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Biomedical subjects

H R Ulfendahl

Publications and source records attributed to H R Ulfendahl.

At least 19 recordsLinked to original sources
PubMed1999

Effect of furosemide or mannitol before injection of a non-ionic contrast medium on intrarenal oxygen tension.

Oxygen tension (pO2) in rat renal cortex and outer medulla was studied after an intravenous injection of mannitol or furosemide, followed 10 minutes later by an intravenous injection of the non-ionic X-ray contrast medium (CM) iopromide (370 mg iodine/ml). Ten minutes after mannitol injection, before injection of CM, pO2 in the medulla had decreased from a control level of 32 +/- 3 to 28 +/- 4 mm Hg. The addition of CM caused a further decrease, to 24 +/- 5 mm Hg, which was a significant reduction. Ten minutes after furosemide injection the pO2 in the medulla had increased significantly, from a control value of 32 +/- 2 to 44 +/- 4 mm Hg. Injection of CM caused a significant decrease in pO2 to 37 +/- 3 mm. Ringer's solution (n = 6) caused no changes. We conclude that pretreatment with mannitol or furosemide does not prevent the CM-induced decrease in pO2 in the outer medulla.

Animals↗
PubMed1998

Injection of low and iso-osmolar contrast medium decreases oxygen tension in the renal medulla.

The oxygen tension (PO2) in the renal cortex and outer renal medulla in 26 rats was studied by use of oxygen microelectrodes before and after injection of x-ray contrast media (CM). The CM, iopromide, ioxaglate and iotrolan were administrated intravenously in iodine equivalent doses (1,600 mg iodine/kg body wt). Ringer's solution was used as the control. In the outer medulla, all three CM induced a decrease in PO2: iopromide (N = 6) from 30 +/- 3 to 18 +/- 4 mm Hg; ioxaglate (N = 7) from 32 +/- 6 to 15 +/- 4 mm Hg; and iotrolan (N = 6) from 36 +/- 3 to 14 +/- 4 mm Hg. All these decreases were significant. After the injection of Ringer's (N = 7) there was an increase from 34 +/- 3 to 35 +/- 3 mm Hg. In the cortex a slight decrease was noted for injection of CM, but this was significant only after injection of iotrolan. All tested contrast media decrease PO2 in the outer renal medulla, which may partly explain contrast medium-induced acute renal failure.

Acute Kidney Injury↗
PubMed1998

Iodine concentrations in the rat kidney measured by X-ray microanalysis. Comparison of concentrations and viscosities in the proximal tubules and renal pelvis after intravenous injections of contrast media.

PURPOSE: To measure the iodine concentrations in the proximal tubules and renal pelvis after i.v. injections of contrast media (CM) at 1600 mg I/kg b.w., using a micropuncture technique and X-ray microanalysis. MATERIAL AND METHODS: The correlation between the viscosity of each CM and its iodine concentration was evaluated and the viscosity of the fluid in the proximal tubule and renal pelvis was estimated in rats. RESULTS: After iotrolan injection, the iodine concentration in the proximal tubular fluid had increased to values about three times higher than those reached with diatrizoate, iohexol and ioxaglate. Similarly, iotrolan tended to produce a higher iodine concentration in the renal pelvis than did the other CM. The urine viscosity in the renal pelvis was much higher after the iotrolan injection than after the other CM injections. CONCLUSION: High urine viscosity after iotrolan injection can at least partly explain our previous findings of a prolonged increase in tubular hydrostatic pressure and a prolonged decrease in the single nephron glomerular filtration rate after administration of this CM.

Animals↗
PubMed1997

Measurements of oxygen tension in the rat kidney after contrast media using an oxygen microelectrode with a guard cathode.

