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Biomedical subjects

K Aukland

Publications and source records attributed to K Aukland.

At least 55 records · Page 3Linked to original sources

Measurement of interstitial fluid pressure: comparison of methods.

Interstitial fluid pressure (IFP), i.e., the pressure in a saline-filled tube brought into contact with the interstitium, has been measured in cats with two "acute" [micropipettes and wick-in-needle (WIN)] and two chronic (perforated and porous capsules) methods. In a control situation, similar pressures of -1.5 and -1.6 mm Hg were recorded in skin with micropipettes and both types of capsules, respectively, while WIN pressure in subcutis was -1.2 mm Hg. IFP in skeletal muscle was -0.5, -0.5, and -1.1 mm Hg as recorded with micropipettes, WIN, and porous capsules, respectively. During infusion of Ringer's solution, pressures in both types of capsules rose by 4 to 6 mm Hg, while pressure recorded with the acute methods increased by 1 to 1.5 mm Hg only. Two hours after infusion all techniques gave similar pressures. Peritoneal dialysis for 2 hours reduced micropipette and WIN pressures by 3 to 4 mm Hg. Pressure in perforated capsules fell by 10 mm Hg during dialysis and remained low for an additional 2 hours, while porous capsule pressure fell by 7 mm Hg during dialysis but thereafter increased and reached the pressure recorded with micropipettes and WIN 2 hours after ended dialysis. In both overhydration and dehydration, capsules probably react to changes in interstitial fluid colloid osmotic pressure; in overhydration the capsules react also to changes in capillary pressure, resulting in the discrepancy between chronic and acute methods during non-steady-state conditions. In conclusion, acute and chronic methods record similar pressures during steady-state conditions, but the chronic methods are sensitive to changes in vascular pressure and interstitial fluid colloid osmotic pressure and are therefore not suitable for measuring the changes that occur in IFP within a few hours.

Animals↗

Wick sampling of interstitial fluid in rat skin: further analysis and modifications of the method.

UNLABELLED: We compared modifications of the wick technique for analysis of interstitial fluid in rat subcutis. Nylon wicks were implanted for 60 min in back skin of rats after anesthesia with pentobarbital or after sacrifice by potassium chloride injection. Wicks were implanted dry or loaded with saline or varied dilutions of rat serum. Implantation of dry wicks and wicks loaded with diluted serum in living, anesthetized animals produced similar results; the protein concentration of wick fluid averaged about 60% that of the plasma protein concentration. The saline loaded wicks produced wick fluid with a lower protein concentration, average about 45% that of plasma protein concentration. The lower concentrations apparently resulted from simple dilution. Wick fluid sampled from dead animals had similar total protein concentrations, but in the dead animals there was a lower concentration of the large plasma proteins and a relatively higher concentration of the smaller proteins. CONCLUSIONS: Wick implantation in living animals causes a transitory inflammatory reaction and a decrease in the size selectivity of macromolecular sieving, but local osmotic forces bring about a concentration equilibrium with undisturbed interstitium. Implantation of dry wicks in subcutis either in vivo or post mortem provides a simple, direct method for sampling the total protein concentration and colloid osmotic pressure of interstitial fluid. Implantation of dry wicks postmortem permits measurement of individual component protein concentrations and evaluation of molecular selectivity between plasma and interstitium.

Animals↗

An attempt to measure glomerular plasma flow by the cationic dyes alcian blue and ruthenium red.

Autoradiography showed that 3H-labelled alcian blue injected into the rat renal artery was concentrated in the glomeruli. To test if the uptake could be used as a measure of local glomerular plasma flow, the one-pass extraction was measured in 19 rats. The average extraction was 31.9% (SD 8.0%). Impurities and heterogeneity of the tracer as well as reversible binding to erythrocytes may have contributed to the low estimated extraction. The average extraction of 103Ru-ruthenium red was 26.3%. We conclude that neither of these dyes are suitable for measurement of glomerular plasma flow.

Alcian Blue↗

Interstitial colloid osmotic and hydrostatic pressures in human subcutaneous tissue during early stages of heart failure.

Subcutaneous oedema is a common finding in heart failure. However, some patients have reduced cardiac pump function without oedema. The aim of this study was to investigate whether local mechanisms in subcutaneous tissue contribute to oedema prevention. A reduction in interstitial colloid osmotic pressure (pii) and a rise in interstitial fluid hydrostatic pressure (Pi) will both counteract a rise in capillary filtration caused by heart failure. Cardiac catheterization was done in 22 angina pectoris patients without visible oedema. Two days later pii was measured with a wick method and Pi was measured with a wick-in-needle method. Both parameters were measured in subcutaneous tissue on thorax at heart level and on the ankle. Plasma volume was determined by 125I-albumin and extracellular volume measured with 35SO4. Parameters of cardiac pump function ranged from normal to clearly pathological values. Mean pii was 13.0 mmHg on thorax and 8.3 mmHg on the ankle. Pi averaged -2.1 mmHg on thorax and -1.5 mmHg on the ankle. Statistically significant (P less than 0.05) correlations were found between pii on thorax and left ventricular end diastolic pressure (rs -0.40) and pii on thorax and cardiac index (rs 0.42). Pi was positively correlated to right atrial pressure (rs 0.50). Body fluid volumes were normal or moderately reduced. The study shows that a reduction in cardiac pump function is associated with a reduction in pii and a rise in Pi. These changes may help to prevent oedema formation in the early stages of heart failure.

