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Biomedical subjects

M Wolgast

Publications and source records attributed to M Wolgast.

At least 55 records · Page 3Linked to original sources
PubMed1987

Functional characteristics of peritubular capillary membrane in rat kidney.

The permeability characteristics of the peritubular capillary membrane in the rat kidney were investigated on the basis of the transport of hippuran, inulin, myoglobin, horseradish peroxidase, albumin, and gamma-globulin from peritubular capillary blood to renal hilar lymph. Data obtained in a previous investigation on single-nephron plasma flow, filtration fraction, net driving force, and fluid reabsorption along the peritubular capillary were also used. The data were analyzed in a computer-based model taking into account the transport both by diffusion and by convection. The results show that the membrane contains a few large pores through which the plasma proteins leak out into the renal interstitium and a system of several smaller pores responsible for the fluid reabsorption. The mean equivalent radius of the large pores was estimated from the larger molecular probes to be approximately 180 A (range 150-225 A), and the corresponding total pore area over pore length was estimated at 3 X 10(-4) cm (range 6 X 10(-4) to 1 X 10(-4) cm). The small-pore system was analyzed from the transport of hippuran, inulin, and myoglobin and from fluid reabsorption and showed a pore radius of somewhat below 20 A and pore areas over pore length of 50 cm. Here, the fluid reabsorption and the transport of hippuran turned out to be a sensitive marker of the pore area and the transport of inulin and myoglobin of the pore radius.

Animals↗
PubMed1987

A method for studying the effect of vasoactive substances on glomerular filtration without affecting the central haemodynamics.

A method for microcatheterization of rat kidneys was developed. The catheter consists of 50-100 micron thick polyethylene tubes, and is inserted into the interlobular or arcuate arteries via a lumbar artery. The technique makes it possible to perfuse a small number of nephrons with very high doses of vaso active substances without affecting the nephrons in the vicinity or the central haemodynamics. By adding labelled inulin to the perfusate it is also possible to calculate the amount of drug reaching the nephron under study. It was shown that the catheterization and perfusion with Ringer solution per se have no effect on the nephron function. Perfusion with very high doses of acetylcholine was found to have a selective effect on the area perfused but caused no changes in central haemodynamics, or on nephrons in unperfused areas. It is concluded that the technique is suitable for use in studies concerning the handling of high doses of vasoactive substances by the nephron.

Animals↗
PubMed1985

Long-term recovery of superficial and deep glomeruli after acute renal failure evoked by warm ischemia.

A study was made on the number of glomeruli in the outer cortex, midcortex, and inner cortex 4 weeks after 45 min of warm ischemia, using alcian blue to stain functioning glomeruli. During this time the stainable glomeruli in the kidney as a whole had decreased in number from 32,000 to 16,800. The superficial glomeruli were reduced by only about 30%, whereas in the juxtamedullary zones the number of functioning nephrons were reduced by 80%. This shows that the juxtamedullary nephrons are the most susceptible to degeneration in the recovery phase of acute renal failure caused by ischemia. The decrease in the number of glomeruli was accompanied by a reduction in total glomerular filtration rate to about the same extent. In contrast, the kidney weight was reduced by only about 20%, suggesting compensatory hypertrophy of the remaining tubules. Fluid reabsorption, urine osmolality, and potassium-secreting ability also remained decreased. The contralateral kidney responded with a compensatory hypertrophy and an increase in glomerular filtration rate, whereas the number of glomeruli in the cortex as a whole and in the individual cortical zones in this kidney remained the same as in control kidneys. It is suggested that the trapping of red cells in the juxtamedullary circulation seen soon after restoration of circulation to kidneys subjected to warm ischemia will also cause a further degeneration of the juxtamedullary nephrons.

Acute Kidney Injury↗
PubMed1984

The cortical and medullary blood flow at different levels of renal nerve activity.

The effect of (1) renal denervation and (2) stimulation of the renal nerve on the regional renal blood flow were determined by the Rb uptake method. Under control conditions the total renal blood flow was 3.64 +/- 0.09 ml X min-1 X g-1 tissue increasing significantly (p less than 0.02) to 4.39 +/- 0.28 ml X min-1 X g-1 after denervation. Upon stimulation of the peripheral portions of the sectioned renal nerves the blood flow decreased almost linearly with the frequency of stimulation reaching 0.99 +/- 0.24 ml X min-1 X g-1 at 10 Hz. Utilizing the relation between blood flow and stimulation frequency the control blood flow correspond to a spontaneous activity of 1.5 Hz. As expected the cortical blood flow responded in the same way as for the total renal blood flow. In the renal medulla denervation gave a much more pronounced response where e.g. the inner medullary flow increased from 0.88 +/- 0.09 to 1.30 +/- 0.16 ml X min-1 X g-1, i.e. a 50% increase (p less than 0.05). Stimulation with 2 Hz produced a steep fall in the blood flow, whereafter it decreased linearly with the stimulation frequency reaching 0.11 ml X min-1 X g-1 at 10 Hz stimulation. This demonstrates again that the renal medulla is sensitive to renal nerve activity primarily in the low level range. It should be remarked, however, that the 86-Rb uptake method reflects the effective blood flow, which might differ from the blood flow in absolute terms.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

The reno-renal reflex; evaluation from renal blood flow measurements.

