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P Liss

Publications and source records attributed to P Liss.

30 records · Page 2Linked to original sources

Hypoperfusion in the renal outer medulla after injection of contrast media in rats.

PURPOSE: The effect on regional renal blood was studied after injection of nonionic iso-osmolar iotrolan or ionic high-osmolar iothalamate. MATERIAL AND METHODS: Laser-Doppler flowmetry was used to measure outer medullary (OMBF) and superficial cortical blood flow (CBF) simultaneously in anesthetized rats. Iotrolan (320 mOsm/kg H2O) was injected i.v. at a dose of 600 mg I/kg b.w. (normal dose) over 2 min or 1,600 (high dose) mg I/kg b.w. over 2 or 8 min. Iothalamate (2,580 mOsm/kg H2O) was injected i.v. at a dose of 1,600 (high dose) or 2,900 (extremely high dose) mg I/kg b.w. over 2 min. RESULTS: At the normal dose and 2-min injection of iotrolan, OMBF was reduced by 25+/-9% over 20 min. The high dose of iotrolan injected over 8 min resulted in a reduction in OMBF slightly smaller (17+/-9%) than that induced by the normal dose but lasting longer (30 min). Compared to the normal dose, the high dose and fast (2 min) injection of iotrolan resulted in a greater and more prolonged decrease in OMBF (32+/-6% lasting 50 min). After the high dose of iothalamate (1,600 mg I/kg) there was a decrease in OMBF by 21+/-6%, lasting 30 min. An extremely high dose (2,900 mg I/kg b.w.) gave a heterogeneous response with a mean increase in OMBF of 48+/-24% occurring 60 min after the injection. CONCLUSION: Iso-osmolar and high-osmolar contrast media (CM), at normal and high doses, decrease OMBF, while an extremely high dose of iothalamate may result in an increase. The depression of outer medullary perfusion may have implications for CM-induced acute renal failure in view of the vulnerability of this region to a decrease in oxygen tension.

Animals↗

The haemodynamic effects of iodinated water soluble radiographic contrast media: a review.

All classes of iodinated water-soluble radiographic contrast media (RCM) are vasoactive with the iso-osmolar dimers inducing the least changes in the vascular tone. The mechanisms responsible for RCM-induced changes in the vascular tone are not fully understood and could be multifactorial. A direct effect on the vascular smooth muscle cells causing alterations in the ion exchanges across the cell membrane is thought to be an important factor in RCM-induced vasodilatation. The release of the endogenous vasoactive mediators adenosine and endothelin may also play a crucial role in the haemodynamic effects of RCM particularly in the kidney. In addition, the effects of RCM on blood rheology can cause a reduction in the blood flow in the microcirculation. The purpose of this review is to discuss the pathophysiology of the haemodynamic effects of RCM and to offer some insight into the biology of the endothelium and vascular smooth muscle cells as well as the pharmacology of the important vasoactive mediators endothelin and adenosine.

Adenosine↗

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↗

Measurements of oxygen tension in native and transplanted rat pancreatic islets.

This study was performed to measure the oxygen tension before and after revascularization of pancreatic islets transplanted beneath the renal capsule and to investigate to what extent this was affected by acute and chronic hyperglycemia. In addition, the oxygen tension in islets within the pancreas was determined. PO2 was measured with a modified Clark electrode (tip 2-6 microm o.d.). Within native pancreatic islets, the mean PO2 was higher (31-37 mmHg) than within the exocrine pancreas (20-23 mmHg). The mean oxygen tension in the transplanted islets the day after implantation was half of that recorded in native islets (14-19 mmHg) and did not differ between normoglycemic and diabetic recipients. At 1 month after transplantation, when revascularization had occurred, the mean PO2 in the islet grafts was 9-15 mmHgf in normoglycemic animals but was lower (6-8 mmHg) in diabetic animals, whereas the blood perfusion of the transplants, as measured with laser-Doppler flowmetry (probe diameter 0.45 mm), was similar in both groups. The mean oxygen tension in the superficial renal cortex surrounding the implanted islets was similar in all groups and remained stable at 13-21 mmHg. Intravenous administration of D-glucose (1 g/kg) did not affect the oxygen tension in any of the investigated tissues. We conclude that the mean PO2 in islets implanted under the renal capsule is markedly lower than in native islets, not only in the immediate posttransplantation period but also 1 month after implantation, i.e., when revascularization has occurred. Furthermore, persistent hyperglycemia in the recipient leads to a further decrease in graft oxygen tension. To what extent this may contribute to islet graft failure is at present unknown.

3-O-Methylglucose↗

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↗

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↗

Effects of contrast media on renal microcirculation and oxygen tension. An experimental study in the rat.

It has been suggested that nephrotoxic effects of X-ray contrast media (CM) are exerted via renal medullary hypoperfusion and hypoxia. This study was therefore undertaken to investigate the effects of CM injection on renal medullary microcirculation and oxygen tension. Red blood cell velocity (VRBC) in the renal medullary vessels was measured by a cross-correlation technique and was found to be decreased by mannitol and by all CM tested except ioxaglate. The incidence of red blood cell aggregation and cessation of blood flow in the renal medullary vessels was estimated with use of a score based on visual observations. All tested CM and mannitol induced aggregation in the renal medullary vessels. The ionic CM ioxaglate was found to induce the least aggregation. Modified Clark PO2 microelectrodes with a guard cathode were constructed and adapted for tissue PO2 measurements. PO2 was measured simultaneously in the renal cortex and outer renal medulla. The PO2 in rats with blood pressure (BP) above 80 mm Hg was found to be lower in the medulla than in the cortex. In rats with BP below 80 mm Hg the PO2 was paradoxically higher in the outer medulla than in the cortex, probably due to a decrease in the glomerular filtration rate and hence in sodium uptake from the tubules. After injection of all tested CM, PO2 in the renal cortex remained unchanged, while in the outer medulla it decreased. There was no difference in the decrease in PO2 between the tested CM. The decrease in outer medullary PO2 was prevented by injection of furosemide but not by injection of mannitol. A decrease in VRBC and PO2 in the renal medulla may be an underlying cause of CM-induced acute renal failure.

Acute Kidney Injury↗

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↗

Interruption of dot processing by a backward mask.

A white target field with 0-10 randomly positioned black dots was presented for 20 ms, and followed by a patterned mask with a duration of 200 ms. Subjects reported target numerosity, with strict or lax criteria. Numerosity functions, and control forced-choice discrimination results, supported an interruption model for backward masking by pattern, even for stimulus onset asynchronies as short as 50 ms. When the same targets were degraded by reducing their contrast, but not otherwise masked, results supported an integration model.

Discrimination Learning↗