Adult↗

Protein concentration of lymph and interstitial fluid in the rat tail.

Lymph was collected from tail lymphatics of anesthetized rats, subcutaneous interstitial fluid was obtained by implanting nylon wicks, and tendon interstitial fluid was obtained by centrifugation of pieces of tendon. Spontaneous lymph flow rates averaged 70 nl X min-1 X g skin-1. Protein concentrations and colloid osmotic pressures of sampled fluids differed significantly. Tail lymph had the highest protein concentration relative to plasma [lymph-to-plasma ratio 0.71 +/- 0.03 (SE) n = 10], followed by wick fluid (0.62 +/- 0.02, n = 9), with tendon fluid lowest (0.50 +/- 0.03, n = 10). Albumin and immunoglobulin G (IgG) concentrations in samples of tail skin and tendon were assayed by rocket immunoelectrophoresis. Comparison of their distribution volumes at lymph or tendon fluid concentrations, respectively, with interstitial fluid volumes measured as 2-h 51Cr-ethylenediaminetetraacetic acid space minus 5-min 125I-albumin space indicated that 50-60% of the interstitial volume in these tissues is not available for distribution of albumin or IgG. Low lymph flow and high interstitial protein content of rat tail indicate a slow turnover of interstitial protein. This suggests that interstitial washout of protein plays a role in limiting edema only after a sustained or chronic increase in fluid filtration.

Albumins↗

Hemodynamics and interstitial fluid pressure in the rat tail.

Blood flow in the rat was measured during pentobarbital anesthesia by plethysmographic and thermometric techniques. Tail arterial and venous pressures (Pa and Pv) were measured by glass micropipettes and interstitial fluid pressure (PIF) by wick-in-needle technique. Large pressure gradients were measured along the tail, Pa decreasing and Pv increasing toward the tip. In the vasoconstricted tail, distal arterial and venous pressures (Pad and Pvd, respectively, 10 cm from the tail root) were 55 and 11% of aortic pressure (PA), while PIF was 0-2 mmHg. Plasma volume expansion increased blood flow by a factor of 10 to 35. Pad rose to 74% and Pvd to 20% of PA. PIF increased to 15 mmHg, in parallel with Pv. Venous stasis (cuff pressure 14.7 mmHg) increased PIF and Pv by 3.5 and 9 mmHg, respectively, while tail volume increased by 0.4 to 1.2%. In conclusion, the large flow increase induced by plasma volume expansion depends strongly on dilation of the tail artery, with two- to threefold increase in internal radius. Simultaneously the tail veins relax and expand. Subcutaneous tissue is compressed between the expanding vessels and the tight skin, and PIF increases almost sufficiently to prevent a rise in net capillary filtration pressure. This immediate edema-preventing mechanism is less efficient during venous stasis, which presumably does not induce "active" dilation of the tail vessels. Similar mechanisms probably exist in other "encapsulated" tissues.

Animals↗

Distribution of body fluids: local mechanisms guarding interstitial fluid volume.

The plasma volume is determined by fluid influx through drinking and outflux by renal excretion. Both fluxes are regulated according to plasma volume and composition through arterial pressure, osmoreceptors and vascular stretch receptors. As to the remaining part of the extracellular volume, the interstitial space, there is no evidence that its volume (IFV), pressure or composition are sensed in such a way as to influence water intake or excretion. Nevertheless, IFV is clearly regulated, often pari passu with the regulation of plasma volume. However, there are many exceptions to parallel changes of the two compartments, indicating the existence of automatic, local mechanisms guarding the net transfer of fluid between plasma and interstitium. Thus, a rise in arterial and/or venous pressure, tending to increase capillary pressure and net filtration, is counteracted by changes in the "Starling forces": hydrostatic and colloid osmotic pressures of capillary blood and interstitial fluid. These "oedemapreventing mechanisms" (A. C. Guyton) may be listed as follows: Vascular mechanisms, modifying capillary pressure or interstitial fluid pressure (IFP). Increased transmural vascular pressure elicits precapillary constriction and thereby reduces the rise in capillary pressure. Counteracts formation of leg oedema in orthostasis. Venous expansion transmits pressure to the interstitium in encapsulated organs (brain, bone marrow, rat tail). Mechanisms secondary to increased net filtration, A rise in IFV will increase IFP, and thereby oppose further filtration. Favoured by lowcompliant interstitium. Reduction of interstitial COP through dilution and/or washout of interstitial proteins. A new steady state depends on increased lymph flow. Increased lymph flow permits a rise in net capillary filtration pressure. Low blood flow and high filtration fraction will increase local capillary COP.