Stimulation of the intact renal nerve bundle at a frequency of 5 Hz was found to affect not only the blood flow of the ipsilateral kidney, but also the contralateral kidney responded with a 15% reduction in its total and regional renal blood flow. If the nerves were cut proximal to the stimulation electrodes, the ipsilateral kidney, as before, responded with a reduction in its blood flow, but now the contralateral kidney remained almost unaffected. If, on the other hand, the nerves were cut distal to the stimulation electrode, meaning that only efferent nerve fibres will be activated, the contralateral kidney responded with the same 15% fall in its blood flow. If the afferent fibres of the ipsilateral kidney were stimulated as before, but the contralateral kidney was denervated, no reduction of the blood flow of the contralateral kidney could be established. It was furthermore noted that stimulation of afferent fibres resulted in a prompt rise in the systemic blood pressure with subsequent normalization after interruption of the stimulus. It is concluded that the general sympathetic tone is determined also by receptors within the kidneys. The signals reach the central nervous system via afferent fibres, and act to increase the sympathetic tone with concomitant rise in the systemic blood pressure and increased efferent renal nerve activity with subsequent reduction of the renal blood flow.

Afferent Pathways↗
PubMed1984

Renal interstitial volume of the rat kidney.

The intravascular plasma volume and the interstitial volume of the rat kidney were determined by an indicator dilution method with a bolus injection of 125-I-labelled human serum albumin and 51-Cr-EDTA into the renal artery and subsequent recording of the indicator-dilution curves in the venous effluent, sampled at intervals of 0.33 s. The curves allowed determination of both the mean transit time of the two indicators and total renal plasma flow. The volumes of distribution were obtained by multiplying these two factors. Under control conditions the plasma volume was 93.0 +/- 11.2 microliters/100 g rat (mean +/- SE), which is 17.9% of the total kidney volume. The interstitial volume was 68.3 +/- 8.6 microliters/100 g, corresponding to 13.1% of the total kidney volume. During expansion with 0.15 M NaCl, 10% of body weight, the plasma and interstitial volumes were not significantly increased. The values for the two volumes were 101.6 +/- 9.7 and 72.8 +/- 6.8 microliters/100 g, respectively. The kidney weight showed, in contrast a clear increase from 539 to 670 mg/100 g, reflecting the expansion of the proximal and distal tubules due to the increased glomerular filtration rate. It is concluded that although the saline load produced a rise in the renal interstitial pressure, the expected expansion of the interstitium became small, due to the parallel expansion of both the vascular and tubular systems which compress the renal interstitium.

Animals↗
PubMed1984

Effect of renal nerve stimulation on the activity of the tubuloglomerular feedback mechanism.

The influence of renal nerve stimulation on the tubuloglomerular feedback mechanism was studied on anaesthetized rats. The analyses was made by comparing the single-glomerular filtration rate (SNGFR) measured from late proximal tubules with SNGFR measured from distal tubules in the same nephron. In the former situation the flow to the macula densa cells is interrupted and in the latter the macula densa is influenced by the flow passing by. In the control situation the SNGFR measured proximally was 47.7 +/- 2.2 nl . min-1 (mean +/- SE) and 40.1 +/- 1.8 measured distally indicating an activated tubuloglomerular feedback. During renal nerve stimulation (2-3 Hz), the SNGFR fell to 38.5 +/- 2.3 and 33.5 4/- 1.7 when measured proximally and distally, respectively. The results indicate that the tubuloglomerular feedback mechanism is unaffected by renal nerve stimulation.

Animals↗
PubMed1983

Dynamics of glomerular ultrafiltration in the neonate kidney.