The oxygen tension (PO2) in the rat kidney was studied by modified Clark microelectrodes. Changes in PO2 were measured in the renal cortex and outer medulla after intravenous injections of the X-ray contrast medium (CM) diatrizoate, 370 mg iodine/mg body weight. Injection of diatrizoate caused a slight fall in PO2 in the renal cortex (from 42 +/- 4 to 38 +/- 4 mm Hg). In the medulla PO2 decreased significantly (from 34 +/- 6 to 20 +/- 4 mm Hg). Ringer's solution did not induce any changes.

Animals↗
PubMed1997

Intrarenal oxygen tension measured by a modified clark electrode at normal and low blood pressure and after injection of x-ray contrast media.

The oxygen tension (pO2) in the rat kidney was studied using a Clark microelectrode with a guard cathode behind the sensing cathode. The mean (+/- SEM) outer tip diameter of the electrodes used was 5.5 +/- 1.9 microm. The zero-pO2 current amounted to 12.5 +/- 0.9 pA at 37 degrees C; at air saturation it was 252 +/- 22.9 pA. Rats with a systolic blood pressure (BP) above 80 mmHg (where 1 mmHg = 133 Pa) showed an average pO2 in the cortex of 45 +/- 2 mmHg and in the outer medulla of 31 +/-1 mmHg. In rats with a BP below 80 mmHg a paradoxically high outer medullary pO2 of 40 +/- 4 mmHg was found, while the pO2 in the cortex was 27 +/- 4 mmHg. Changes in pO2 were also noted in the renal cortex and outer medulla after intravenous injections of the x-ray contrast medium diatrizoate (370 mg iodine/ml). In rats with normal BP, injection of diatrizoate caused a slight fall in pO2 in the renal cortex, from 42 +/- 4 to 38 +/-4 mmHg. In the medulla pO2 decreased significantly from 34 +/- 6 to 20 +/-4 mmHg. Ringer's solution did not induce any changes.

Animals↗
PubMed1996

Effects of contrast media and mannitol on renal medullary blood flow and red cell aggregation in the rat kidney.

Hemodynamic factors may play a role in the development of acute renal failure following administration of contrast media (CM). In this study the effect of intravenous injection of contrast media and mannitol on red blood cell velocity (VRBC) and red blood cell aggregation in renal medullary vessels was studied in 58 rats. Renal medullary blood flow was investigated by a cross-correlation technique and by a visual aggregation score. The CM, namely diatrizoate, iopromide, iohexol, ioxaglate, iotrolan, were given in iodine equivalent doses (1600 mg/kg body wt). Mannitol (950 mOsm/liter) and Ringer's solution were used as controls. The same vessels were studied 30 minutes before and 30 minutes after injections. VRBC decreased significantly after injection of diatrizoate, iopromide, iohexol, iotrolan and mannitol. Ringer's solution and ioxaglate did not significantly alter medullary blood flow, while iotrolan and mannitol caused the largest decreases in VRBC. All CM and mannitol caused both red cell aggregation and cessation of blood flow. The decrease in blood flow and increase in red blood cell aggregation after injection of CM and mannitol may partly explain the occurrence of contrast medium-induced acute renal failure.

Acute Kidney Injury↗
PubMed1993

Effect of intravenous contrast media on proximal and distal tubular hydrostatic pressure in the rat kidney.

The effect of i.v. injection of contrast media (CM, 1,600 mg I/kg b.w.) on proximal and distal tubular hydrostatic pressure (PTHP, DTHP) in the rat was investigated using a micropuncture technique. The PTHP and DTHP after injection of diatrizoate, iohexol, ioxaglate, or mannitol returned to control values within approximately 20 min. However, following iotrolan injection PTHP was still elevated above control levels after 35 min while DTHP remained elevated throughout the experiment (50 min). Iotrolan has a lower osmotic potential than the other CM when given in equivalent iodine doses. The concentration of iotrolan may thus increase more along the tubules than the other CM and consequently lead to a higher viscosity of urine, resulting in increases in PTHP and DTHP. The high intratubular pressure induced by iotrolan may explain our previous findings of reduced single nephron glomerular filtration rate caused by this CM.