Animals↗

A telemetric technique for studies of venous pressure in the human leg during different positions and activities.

The pressure in the saphenous vein of the lower leg was monitored by ordinary ECG telemetry equipment supplied with a pressure transducer, a chopper and an extra filter. In eight healthy volunteers venous pressure averaged 80 +/- 5 (SD) mmHg in the standing position and 21 +/- 10 (SD) mmHg during slow walking. When the subjects were occupied with laboratory work in upright position the mean venous pressure was 40-50 mmHg, similar to that obtained sitting at a desk: 48 +/- 5 (SD) mmHg.

Adult↗

Capillary transport of H2 gas generated locally in renal tissue.

Previous measurements by microspheres have shown a higher blood flow in outer cortex and a lower blood flow in inner cortex than found by diffusible tracers. During vasodilation microspheres have indicated a disproportionate increase in deep cortical blood flow, whereas diffusible tracer distributions remained unchanged. These discrepancies could possibly be explained by a variable net inward transport of diffusible tracers in postglomerular vessels, the transport existing in control, but disappearing during vasodilation. To test this hypothesis H2 gas was produced electrolytically for 1 s at a platinum electrode in midcortex and the resulting gas concentration curve measured polarographically at two electrodes placed above and below the source. Analysis of a mathematical model showed that the ratio of the curve maxima at the two electrodes (Cmo/Cmi) would best reveal a radial net transport. Average Cmo/Cmi at 25 positions in 7 clamped dog kidneys was close to unity, but rose to 1.24 at control flow. During acetylcholine infusion Cmo/Cmi rose to 1.68. Local washout rates at the two electrodes increased equally. Calculations indicated a small outwardly directed net transport in control (3 X 10(-4) cm/s), becoming slightly reinforced during vasodilation (5 X 10(-4) cm/s). Thus the control transport direction is opposite to the hypothesis, and the change during vasodilation was estimated to be too small to explain the disparity between diffusible tracer uptake and microsphere distribution in control. H2 concentration maximum was obtained earlier under control flow than in the clamped kidney, indicating an increase in apparent D of the gas in tissue from 3 X 10(-5) cm2/s to 5 X 10(-5) cm2/s, probably due to mixing of H2 gas in the capillary net work.

Acetylcholine↗

A mathematical analysis of the myogenic hypothesis with special reference to autoregulation of renal blood flow.

To test the hypothesis that autoregulation of renal blood flow could result from myogenic regulation of arterial/arteriolar wall tension, we have explored a model based on the assumptions that (1) each preglomerular vessel segment reacts to a change in transmural pressure by altering its internal radius until the initial change in wall tension is reduced by a gain factor, (2) postglomerular structural resistance remains unchanged, (3) extravascular tissue pressure equals intrarenal venous pressure, and (4) the renal vascular system can be represented by one unbranched tube. General equations were obtained for flow and segmental radii and pressure as functions of aortic pressure. With a gain factor of 1 and a glomerular capillary pressure of 50% of aortic pressure under control conditions, the model predictions agree well with experimental data in dogs. Increasing aortic pressure from about 60% of control level causes only slight increase of blood flow. A rise in tissue pressure up to 40% of aortic pressure causes only moderate reduction. Changes in vessel radii begin in proximal vessel segments and spread distally toward glomerulus at increasing changes in aortic and tissue pressures from their control levels. Glomerular capillary pressure is autoregulated in proportion to blood flow. The degree of autoregulation is only moderately dependent on the gain factor: A moderate impairment caused by reducing the gain factor from 1 to 0.7 may be compensated by locating the myogenically responsive wall layer a distance 0.2 times the internal radius from the vessel lumen. "Superautoregulation," i.e., a rise in flow at reduced aortic pressure, is not possible. An upper limit of autoregulation is obtained only with the additional assumption of a fall in contractile force at extreme shortening of the muscle fibers. No definitive biological proof has yet been provided for a segmental wall tension-regulating mechanism in the preglomerular vessels, and obviously its existence cannot be proved by a mathematical model. However, if such a mechanism does exist, it can explain most of the renal resistance changes at varying arterial and intrarenal pressures, as well as the observed autoregulation of terminal interlobular arterial pressure.

Aorta↗

Plasma colloid osmotic pressure in venous blood from the human foot in orthostasis.