In the neonate kidney the glomerular filtration rate is generally depressed both in absolute terms and when calculated per gram kidney weight. Micropuncture studies have revealed that this phenomenon is due, not to changes in the driving pressures or the hydraulic conductivity of the glomerular capillary membrane, but to a retarded glomerular blood flow. A retarded flow will thus mean a steep rise in the protein concentration in parallel to the filtration of the protein-free filtrate. The corresponding steep rise of the colloid osmotic pressure will then induce cessation of the filtration in the distal parts of the glomerular capillary. In dehydrated states this phenomenon will be even more aggravated. An extracellular volume expansion with saline induces relaxation of the two arterioles with subsequent rise in the glomerular blood flow. The rise in the colloid osmotic pressure along the capillary is then less and the filtration can proceed along the whole of the glomerulus. Accordingly the glomerular filtration rate will be increased, reaching figures typical of the mature kidney.

Animals↗
PubMed1983

Hydraulic permeability of the peritubular and glomerular capillary membranes in the rat kidney.

The hydraulic conductivity of the peritubular capillary membrane was calculated from 1) single nephron fluid reabsorption and 2) net driving force, i.e. from hydrostatic and colloid osmotic pressures in renal interstitium and peritubular capillary blood, as determined by a micropuncture technique and with use of a computer-based model. Under control conditions the net driving force was estimated to be 15.4 mmHg and the hydraulic conductivity 1.04 nl/(min . mmHg) per 100 g rat. During extracellular volume expansion with 0.15 M saline, 4% and 10% of body weight, the net driving force decreased to 12.5 mmHg and 6.4 mmHg, respectively, whereas the conductivity increased to 1.85 and 3.14 nl/(min . mmHg) per 100 g rat. The reduction in net driving force was compensated by an increased hydraulic conductivity. In the glomeruli the net driving force for filtration increased from 14.2 mmHg under control conditions to 21.2 mmHg and 25.3 mmHg during saline expansion 4% and 10%, whereas the corresponding hydraulic conductivity de increased from 1.13 nl/(min . mmHg) per 100 g rat to 1.03 and 0.80 nl/(min . mmHg) per 100 g rat during the two expansions. During saline expansion the water permeability of the glomerular capillaries is decreased while that of the peritubular capillaries is increased. These changes in the water permeability will lead to retarded excretion of the excess fluid.

Animals↗
PubMed1983

Impaired medullary circulation in postischemic acute renal failure.

Acute renal failure was induced in heparinized rats by clamping the renal artery for 45 min. Ten minutes after recirculation the intrarenal blood flow distribution was measured. For this purpose labelled microspheres were injected together with 86-Rb chloride. The microspheres were used for determination of cardiac output, total renal and cortical blood flow, and 86-Rb for calculations of medullary blood flow. Total renal blood flow was reduced from 7.6 to 3.8 ml . min-1 . g-1 and cortical blood flow was reduced from 11.7 to 7.0 ml . min-1 . g-1. In the outer stripe of the medulla there was a reduction from 2.5 to 1.4 ml . min-1 . g-1. In the inner stripe there was a more pronounced reduction from 1.8 to 0.2 ml . min-1 . g-1 and in the inner zone from 0.8 to 0.1 ml . min-1 . g-1. The marked reduction in the blood flow to the renal medulla after recirculation is suggestive for a medullary ischemia, which might be responsible for the characteristic dysfunctions in acute renal failure.

Acute Kidney Injury↗
PubMed1982

Postischemic renal failure. Intrarenal blood flow and functional characteristics in the recovery phase.

Intrarenal blood flow, nephron function and whole kidney function were studied in the recovery phase of acute failure induced by 45 min of warm ischemia. Analyses were made 24 h, 7 days and 28 days after the ischemic insult. At 24 h the total renal blood flow was 4.0 ml . min-1 . g-1, decreasing to 1.2 within one week. After four weeks it was normalized to 3.4 ml . min-1 . g-1. The intrarenal blood flow distribution, studied with the 86-Rb extraction method, showed the same pattern of response, with no signs of a persistent heavy reduction in the deeper parts, as was found 10 min after recirculation (Karlberg et al. 1982 a). The contralateral, nonischemic kidney responded with hyperemia in all areas 24 h after the trauma, but after 7 days the values were normal. The function of the superficial nephrons was studied with the micropuncture technique. In the initial phase mainly obstructed nephrons were found, but after four weeks the nephrons were essentially normal. After 24 h the postischemic kidneys were anuric but at 7 days urine production had started and the GFR was 0.1 ml . min-1; this improved to 0.55 ml . min-1 after 4 weeks.

Acute Kidney Injury↗
PubMed1982

Renal medullary blood flow studied with the 86-Rb extraction method. Methodological considerations.