Animals↗
PubMed1992

Tubuglomerular feedback control in long-looped nephrons. Topical minireview.

The tubuloglomerular feedback mechanism is highly activated in juxtamedullary nephrons and considered to play a major role in intrarenal regulation of glomerular filtration rate. The vasculature of juxtamedullary nephrons is highly vasoreactive with a high ability for vasodilation. This vasoreactivity is a prerequisite for an important influence of the tubuloglomerular feedback mechanism on the medullary blood flow and its regulation.

Animals↗
PubMed1991

Sodium and potassium load in the loop of Henle, measured with intact and blocked tubuloglomerular feedback mechanism in juxtamedullary nephrons.

For the juxtamedullary nephrons only the loop of Henle is easily accessible for micropuncture. We have shown that the tubuloglomerular feedback (TGF) mechanism is highly activated in these nephrons. Techniques have been developed for measurements on these nephrons without disrupting the normal flow to the macula densa. The tubular flow rate was measured by a real-time videodensitometric method in juxtamedullary nephrons in Lewis x DA rats. For the determination of tubular fluid composition a small fraction (less than 10%) of the fluid was sampled. Measurements were also performed according to the conventional technique, where all the tubular fluid was sampled. Despite a more than twofold increase in tubular flow rate when the flow to the macula densa region was interrupted, sodium concentration was only reduced by 25%, whereas potassium concentration was reduced by 40%. The results demonstrate that interruption of the urine flow to the macula densa results in a 52% increase in the tubular load of Na in the loop of Henle of juxtamedullary nephrons, and a corresponding increase of 24% for K. Thus, TGF exerts a strong influence on these nephrons which is why previous data on water and electrolyte loads, based on stop-flow measurements, greatly overestimate these loads.

Animals↗
PubMed1990

Effect of papillary exposure on intrarenal distribution of glomerular filtration rate and of plasma flow.

Removal of the renal pelvis in order to expose the renal papilla has been shown to cause impairment of the renal concentrating ability by an unknown mechanism. To study this phenomenon, urine osmolality (Uosm), single-nephron glomerular filtration rate (SNGFR) in outer and inner cortical nephrons and the inner and outer medullary plasma flow were determined. Measurements were performed on groups of rats before (control) and 15, 45 and 90 min after exposure of the left renal papilla. Rats with an intact ureter were studied in parallel to see whether the variables varied within the 90-min period of the study. In all groups of animals with an exposed papilla, Uosm was lower than in non-exposed animals. Outer cortical SNGFR in rats with exposed papillae, regardless of time, was not different from that in control rats. Inner cortical SNGFR after 45 and 90 min of exposure did not differ from that in controls, but after 15 min of exposure it was lower than in control animals. Outer and inner medullary plasma flow did not differ between rats with exposed papillae and controls, irrespective of exposure time. In conclusion, papillary exposure results in a permanent decrease in urine osmolality. This impairment of the concentrating ability cannot be attributed to prolonged changes in renal haemodynamics.

Animals↗
PubMed1988

Effects of intravenous contrast media on cortical and medullary blood flow in the rat kidney.

The effect of slow intravenous infusion of contrast medium (CM) (1600 mg I/kg body weight) on cortical blood flow (BF) and medullary BF in rat kidneys was investigated by laser-Doppler flowmetry on either renal cortex or exposed renal papillas (inner medulla). The effect on cortical BF was evaluated after infusion of either ioxaglate, iohexol, or ioxithalamate. Mannitol and Ringer's solution were used as control substances. The effect on medullary BF was examined after infusion of either ioxaglate, iohexol, iopamidol, ioxithalamate, or mannitol. BF was measured continuously during a 30-minute control period and a 60-minute experimental period, starting with the CM infusion. Cortical BF was unchanged in the ioxaglate group and significantly increased in the iohexol, ioxithalamate, and mannitol groups (P less than .05). Medullary BF was moderately increased in the ioxaglate group (P less than .05) but moderately decreased in the groups that received iohexol, iopamidol, ioxithalamate, or mannitol (P less than .05). The reduction in medullary BF following infusion of the ratio 3.0 nonionic CM and of the ratio 1.5 ionic CM might be one contributory mechanism to the pathogenesis of CM nephropathy, especially in the presence of microangiopathy in the kidney.

