Alleviation of ischaemic acute renal failure by beta blockers: specific tubular receptor blockade or membrane stabilising effect?
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Biomedical subjects
Publications and source records attributed to I Serban.
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Beta-adrenergic blockade by oral propanolol in five cirrhotic patients caused changes in the handling of an acute sodium load. Fractional sodium excretion following an acute saline load increased from 0.69% +/- 0.29 to 1.49% +/- 0.11 (103 microEq/min +/- 7.5 to 129 microEq/min +/- 18) before propranolol administration. After 3 days of oral propanolol 1 mg/kg day, the fractional excretion of sodium by saline loading increased from 0.52% +/- 0.19 to 2.17 +/- 0.19 (109 microEq/min +/- 9 to 178 microEq/min +/- 11). This change was not accompanied by changes in GFR, RPF or in the renin-aldosterone system. The possibility that these changes are caused by a change in the sodium transport at the tubular cell level induced by the beta-adrenergic blockade, is entertained.
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Plasma renin activity (PRA) of infant rats is high until some time between the 3rd and 4th week after birth. Mothers, however, return PRA to normal by 2 weeks post partum. The rate of disappearance endogenous PRA of nephrectomized rats is slower in those animals having gigh PRA than in mature rats. Disappearance curves of endogenous PRA of mothers post partum is also the same as that of normal mature females. Part of the high PRA of the neonate can thereby be the related to the lower rate of destruction. Total kidney renin content increases with age. Renal renin activity (RRA) is low only during the 1st postnatal week when expressed in terms of whole kidney weight and compared to later postnatal times. Although there are some slight differences in the means in older animals, none are statistically significant.
A RIA method for the measurement of RRA is described, based upon the incubation of two dilutions of kidney extract with a fixed amount of EDTA-anticoagulated anephric rat plasma. The RIA of the generated angiotensin I is carried out with the commercially available NEN Kit. Recovery of angiotensin I added to the incubation mixture was 98 percent. There were 113 kidneys with a wide range of renin activity (52 to 1,274 ng. angiotensinl/mg. of kidney per hour) assayed. The within-assay coefficient of variation was uniform throughout the range, equalling 4.4 percent. The between-assay variance was practically identical with the within-assay variance. The confidence interval to the mean RRA level of one pair of readings was 5.4 percent of this mean.
The effect of saline loading was compared in two types of experimental acute renal failure--due to i.m. administration of glycerol or to anoxia. In the glycerol model, chronic saline loading for about three weeks prior to the experiment achieved almost complete prevention of the uremia. The blood urea and serum creatinine levels 24 h after the experiment were 44 +/- 2 and 1.3 +/- 0.3 se) mg/dl, respectively. The values for the water-drinking rats were 292 +/- 23 and 3.7 +/- 0.4 mg/dl, respectively. In the anoxic model of acute renal failure, produced by uninephrectomy and contralateral renal artery clamping, chronic saline loading reduced the severity of the resultant uremia, although less impressively than in the glycerol model. The blood urea and serum creatinine 24 h after the experiment were 148 +/- 15 and 1.8 +/- 0.2 mg/dl, respectively. The values for the water-drinking rats were 237 +/- 15 and 2.3 +/- 0.2 mg/dl, respectively. Plasma renin activity was similar in the saline-loaded rats in both the toxic and anoxic models. It seems, therefore, that all known models of acute renal failure have at least a common pathogenic mechanism, which can be influenced by chronic saline loading prior to onset of the disease, and which is most probably not renin dependent. In the anoxic model additional factors, which cannot be counteracted by chronic saline loading, are active in the development of uremia.
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The present paper reports on 34 cases of meningococcal meningitis admitted during the last three years to the Clinic of Communicable Diseases of Cluj. The incidence was higher in adolescents and young adults (76%). The clinical form was severe in 10 cases, medium in 19 cases and mild in 5 cases. All the patients recovered, with a mean duration of the disease of 9-12 days. No sequelae or relapses were recorded. The treatment was based upon penicillin G, 15 million U/day. In 17 cases sulfonamides were associated and in 5 cases chloramphenicol and ampicillin. In 29 cases intravenous, intramuscular or oral cortisone was administered and in 5 cases intrathecally. The results obtained in the cases treated only with penicillin were identical to those obtained by an associated therapy. Worthy of note was the decrease of the sensitivity of meningococci to sulfonamides and chloramphenicol and their increased resistance to tetracyclin and erythromycin.
