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T Bilde

Publications and source records attributed to T Bilde.

At least 37 records · Page 2Linked to original sources
PubMed1980

The effect of chlorpromazine pretreatment on the vascular function of kidneys damaged by warm ischaemia and cold storage in Collins' solution.

Vascular resistance was determined in 40 rabbit kidneys after graded warm ischaemia up to 60 minutes and preservation in Collins' solution for 24 and 48 hours. Half of the animals were treated with chlorpromazine 3.5 mg/kg before induction of the ischaemia. Vascular function was determined during short-term perfusion with TIS-U-SOL at 4 degrees C. The experiments showed that warm ischaemia of 30 and 60 minutes duration gave an increase in vascular resistance. The increase was, however, smaller in kidneys pretreated with chlorpromazine. Preservation in Collins' solution for 24 and 48 hours did not change this correlation. Determination of the weights and thereby formation of oedema showed that all kidneys preserved had a small increase in weight. No difference was found between pretreated kidneys and untreated kidneys. It is concluded that pretreatment with chlorpromazine is capable of diminishing vascular contraction during the warm ischaemic period and that preservation in Collins' solution for up to 48 hours does not alter this beneficial effect.

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PubMed1980

The 125I-Hippuran renogram in rabbit kidneys after graded warm ischaemia.

125I-Hippuran renography was performed after temporary renal arterial clamping in contralateral nephrectomized rabbits. Mean renograms for the experimenttal groups were calculated for 0, 1, 1 1/2, 2, 2 1/2 and 3 h of warm ischaemia. The appearance phase, the 1 min uptake phase and excretion ratio were evaluated. The kidney function was monitored by serum-creatinine. Warm ischaemia of 1, 1 1/2 and 2 h resulted in a late maximum peak and delayed excretion, and for the last group in an accumulation curve. The uptake capacity was normal for these groups. Protracted ischaemia of 2 1/2 and 3 h affected also the appearance and uptake phase resulting in a slower and decreased Hippuran uptake of 50% and 34% respectively. Duration of warm ischaemia and changes in the renogram were well correlated. A normal uptake phase predicts restitution of the kidney function and 100% survival.

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PubMed1979

Renographic evaluation of kidney preservation with chlorpromazine.

The effect of chlorpromazine pretreatment of kidneys then damaged by warm ischemia was investigated. The ischemia was inflicted on rabbit kidneys by renal arterial occlusion of 1 1/2 and 3 hours' duration after contralateral nephrectomy. Pretreatment with chlorpromazine, 3.5 mg/kg, was given intravenously before arterial clamping. I-125 Hippuran renography was performed before clamping, immediately after clamp release, and at 2, 4, 6, and 14 days later. Serum creatinine and survival rate were followed. Comparison with untreated control groups was made. The effect on tubular function was investigated by measuring I-125 Hippuran uptake in pretreated slices of renal cortex (compared with untreated contralateral kidney) 48 hr after circulation was restored to the ischemic kidney. Chlorpromazine pretreatment improved recovery from ischemic damage: the renograms showed improved Hippuran uptake after clamp removal, and return to normal was faster. Survival rate after 3 hr of ischemia increased from 1/10 to 6/10 in the pretreated group, and serum creatinine recovered earlier. Hippuran uptake in slices of cortex showed no significant improvement because of pretreatment. It is concluded that the beneficial effect of chlorpromazine pretreatment must be because of decreased vascular resistance, leading to long-lasting increased postischemic renal blood flow.

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PubMed1978

Vascular function in kidneys preserved by simple cold storage in Sacks' or Collins' solutions.

Vascular resistance was determined in 40 kidneys after preservation in Collins' or Sacks' solution for 24 and 48 hours. Kidneys without warm ischaemia and kidneys with up to 60 min of warm ischaemia prior to preservation were investigated, vascular resistance was determined during short time perfusion with Tis-U-Sol at 4 degrees. The experiments showed that cold preservation of kidneys with no warm ischaemia or 15 min of warm ischaemia gave a small increase in vascular resistance, independent of the solution used. 30 and 60 min of warm ischaemia gave a considerable increase in vascular resistance, but less increase was found in kidneys preserved in Sacks' solution. Determination of the weights and thereby formation of oedema showed slight dehydration in kidneys preserved in Sacks' solution. Kidneys preserved in Collins' solution showed small increase in weight. No correlation was, however, found between the vascular resistance and degree of oedema.

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PubMed1977

The effect of chlorpromazine pretreatment on renal function and pathology in kidneys damaged by warm ischaemia.

The influence of chlorpromazine pretreatment on kidney function and survival after temporary occlusion of the renal artery was investigated. Three hours of clamping of the renal artery and contralateral nephrectomy was performed in a group of ten rabbits pretreated with 3.5 mg/kg chlorpromazine and compared with a previously published control group of untreated animals. Chlorpromazine pretreatment improved survival. The kidney function, estimated by serum-creatinine, showed an earlier onset of function and the surviving animals regained nearly normal function. Histological examination revealed mild to moderate ischaemic changes, whereas the control group showed more profound damages.

