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Biomedical subjects

J Tange

Publications and source records attributed to J Tange.

11 recordsLinked to original sources
PubMed1987

Atrial natriuretic peptide in dehydrated Long-Evans rats and Brattleboro rats.

Atrial natriuretic peptide (ANP) was measured by radioimmunoassay in atrial and plasma extracts from normal Long-Evans (LE) rats and Brattleboro-strain diabetes insipidus (DI) rats. LE rats, dehydrated for 72 hours, had an increased plasma osmolality and plasma vasopressin. They also demonstrated a higher atrial immunoreactive ANP (IR-ANP) content than hydrated animals (72 hr dehydration: 178.2 +/- 30.4 micrograms/g wet weight atria, mean +/- SE, control: 60.4 +/- 8.2; P less than 0.001). Plasma IR-ANP in dehydrated LE rats tended to be lower than hydrated LE but this was not statistically significant [72 hr dehydration: 61.9 +/- 5.9 pg/ml, control: 82.4 +/- 8.2]. IR-ANP concentration in atrial extracts from DI rats, without detectable plasma vasopressin levels but with increased plasma osmolality, was not different from that in hydrated LE rats (DI: 100.6 +/- 13.2 micrograms/g). There was also no significant difference between plasma IR-ANP in DI and hydrated LE rats (DI: 100.2 +/- 11.9 pg/ml). The atrial IR-ANP concentration in DI rats was decreased by infusion with either arginine-vasopressin (AVP) or 1-deamino-8-arginine vasopressin (DDAVP), and plasma IR-ANP was increased significantly by both infusions (AVP: 171.3 +/- 18.1 pg/ml, DDAVP: 179.5 +/- 24.6). Thus, changes in atrial and plasma IR-ANP concentration appeared to be associated with changes in water balance but not with plasma AVP levels, indicating that the changes in volume may be a more important factor controlling ANP release in vivo than vasopressin itself.

Animals↗
PubMed1987

Glomerular epithelial cell lesions in rat renal isografts.

Visceral glomerular epithelial cell lesions--microvillus formation, loss of foot processes, osmiophilic inclusion droplets, balloon-like malformation of cell processes, degeneration, necrosis, and loss of cell processes from capillary basement membranes--are found in rat renal isografts 1 mth after transplantation. The lesions, which are most readily recognized in perfusion-fixed material, are essentially focal, affecting neither all glomeruli, nor all cells in any glomerulus, bear no relation to the degree of interstitial nephritis in the graft, and are associated with albuminuria and with focal capillary sclerosis in some glomeruli. They are not restricted to renal isografts but are found in aging rats, in different experimental models of glomerular disease and in clinical glomerular disorders, again in association with proteinuria and glomerulosclerosis. It is therefore proposed that glomerular epithelial cell damage increases capillary permeability and impairs maintenance of the integrity of the capillary wall, leading to proteinuria and focal glomerulosclerosis.

Animals↗
PubMed1986

Glomerular damage after kidney preservation.

Severe proteinuria occurs during isolated organ perfusion of kidneys removed from SD and DA rats and subjected to 24-hr cold preservation. In both strains increased glomerular permeability was associated with changes in glomerular visceral epithelial cells, particularly cytoplasmic edema and detachment of cells from capillary basement membranes. Foot processes were intact and staining for sialoglycoprotein was retained. The changes were compatible with survival of the isograft kidney after transplantation, but moderate proteinuria was found in some rats after one month. Protein loss in the urine during isolated organ perfusion is very much less in kidneys subjected to 4-hr cold preservation, and the glomerular epithelial cells are normal or show only minimal cytoplasmic edema on electron microscopy. The experiment shows that significant damage to glomeruli may occur during preservation prior to transplantation, and the model itself can be usefully exploited to determine the relation between increased glomerular permeability to albumin and the associated changes in the glomerular capillary wall.

Animals↗
PubMed1985

The influence of the contralateral kidney upon recovery from unilateral warm renal ischemia.

Unilateral warm renal ischemia of 90 min duration was induced in rats and the contralateral normal kidney was removed either immediately or after 1, 2, 4 or 14 d. Contralateral nephrectomy at 2, 4, 14 d increased survival and modified the functional and morphological events of the recovery period. Optimal recovery was obtained by 4 d delay. When contralateral nephrectomy was delayed by 14 d, scarring of the ischemic kidney was more severe suggesting that regeneration of damaged nephrons was impaired when renal homeostasis was sustained by the contralateral kidney. Such biphasic and inverse effects of normal kidney tissue are likely to be important determinants of the natural history of severe unilateral renal damage.

Animals↗
PubMed1984

Studies in renal preservation using a rat kidney transplant model: II. The effect of reflushing with citrate.