Several theories could explain the slow rate of edema formation in the feet of sitting or standing man. One possible mechanism is a rise in local plasma colloid osmotic pressure (pi p). We measured pi p in blood from superficial veins of warm and cold feet during orthostasis. The difference in venous pi p between the foot and the arm averaged 12.8 mmHg (range 9.4-16.1 mmHg) in subjects sitting in a cold room. Hemoconcentration was also reflected as increased hematocrit. These findings support the view that a local increase of pi p in foot capillaries contributes considerably to edema prevention during orthostasis.

Adult↗

Distribution of blood flow in the dog kidney. III. Local uptake of 10 mum and 15 mum microspheres during renal vasodilation and constriction.

Recent studies indicate that intrarenal distribution of blood flow measured with microspheres (Ms) during control conditions depends on Ms size. We therefore compared local flow in outer and middle cortex (C1 and C2) and inner cortex plus the medulla (C3M) using 10.5-12.0 and 13.9-15.0 mum Ms (Ms 10 and Ms 15). One pair of Ms 10 and Ms 15 was injected during control and a second pair at 80% increased or 50% decreased total renal vascular conductance (RVC), as induced by infusion of acetylcholine (Ach) and angiotensin II (Ang) or noradrenaline (NA). All zones participated in dilation and constriction, as indicated by both Ms sizes. Ms 15 underestimated C3M flow as compared to Ms 10, by 19% during control or Ang, and by 3% during Ach (P less than 0.02). The C3M flow fractions increased during Ach and decreased during Ang, whereas NA gave greatly variable results, on average no change. Renal Ms extraction averaged 97.0 +/- 3% for Ms 10, 98.6 +/- 2.4% (S.D.) for Ms 15. About 8% of Ms 10 and less than 1% of Ms 15 were located in peritubular capillaries in each cortical zone. Neither total Ms extraction nor zonal extraglomerular Ms fraction changed over the present RVC range. Thus, the Ms 10 to Ms 15 differences as well as the observed redistribution must be due to differences in local entry of Ms into the afferent arterioles. However, steric restriction of Ms at arteriolar inlets did not play a significant role. The measured redistribution of fractional flow could in part be due to skimming of Ms at arteriolar inlets along the interlobular arteries (i.l.a.), depending on the C3M flow fraction, Ms size and i.l.a. diameter. If the observed fractional flow redistributions were solely due to variable Ms skimming, Ms 15 underestimated C3M flow by 53%, Ms 10 by 43%, during Ang as compared to Ach. Although Ms 10 and Ms 15 may correctly indicate the direction of fractional glomerular flow redistribution, at least Ms 15 overestimates this phenomenon quantitatively.

Acetylcholine↗

Distribution of blood flow in the dog kidney. IV. Reversed net inward postglomerular capillary flow in the cortex after blocking interlobular arteries by 50 mum microspheres.

Simultaneous measurement of glomerular flow by 15 mum microspheres (Ms) and postglomerular capillary flow by 125I-iodoantipyrine (I-Ap) suggest that about 10% of total RBF flow inward through the entire cortex in the postglomerular capillaries of the dog kidney. This flow fraction might be variable (Clausen et al. 1978, 1980) and perhaps even reversible. To test this possibility we injected 50 mum Ms into the renal artery in order to obstruct interlobular arteries and produce a selective reduction of outer cortical glomerular blood flow and postglomerular pressure. The 50 mum Ms reduced total RBF by 50%. In the outer cortex, postglomerular flow measured by I-Ap was significantly less reduced than glomerular flow as measured by 15 mum Ms: Whereas the inward flow fraction from inner cortex to the medulla was maintained, about 5% of RBF now drained from midcortex to outer cortex. This observation support the theory of a variable net postglomerular capillary flow of radial direction in the cortex of the dog kidney.

Animals↗

Skimming of microspheres in vitro: implications for measurement of intrarenal blood flow.

Skimming could result in erroneous estimation of renal cortical blood flow distribution as measured by microspheres. Skimming of microspheres with diameters 10, 12, and 15 micrometers and red blood cells was therefore studied in a model in which an interlobular artery and its first arteriolar branch were simulated by 80- and 30-micrometers-wide slits between glass prisms. The experiments were performed with citrated blood at a hematocrit (Hct) of 40, flow velocities of 3 and 6 cm/s, and branch flow varying from 2 to 25%. At a branch flow fraction comparable to that of a deep arteriole in the dog kidney (3%), Hct in branch blood was 24% lower than that of input blood, whereas 10-, 12-, and 15-micrometers microsphere concentrations were 75, 81, and 87% lower, respectively. The size-dependent skimming was probably caused by wall exclusion in the main channel. Differences in particle inertia did not affect skimming. The results suggest that the disparate local flow values obtained by use of microspheres of different sizes in dog and rat kidneys are due to a size-dependent skimming of the microspheres.

Animals↗