Animals↗
PubMed1988

Renal effects of atriopeptin II and dopamine receptor blockade in acutely volume-expanded rats.

Studies were made of the effects of continuous intravenous infusion of a synthetic atrial natriuretic factor (ANF) or, pre-treatment with the dopamine receptor antagonist haloperidol, on the renal response in anaesthetized rats subjected to volume expansion with an isotonic solution at 2% kg-1 body weight (wt) h-1. A time-control group receiving vehicle alone was studied in parallel. Measurements were compared 75 and 145 min after initiation of the volume expansion. Seventy minutes of Atriopeptin II infusion at 10 micrograms h-1 kg-1 body wt did not significantly alter the glomerular filtration rate [control value 1.29 +/- 0.10 ml min-1 g-1 kidney wt (n = 7, mean +/- 1 SEM), experimental value 1.20 +/- 0.12], but increased sodium excretion by 49% (from 2.87 +/- 0.56 to 4.27 +/- 0.45 mumol min-1). The arterial blood pressure was reduced by 9%. In previous investigations we found that in the same dosage Atriopeptin II increased sodium excretion 10-fold in euvolaemic animals. In the time-control group (n = 7) the response was similar to that in the atrial natriuretic factor-treated animals with the exception that the blood pressure was unaltered. Thus, glomerular filtration rate showed no statistically significant change (1.28 +/- 0.06 vs. 1.27 +/- 0.09 ml min-1 g-1 kidney wt) while the sodium excretion increased by 96% (from 2.29 +/- 0.22 to 4.50 +/- 0.49 mumol min-1). In animals pretreated with haloperidol (n = 5), the natriuretic response to the volume expansion was attenuated and was about ten times below that in the time-control group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

CNS-induced natriuresis during dopamine receptor blockade. Further support for the existence of, at least, two separate natriuretic hormonal systems.

Intracerebroventricular (ICV) stimulation with hypertonic sodium chloride solutions has previously shown indications to stimulate the release of a blood-borne natriuretic factor. Sodium excretion in this situation increases in the order of 10-20 times. Acute isotonic volume expansion has shown to be a potent stimulus for endogenous release of the atrial natriuretic factor (ANF). It has also been demonstrated that the natriuretic response to both volume expansion and exogenously applied ANF can be attenuated by the dopamine receptor blocker haloperidol. The present study was performed to investigate if the natriuretic response to ICV stimulation also could be attenuated with haloperidol, thus indicating similar effector mechanisms as for ANF. A first group of anaesthetized animals was, therefore, pre-treated with haloperidol (H) and then ICV stimulated (H-ICV). A second group of animals was subjected to acute isotonic volume expansion (VE, 2% b.w.h.-1) to evoke the documented ANF release. In a third group of animals pre-treatment with haloperidol was followed by volume expansion (H-VE). In the H-ICV group there was a more than 30-fold increase in sodium excretion, due to an increase both in urine flow rate (more than sixfold) and in the urinary concentration of sodium (more than fourfold). Potassium excretion increased more than eightfold, urine osmolality was unchanged, and blood pressure increased by 7%. In the VE group sodium excretion increased more than 18-fold, consequent to large increases in urine flow rate (more than 23-fold), while the urinary concentration of sodium tended to decrease. Potassium excretion increased more than threefold, urine osmolality decreased by 88%, and blood pressure was unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Increase in proximal tubular fluid reabsorption by renal nerve stimulation. A split oil droplet study.

