappearance of intravenously injected 131I-labelled human serum albumin and 125I-labelled human IgG in eight patients with cirrhosis of the liver. The mean wedged hepatic venous pressure was 22 mmHg (range 13-34). TERIgG and TERalb were on average 8.4± 0.8 %/h (SD), and 7.4 ± 1.9 %/h (SD), respectively and these values are significantly increased compared to normal subjects [TERalb = 5.2±1.0 %/h (SD) and TERIgG = 3.0 ± 0.7 %/h (SD), P<0.001]. The TERIgG/TERalb ratio was on average 0.88 ± 0.20 (SD), which is significantly higher than that of normals [0.58 ± 0.08 (SD), P<0.005]. The results indicated that increased filtration (bulk flow) is the dominant process of the increase microvascular protein escape in cirrhosis, due most likely to increased hepatic, but also to increased extrahepatic splanchnic transcapillary protein flux.

The transcapillary escape from plasma to the interstitial space of albumin and two plasma globulins, IgG and IgM, was studied in man during angiotensin II infusion causing an average increase of 42% in the mean arterial blood pressure. The intravascular mass of each protein was determined before and after 90 minutes' hypertension, in order to obtain a measure of the change in the transcapillary escape rate of each protein. The transcapillary escape rate of albumin was also determined by use of radioiodinated albumin. During the hypertensive period the transcapillary escape rate for all 3 proteins increased. The relative increase was much more pronounced for IgM and IgG (+170%) than for albumin (+75%). The ratio between the transcapillary escape rate and the free diffusion coefficient increased with increasing molecular size, a finding which cannot be explained by simple diffusion. The central and peripheral venous pressure increased and the plasma volume decreased during the angiotensin II infusion period. Our results can best be explained by increased filtration through enlarged pores between the endothelial cells of the microvasculature, owing to the arterial pressure elevation caused by the angiotensin II infusion.

AbstractThe systolic blood pressure on the finger, toe, and ankle has been measured by a strain gauge technique in 10 normal subjects aged 17–31 years and 14 normal subjects aged 43–57 years. The standard deviation in repeated measurements lies between 2 and 6 mm Hg. The finger pressure in the younger group was significantly higher than the corresponding arm pressure ( 9.3 mm Hg, S.D. 6.8), but equalled this in the older group (– 0.5 mm Hg, S.D. 6.6). In the two groups the ankle pressures were 19.3 mm Hg (S.D. 7.5) and 23.6 mm Hg (S.D. 9.5) higher than the systolic arm pressures. The toe pressures were lower than the arm pressures, in the two groups – 4.8 mm Hg (S.D. 6.6) and – 9.8 mm Hg (S.D. 10.7) respectively. The ankle-toe gradient was in the younger group 24.3 mm Hg (S.D. 7.3) and in the older group 33.3 mm Hg (S.D. 12.1). Using mean minus 2.5 X S.D. as the lower limit of normality, arterial stenosis or occlusion in the leg is suggested by ankle pressure below the systolic arm pressure and in the foot by ankle-toe gradient exceeding 43 and 64 mm Hg in the two age groups respectively.

The disappearance rates of locally injected radioactive extracellular ions were studied in hyperemic human skeletal muscle (m. tibialis ant.) in 7 non-diabetics, 4 recently-diagnosed juvenile diabetics and 7 long-term juvenile diabetics with clinical manifestations of diabetic angiopathy. 24Na+ and 131I- were employed as tracers. The local blood flow was estimated by the 133Xenon clearance method.The capillary diffusion capacity, CDC, (Renkin's permeability-surface area product PS) was calculated in terms of the unidirectional flux of the tracers: CDC is the number of ml of interstitial fluid completely rinsed of tracer in the (imaginary) situation of infinitely high capillary blood flow, i.e. when no back-diffusion of tracer occurs.The average values for CDCNa and CDCI were found to be highly significantly increased (p<0.001) in the long-term diabetic group as compared to non-diabetics and recently-diagnosed diabetics: CDCNa=5.8; 4.2; 4.0 and CDCI=8.7; 6.4; 6.2 ml interstitial fluid per 100 g skeletal muscle per minute in the respective groups.It is believed that this increased CDC is due to the presence of diabetic microangiopathy i.e. the thickened capillary basement membrane is probably abnormally leaky to small hydrophilic molecules. The CDC may represent a useful new parameter in the clinical evaluation of diabetic angiopathy.

The theory of calculating the Capillary Diffusion Capacity (CDC) from the observed disappearance rate of a small hydrophilic molecule injected locally is described. The presentation concerns specifically the wash-out during hyperemia of intramuscularly injected tracer amounts of 24Na+, 131I-, and 51Cr-ethylene-diamine-tetra-acetate (a monovalent chelate-anion, 51Cr - E.D.T.A.). The CDC is calculated in the unit of moles/(mol/ml)/100 g muscle/min, a unit which allows one directly to compare the CDC of different tracers in contrast to hitherto used units. The technically simple local clearance method for determining CDC is critically commented on, with particular reference to 1) the size of the interstitial volume after the local injection, 2) the possible limitation of tracer movement within this volume, 3) the small degree to which the various extracellular tracers used may pass into the intracellular space. It is concluded that the local clearance method must be validated by experiments comparing it to the more direct, but more cumbersome, Chinard-Crone double indicator technique, which is based on intra-arterial injection and multiple venous samples.