Biomedical subjects

L Karlberg

Publications and source records attributed to L Karlberg.

22 records · Page 2Linked to original sources

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↗