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PubMed1977

The effect of chlorpromazine pretreatment on the vascular resistance in kidneys following warm ischaemia.

In studies of 45 rabbits pretreated by chlorpromazine, clamping of the renal artery was performed. Chlorpromazine 3.5 mg/kg was given intravenously 15 min before arterial clamping. The duration of the clamping period ranged from 0 to 180 min. After removal of the kidneys the influence of the pretreatment on the vascular resistance was examined in perfusion studies. Resistance patterns were measured during hypothermic perfusion. The results were compared with an identical group without pretreatment. The vascular resistance rose with the duration of clamping but was lower than in the control group. The maximal resistance attained after 60 min of clamping was approximately 50% lower. In another series of chlorpromazine pretreated animals clamping of the renal artery for 180 min was followed by reestablishment of the circulation for 24 and 48 hours. Perfusion studies were performed on kidneys after removal. The results were compared with a group without pretreatment. The vascular resistance was found to return to normal values more rapidly when the animals had been pretreated with chlorpromazine.

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PubMed1977

The influence of warm ischaemia on renal function and pathology.

Temporary occlusion of the left renal artery for 0-180 min after contralateral nephrectomy was undertaken in 51 rabbits. The correlation between the injury of warm ischaemia and kidney function, survival and histology was evaluated. After 0, 60, 90 and 120 min occlusion, all animals survived and normal renal function was restored. After occlusion for 150 min only 4 of 10 animals survived, and normal renal function was not re-established. 180 min occlusion was detrimental to the animals. Only one out of ten survived with severely damaged kidney function. Histological findings were consistent with the experimental observations of renal function.

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PubMed1977

The effect of chlorpromazine and heparin pretreatment on kidney viability and function after warm ischaemic damage.

The influence of chlorpromazine and heparin pretreament on kidney function and histology has been investigated in rabbit kidneys damaged by warm ischaemia. Three experimental groups were investigated. One in which animals were pretreated with heparin, one group pretreated with heparin and chlorpromazine, and one group without pretreatment. The left renal artery was temporarily clamped for 3 hours and the kidneys recirculated. After 2-3 weeks a delayed contralateral nephrectomy was made, and after another 2-3 weeks all kidneys were studied histologically. Kidney function was measured by determination of serum-creatinine. The experiments showed, that all animals survived with impaired renal function. Pretreatment with chlorpromazine and heparin did not affect the final results. Secerity of the ischaemic damage, histologically evaluated was the same in all groups.

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PubMed1976

The integrity of tubular cell function after preservation in Collins' or Sacks' solution.

Collins' solution is an excellent medium for kidney preservation by simple cold storage before transplantation. Efforts by Sacks et al. to improve this technique by modifying the composition seemed promising. A comparison between ability of these two media to preserve the tubular cell was attempted. The viability of the tubular cells was evaluated by measuring the 125 I Hippuran uptake in cortex slices taken from kidneys preserved for 24 and 48 hr in the respective solutions. Kidneys exposed to as well as kidneys not exposed to warm ischaemia were used. Collins' solution was found to be superior in protecting the cell function. Nonetheless intracellular oedema during preservation was greater after preservation in this solution as compared with cells preserved in Sacks' solution.

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PubMed1976

Vascular resistance in hypothermically perfused kidneys damaged by warm ischemia.

Vascular resistance was determined during hypothermic perfusion of rabbit kidneys after various periods of warm ischemia. Ischemia was induced by clamping of the renal artery, or of the renal artery and vein, in situ. Studies were made after periods of clamping ranging from 0 to 180 min. The perfusing fluid was 5% Dextran of low molecular weight in balanced saline solution (Tis-U-Sol), with addition of 5 mg % Papaverin. When the renal artery was clamped for more than 15 min, vascular resistance increased. Maximal resistance was reached after 60 min of clamping, and was 3 times as high as that value in the control group of kidneys which were not clamped. The vascular resistance attained after 60 min of clamping did not further increase when clamping was maintained for 180 min. When both the renal artery and the renal vein were clamped vascular resistance first increased after 30 min. Maximal resistance was reached after 60 min of clamping, but was only 1/2 of that level seen when the renal artery alone was clamped.

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PubMed1976

The influence of an agonal phase on the vascular resistance of the kidney measured during hypothermic perfusion studies.

The influence of the agonal phase on the rabbit renal vascular resistance during warm ischemia was studied in 24 hypothermic perfusion experiments. The agonal phase was induced by tracheal clamping in anesthetized animals. The interval from strangulation to cardiac arrest was, on average, 8.1 min. Kidneys were removed between 0 and 60 min after cardiac arrest. Comparison with an earlier study where warm ischemia was induced by clamping of the renal artery shows that the agonal phase is not a significant factor in that renal vascular resistance is not increased.