This study investigated the possible beneficial effects of reflushing renal grafts with isotonic citrate solution. Rat kidneys were initially flushed with isotonic citrate or with Hartmann's solutions at O C. After 2 hr, half the kidneys of each group were reflushed with isotonic citrate; 22 hr later, all kidneys were transplanted into rats of the same inbred strain. All animals receiving kidneys flushed with Hartmann's solution died, whereas reflushing such kidneys with isotonic citrate significantly ameliorated the deleterious effects of Hartmann's solution. All animals receiving citrate-flushed kidneys survived with relatively good renal function and morphology. However, reflushing itself is not a beneficial procedure and is only of value where an ineffective preserving solution has been used to flush the kidneys initially. There is evidence that some of the adverse effects of flushing develop in the renal medulla.

Animals↗
PubMed1983

An experimental model for assessment of renal recovery from warm ischemia.

A study was made of the acute and chronic (15 days) functional and morphologic effects on the rat kidney of warm ischemia and contralateral nephrectomy, in order to define a suitable animal model for testing renal transplant preservation techniques when warm ischemia is a contributing factor. Spontaneous recovery from 30-min warm ischemia was complete, and the model was consequently unsuitable; the high mortality from 90 min was unacceptable. Warm ischemia of 60 minutes produced severe renal tubular necrosis, an acceptable mortality, residual morphologic damage, and impairment of isolated kidney perfusion parameters at 15 days. Renal function in vivo was normal in many of these animals, despite appreciable residual morphologic changes, and it is evident that functional data alone are not sufficient for assessment of preservation regimens.

Animals↗
PubMed1983

Studies of renal preservation using a rat kidney transplant model. Evaluation of citrate flushing.

Rat kidneys were flushed with isotonic citrate solution, hypertonic citrate solution, or Collins's C2 solution, and were stored hypothermically for 24 hr before transplantation into another rat of the same inbred colony. The number of animals surviving for one month was greatest with isotonic-citrate-flushed kidneys (82%), and least with Collins's C2 solution (27%). Functional and morphological damage after transplantation was consistently greater in Collins's-flushed grafts, as compared with citrate-flushed grafts. Best results were attained with the isotonic-citrate flushed grafts. Seven days after contralateral nephrectomy all surviving animals had elevated serum creatinine and urea concentrations, along with decreased creatinine clearance, and they had secreted large volumes of dilute urine. Renal function was best in animals with isotonic-citrate-flushed grafts. After one month, significant improvement in urine osmolality, creatinine clearance, and serum creatinine had occurred only in the rats with citrate-flushed grafts. There were no significant differences between the citrate groups. All surviving rats had some residual renal cortical damage, but severe interstitial nephritis (greater than 30%) was much less frequent in the citrate groups.

Animals↗
PubMed1983

Recovery of renal function after warm ischemia. I. The effect of chlorpromazine and phenoxybenzamine.

The effects of treatment with chlorpromazine (4 mg/kg) and phenoxybenzamine (1 and 5 mg/kg) on renal function and morphology after warm ischemia and contralateral nephrectomy were studied. Chlorpromazine pretreatment by intravenous injection 15 min before warm ischemia of 60 min resulted in the survival of all animals (cf. 75% in untreated group), with better renal function in the first week. Necrosis of the proximal convoluted tubule and ultimate residual cortical damage were less severe than in the untreated groups. Chlorpromazine was also beneficial after 75 min warm ischemia, although mortality was not reduced. Administration of chlorpromazine just prior to revascularization was ineffective, suggesting that sufficient concentration of the drug must be present in the kidney during the ischemic period or immediately after revascularization. Chlorpromazine probably protects the proximal tubular cells from ischemic damage. Phenoxybenzamine (1 mg/kg) was ineffective when administered 15 min before warm ischemia. A higher (5 mg/kg) dosage of the drug proved to be detrimental.

Animals↗
PubMed1982

The influence of metabolic variation on analgesic nephrotoxicity. Experiments with the Gunn rat.

The analgesics aspirin and paracetamol administered as single I.V. doses produce renal lesions in the homozygous Gunn rat. The lesions affect both cortex and medulla but are less severe than the renal lesions of analgesic nephropathy. By contrast the reactive compounds p-aminophenol and 5-aminosalicylic acid which are known to cause renal damage in other less susceptible strains respectively produce cortical and medullary renal lesions in homozygous Gunn rats which are as extensive as those found in patients with analgesic nephropathy. The increased frequency of renal lesions from the analgesics aspirin and paracetamol as compared to heterozygous and albino rats and the increased severity of the lesions due to p-aminophenol and 5-aminosalicylic acid is considered to be at least partly due to impaired glucuronide formation and consequent delayed excretion of nephrotoxic substances.

Acetaminophen↗
PubMed1980

Renal metabolism of paracetamol: studies in the isolated perfused rat kidney.

1. The metabolism of [3H]paracetamol has been studied in the perfused rat kidney. Seventy-four per cent of filtered paracetamol was reabsorbed. Paracetamol appeared in the urine; 90% was unaltered but 10% appeared as metabolites: the glucuronide, sulphate, mercapturic acid and cysteine conjugates. 2. At concentrations of paracetamol of 1--3 mmol/l no impairment of renal physiological function was observed. 3. The presence of the mercapturic acid and cysteine conjugates in the urine demonstrates the capacity of the kidney for oxidative metabolism of paracetamol and hence the formation of potentially toxic intermediates.

Acetaminophen↗