The 86-Rb extraction method was applied for a study of regional renal blood flow. In the cortex, a sampling time of 30 s led to an underestimation by about 15% as compared with the microsphere method. This was due to incomplete cortical cellular extraction of rubidium with subsequent rapid wash-out the tracer. In the renal medulla, a sampling of 30-60 s gave valid data with almost complete extraction. A sampling time of only 10 s, i.e. a time similar to the intravascular transit time, gave rise to a 50% underestimation of the inner medullary blood flow. Errors due to transport of rubidium by the tubular fluid were investigated in detail. A theoretical analysis based on equilibrium data revealed a maximal error of about 5%. Studies with micropuncture of distal tubules and studies of the urinary transport showed no or negligible contamination from tubular urine. Under control antidiuretic conditions the blood flow in the cortex was 5.2 +/- 0.2 ml . min-1 . g-1 (mean +/- SE, n = 16), in the outer stripe of the outer zone 2.2 +/- 0.1, in the inner stripe 1.5 +/- 0.1 and in the inner zone 0.69 +/- 0.06.

Animals↗
PubMed1982

Hemodynamic alterations in ischaemic acute renal failure.

It is concluded that the condition of 'acute renal failure' starts in the first minutes after restoration of the circulation, following the ischemic period. The aggregation of red blood cells in the renal medulla with the subsequent cessation of medullary blood flow represents an important factor causing both the reduced urinary concentrating ability and the depressed urinary potassium concentration. The persisting medullary ischemia leads to cellular swelling and eventually to cell necrosis, which in turn results in a mechanical obstruction of the tubular lumen in the region of the loops of Henle and the medullary collecting ducts. In contrast, the anuria which is evident weeks after the primary damage, seems to be caused by the release of vasoconstrictor principles, whose origin is unclear, but it seems not to be mediated via the renal nerves, since the same symptoms are found in transplanted kidneys. Therapeutic endeavors using heparin, saline expansion and mannitol to improve the rheological characteristics of the blood seems to be of limited value. Infusion of hyperoncotic albumin during the ischemic period, however, seems to be of some benefit, since glomerular filtration is better preserved. The addition of ATP and magnesium, glucose or adjustment of the acid base status with buffers has not been encouraging in the present models, in which glomerular filtration rate is reduced to only a few percent of control.

Acute Kidney Injury↗
PubMed1982

Nephron function in postischemic acute renal failure.

Acute renal failure was induced in rats by clamping the renal artery for 45 min. After reestablishing renal blood flow, tubular heterogeneity was observed, with (1) seemingly normal tubules, (2) dilated tubules and (3) collapsed tubules. Micropuncture techniques were used to examine the hydrostatic pressures in the different nephrons and superficial vessels, and also to determine single nephron glomerular filtration rate. The dilated tubules showed minimal filtration, due to an elevated intratubular pressure probably caused by obstructions; in these nephrons filtration could be induced by lowering the intratubular pressure. In the "normal" nephrons there was some filtration, as the proximal tubular pressure was only moderately increased. No filtration took place in the collapsed type, probably as a result of glomerular ischemia and consequently decreased glomerular capillary pressure. The kidneys also exhibited isosthenuric polyuria with a reduced potassium secretion. It is suggested that a medullary ischemia will lead to interstitial and intracellular edema and eventually cell necrosis with subsequent formation of obstructions in the loops of Henle. The obstructions would explain the increase in proximal tubular pressure and the decrease in total kidney filtration to about 5% of the normal. It is proposed that the deficient urine concentration ability and the inhibited potassium secretion are caused by the ischemic damage to the renal medulla.

Acute Kidney Injury↗
PubMed1982

Erythrocyte and albumin distribution in the kidney following warm ischemia. A study in rats.

A dark zone of probably stagnant erythrocytes, localised primarily to the inner stripe of the outer medulla, is always found in acute renal failure caused by clamping of the renal artery for 45 min. To test the possible accumulation of red cells, the regional renal red cell content was investigated with 51Cr labelled red cells injected before, during and 10 min after the recirculation. Analyses were made of the volumes of (1) cells remaining from the period of clamping, (2) cells aggregated 0--10 min after recirculation and (3) cells still circulating 10--20 min after recirculation. In the inner stripe the total red cell volume was 21.8 +/- 2.2 microliter . 100 mg-1 (control value 9.3 +/- 0.6), where 26% remained from the period of clamping, 46% had accumulated 0--10 min after recirculation, and only 28% had entered the region 10--20 min after recirculation. The same pattern of response, though less pronounced, was also found in the inner zone. In the cortex the total red cell volume was 6.3 +/- 1.2 microliter . 100 mg-1 (control value 4.4 +/- 0.3), where 24% remained from the period of clamping, 32% were accumulated and 44% remained circulating. The plasma volume as investigated from 131I-labelled albumin was markedly increased in all zones, probably due to extravasation of the tracer. It is suggested that red cell accumulation plays an important role for the medullary ischemia found in ischemic acute renal failure.

Acute Kidney Injury↗