Over a six year period, in the Clinic of Communicable Diseases of Cluj Napoca, 2301 patients with staphylococcal infections were admitted to the Clinic, representing 8% of the total number of patients admitted, and 3513 staphylococcal strains were isolated. A number of 43 of the 2301 patients died (1.8%), but staphylococcal infection was actually the cause of death in only 35 cases (1.5%) (septicemia, staphylococcal meningitis and pulmonary infections). Eight of the patients died from the basic disease (hepatitis, tetanus, paratyphoid C fever etc.). A number of 2246 Staphylococcus hemolyticus aureus, 80 non-hemolytic Staphylococcus aureus and 162 Staphylococcus albus strains were isolated; most of the strains were resistant to antibiotics in different proportions.
Specific beta-adrenergic receptors were demonstrated in the urinary bladder of adult and developing rats, by direct tissue binding with LD [125I]-cyanopindolol (CYP). The maximum number of binding sites (Bmax) was 167 +/- 25 fmol/mg membrane protein and the dissociation constant (KD) equalled 61 +/- 33 pM. The Hill slopes of the LD [125I]-CYP binding showed a single class of noncooperative receptor sites. The rank order of potency of agonist competition for LD [125I]-CYP binding suggests that the receptors are mostly of the beta 2 subtype. Beta-adrenergic receptor density was approximately half in the first 10 days of life (Bmax 63 to 77 fmol/mg protein) compared with the older age-groups studied (Bmax 91 to 167 fmol/ng protein). On the 1st day after delivery, the calculated beta-adrenergic receptor number/bladder was 9.4, and it increased significantly with age to 2,496 in the adult rat. This is a 250-fold increase in the number of receptors/bladder, while only a 20-fold increase in membrane protein and a five- to sixfold increase in the bladder weight was observed. Thus, an age-dependent increase of beta-adrenergic receptors on the cell membrane surface area occurred in the developing urinary bladder of the rat.
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The presence of HBs Ag was determined by contraelectrophoresis in 500 convalescents after hepatitis B, at the moment of discharge and after 1--3 and 6 months. Antigen carriage is prolonged in hepatitis B, 51% of the convalescents being positive on discharge and 10% remaining persistent carriers. This was more frequent in males, young adults and those who had suffered from mild, prolonged forms of the disease. As only 42% of the patients became negative within the first 20 days of hospitalization it became necessary to prolong their stay in hospital and to follow up the patients subsequently in an out-patient unit.
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Anti-HA antibodies were determined by radioimmunoassay according to the HAVAB-ABBOTT technique in 244 subjects, of whom 194 without hepatic involvement, 25 with non B hva and 25 former non B hva patients. Anti-HA anti-bodies were found in 67% of the healthy subjects and 100% of the patients and former hva cases. The incidence of anti-HA antibodies increases with age being in 30% of children and 83.5% of adults. A peak incidence was found between the ages 21 and 30 years. In the district investigated subclinical infection with HVA was frequent, beginning in childhood and up to the age of 30 years. The qualitative HAVAB test is adequate for epidemiological investigations; a quantitative variant is necessary for the diagnosis.
The incidence, aetiology, evolution, prognosis and treatment of PTH was studied in 253 cases selected from among 7224 patients with acute viral hepatitis, admitted to hospital during the 1973-1979 period. Following the rational application of transfusion and elimination of hepatitis virus B carriers, there was a three-fold decrease in the frequency of PTH. Control of the donors by contra-immunoelectrophoresis showed that PTH type B represents at least 26.8% of the total number of PTH. In order to eliminate PTH type B a more sensitive technique should be used in order to detect HBs Ag in the donors. The treatment being complex and hospitalization prolonged, the cost of PTH patients is greater than that of acute viral hepatitis patients, in general, justifying the additional expenses required for the prevention of PTH.
The behaviour of antialbumin antibodies (AAA) was tested by immunodiffusion in 284 patients suffering from acute viral hepatitis. AAA were found in more than 80% of the cases, and in only 16% of the control lot. The AAA titer was higher the more severe was the clinical form of the disease. As the AAA titer appears to be a marker of functional alterations of the hepatocyte, the test might be used to check the recovery of convalescents after acute viral hepatitis.