The influence of renal sympathetic nerve stimulation on fluid reabsorption in the proximal tubules was studied in anaesthetized male Sprague-Dawley rats. Direct stimulation with a frequency of 2 Hz was applied, and a modification of the split oil droplet technique was used. The fluid reabsorption was determined as the half-time (t1/2) of the shrinking droplet. In the control situation t1/2 was 30.7 +/- 3.4 s. On stimulation at 2 Hz, t1/2 decreased in all nine rats studied by an average of 25 +/- 5%, to 22.4 +/- 2.6 s (P less than 0.01). The decrease in t1/2 indicates an increased rate of proximal tubular fluid reabsorption. The results support the concept that the anatomically established adrenergic innervation of renal proximal tubules participates in the direct regulation of tubular fluid reabsorption, a role which might be important in the control of the extracellular volume.

Animals↗
PubMed1988

The calcium entry blocker verapamil increases red cell flux in the vasa recta of the exposed renal papilla.

To investigate the vasoreactivity of the vessels of the juxtamedullary vasculature, measurements were made of the red blood cell flux (Qrbc) in the vasa recta of the exposed renal papilla of anaesthetized rats by means of fluorescently labelled erythrocytes. The flux was measured before and after intravenous administration of the calcium entry blocker verapamil, which was infused in two different doses. A control group receiving vehicle was studied in parallel. The lower dose of verapamil (0.6 mg h-1 kg-1 body wt) increased Qrbc by 30 +/- 6% (n = 9, P less than 0.05, mean +/- 1 SEM) and reduced the systemic blood pressure by 6% (P less than 0.05). The osmolality of urine samples from the papillary tip remained statistically unchanged (1199 +/- 60 vs. 1186 +/- 102 mosM kg-1 H2O). In the animals receiving the higher dose of verapamil (2.4 mg h-1 kg-1 body wt), Qrbc increased by 39 +/- 7% (n = 10, P less than 0.05) and the blood pressure was reduced by 9% (P less than 0.05), while urine osmolality was unchanged (1104 +/- 110 vs. 1264 +/- 123 mosM kg-1 H2O). In the time control group there was no statistically significant change in Qrbc (+6 +/- 8%, n = 10), blood pressure or urine osmolality (1006 +/- 61 vs. 1091 +/- 70 mosM kg-1 H2O). The verapamil-induced increase in Qrbc is probably mainly mediated by a relaxation of the afferent arteriole of the juxtamedullary nephrons. The results confirm our previous indication of a high vasoreactivity in the vessels of the juxtamedullary vasculature.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Atrial natriuretic factor, urinary catechol compounds and electrolyte excretion in rats during normal hydration and isotonic volume expansion. Influence of dopamine receptor blockade.

To investigate the influence of acute isotonic volume expansion (VE) on the plasma concentration of atrial natriuretic factor (ANF), the excretion of catechol compounds and electrolytes and the whole kidney glomerular filtration rate (GFR), these variables were measured before and during 60 min of VE (2% of body weight per hour). Atrial natriuretic factor was measured at the end of the experiment. In a control group (n = 7) without volume expansion, plasma ANF was 58 +/- 4 pg ml-1. The excretion of sodium, dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), noradrenaline (NA) and GFR did not change during the control study. In VE animals (n = 7) plasma ANF was 82 +/- 7 pg ml-1, significantly higher than in the control group. Sodium excretion increased more than 17-fold. The excretion of the DA increased by 38% and that of DOPAC by 30%. Noradrenaline excretion remained unchanged while GFR increased by 20%. In haloperidol-pretreated animals subjected to VE (n = 7), plasma ANF was 81 +/- 8 pg ml-1 during VE, significantly higher than in the control animals. Although the sodium excretion increased more than ninefold in this group during VE, this increase was only 55% of that in the VE group not given haloperidol. The DA and DOPAC excretion was increased by haloperidol, indicating a feedback effect of receptor blockade. DOPAC excretion was not increased further by VE, but the excretion of DA increased by 15% and GFR increased by 19%.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