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.

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.

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.

No abstract

The pressure conditions at the distal end of the interlobular arteries and in the interlobular veins were investigated from the pressures obtained in superficial small arteries and veins, accidentally found on the kidney surface, during the subsequent blockade of the blood stream in the down-stream and up-stream direction, respectively. The results suggested a hydrostatic pressure in the distal end of the interlobular arteries of about 85 mm Hg under normotensive conditions-a pressure which remained fairly constant when the perfusion pressure in the renal artery was decreased within the autoregulation range. The results indicate a considerable pressure drop of about 40 mm Hg along the interlobular arteries. During hypotension this pressure drop decreased, implying a decreased resistance in the interlobular arteries, i.e. a typical autoregulative response. The pressure in the interlobular veins amounted to about 5 mm Hg, which is a few mm Hg higher than that in the renal vein and about 7 mm lower than that in the peritubular capillary network. The results suggest a flow resistance located somewhere between the peritubular capillaries and the intrarenal veins. This resistance is not influenced by vasoactive substances but it is decreased when the systemic venous pressure is raised above 10 mm Hg. The resistance seems to act in the direction of protecting the peritubular capillaries from minor changes in the central venous pressure.