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PubMed1976

The effect of temporary clamping of the renal vessels on the vascular resistance in rabbit kidneys.

In studies of 45 rabbits, either the renal artery (35 animals), or the renal artery and vein (10 animals) were clamped in situ. The effect of the clamping--of the warm ischemia--on the vascular resistance of the kidney after reestablishment of the circulation was examined in perfusion studies made after removal of the kidneys from groups of 5 animals between 1 and 5 days after revascularization. Resistance patterns were measured during hypothermic perfusion. The results confirm earlier findings that vascular resistance increases in proportion to the duration of warm ischemia up to 60 min, but not thereafter. The renal vascular resistance falls over the days following revascularization, more slowly after longer periods of ischemia. Thus after 60 min of warm ischemia the vascular resistance became normal within 24 hours, but after 180 min of warm ischemia, the normal resistance range was not reached until 96 hours after reestablishment of the circulation. When both the renal artery and the renal vein were clamped, the pattern was the same but much less emphatic. The vascular resistance never attained such high values as seen after clamping of the renal artery alone, and became normal after 24 hours of revascularization, even when the period of warm ischemia was as long as 180 min.

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PubMed1976

The collateral blood flow and hippuran clearance of the rabbit kidney after occlusion of the renal artery.

The collateral blood flow to the rabbit kidney was determined by two methods: (1) measurement of the venous flow after clamping of the renal artery and (2) Hippuran clearance of the clamped kidney. The collateral blood flow was found to be 0.012 ml/min/g kidney equivalent to 0.2% of the entire blood flow to the rabbit kidney. Compared with collateral blood flow in other mammals (as humans and dogs) with a collateral flow of 6.2% of the normal flow, the collateral blood flow in the rabbit is very modest. The cranial ureteric artery contributes more than 90% of the entire blood flow, while capsular perforants, important in other mammals, play no role in the supply of the rabbit kidney. Only 50% of the collateral blood flow passes the tubular system. Flow to the medulla calculated from Hippuran clearance was 35% greater than flow to the cortical part of the kidney. The subcapsular cortical tubuli were able to absorb Hippuran from the peritoneal fluid and surrounding tissues after the kidney was dissected free from its surroundings and all vessels severed. Absorption corresponded to an arbitrary serum flow of 0.0002 ml/min/g.

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PubMed1976

The uptake of hippuran in kidney slices employed as a viability test.

125J Hippuran uptake in slices from rabbit kidneys was measured in kidneys damaged by warm ischaemia alone as well as by warm ischaemia combined with 24 hours of cold ischaemia. The Hippuran uptake was calculated as the ratio between radioactivity in the slices and the activity in the incubation medium as a slice/medium ratio (S/M). S/M was unchanged after 15 minutes, 30 minutes and 1 hour of warm ischaemia, while in kidneys exposed to 2 hours of warm ischaemia a 15% decrease in S/M ratio compared with control values was noted. A 53% decrease was observed after 3 hours of warm ischaemia and 73% and 91% after 4 and 5 hours respectively. Twenty-four hours of cold ischaemia alone did not alter the Hippuran uptake, but prolonging this with 15 minutes of warm ischaemia precipitated a significant fall (25%) in S/M. This value remained constant during the first hour of warm ischaemia, but a fall of 64% was observed after 2 hours of warm and 24 hours of cold ischaemia. These findings were in agreement with experiments on kidneys damaged by arterial occlusion and recirculated. Two hours of warm ischaemia was the maximal damage the kidneys could endure and still regain normal function. After simple preservation methods with Collins solution for 24 hours, 1 additional hour of warm ischaemia was the maximal ischaemic damage the kidney was able to withstand. Hippuran uptake in kidney slices appears to be well correlated to the kidneys' ability to regain normal function after ischaemic damage.

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PubMed1976

The effect of chlorpromazine pretreatment on tubular function in kidney preservation.

The effect of Chlorpromazine pretreatment on tubular function was investigated. Hippuran uptake in cortex slices from rabbit kidneys was measured after one hour of incubation in a medium containing Hippuran. Before measurement the kidneys were exposed to varying periods of warm ischaemia or/and cooled and preserved for 24 hours in Collins solution. Chlorpromazine treated and untreated groups of animals were compared, the results obtained were identical in both groups. In contra distinction to these findings, addition of Chlorpromazine to the incubation fluid inhibited uptake of Hippuran in the kidney slices. The effects of pretreatment with Chlorpromazine on the kidney function after ischaemic damage were demonstrated. Serum-creatinine and survival were compared in a treated and an untreated group after 3 hours of temporary clamping of the renal artery. Pretreatment resulted in earlier onset of function and better survival. It is concluded that the antimetabolic effect of Chlorpromazine is opposed to its vasodilatory properties is of little practical importance for the viability of the kidney damaged by ischaemia.

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