Superoxide radicals (SR) in the pathophysiology of ischemic acute renal failure (ARF).
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to E Bartoli.
Explore the source record for details and available documents.
In a previous study, we described a new method [3] to measure Na reabsorption by each segment of the human nephron independently. Reabsorption was expressed as equivalent volumes of solute-free water (CH2O) generated by the loop of Henle (CH2O-HL) and by the distal tubule (CH2O-DT), and dissipated by back diffusion (BD) across collecting ducts (CH2O-BD). These data were obtained during maximal water diuresis (MWD). The present study was undertaken to calculate CH2O-HL by experiments performed during maximal antidiuresis (MA). For this purpose, a new theoretical approach was devised, described by algebraic equations which allowed calculations of segmental transport during MA alone, where only CH2O-HL could be calculated independently. The study was performed on 14 normal volunteers who were studied twice by clearance measurements, firstly during MWD and again during MA. In each experiment, clearance periods were performed during baseline conditions and during the administration of furosemide (0.7 mg/kg bolus injection followed by 0.06 mg/kg/min maintenance infusion). From the values measured during either condition, segmental reabsorption was calculated. During MWD, CH2O-HL averaged 19.4 + 10.4, during MA 20.4 + 8.0 ml/min/GFR X 100; p greater than 0.05. The paired measurements were significantly correlated (r = 0.80; p less than 0.01). These data demonstrate that CH2O-HL obtained with the original theory is a reproducible result that can be confirmed with independent measurements obtained during different experimental conditions. Thus, measurements of segmental Na transport in the human nephron are feasible and can contribute important informations on disease states.
Explore the source record for details and available documents.
The results of a study conducted using a new loop diuretic, Azosemide, on a group of 45 patients suffering from hypertension and oedema are reported. Thirty patients were studied in an open trial and in association with other drugs. The remaining 15 exclusively hypertensive patients, were studied in a controlled trial against Indapamide. The patient's standing and recumbent arterial pressure was monitored and all were given periodic weight checks. In the 1st group, Azosemide brought about a significant reduction in arterial pressure, without modifying body weight, but caused considerable weight loss (from 71 to 64 kg) (P less than 0,01) in the oedema patients without altering arterial pressure. In the 2nd group of hypertensive patients, a significant fall in arterial pressure (from 166 to 138 mmHg) was observed, most notably after Azosemide treatment. None of the patients revealed side effects, or alterations in laboratory parameters. It is therefore suggested that Azosemide--given its effectiveness and ease of application--is particularly useful for the diuretic treatment of hypertensive and oedematous patients.
It is possible to quantitatively estimate Na and water transport by each segment of the human nephron during maximal water diuresis (MWD) with a newly developed technique. The present study describes a new development whereby Na reabsorption by the ascending limb of Henle's Loop can be measured during a test of maximal antidiuresis (TMA) and compared with that obtained in separate experiments during MWD. In experiments performed on eight subjects, Henle's Loop reabsorption, expressed as equivalent volume of solute-free water generated, was 23.9 +/- 3.7 during MWD, 24.5 +/- 2.3 ml/min/100 ml GFR in TMA, p greater than 0.05; r = 0.68, p less than 0.05. Thus, our new method is reproducible and theoretically correct.
Explore the source record for details and available documents.
Muzolimine, a new diuretic, is known to act by inhibiting Na transport along the ascending limb of Henle's loop. Because of its ineffectiveness when perfused into the lumen, and as a result of experiments on frog skin, it is believed that muzolimine acts from the serosal cell side, unlike all other diuretics. We decided to assess the site of action of muzolimine (mucosa versus serosa) by experiments on rats. The animals were anesthetized, both ureters cannulated, and a hydronephrosis established in the left kidney by applying a counterpressure to the ureter, slowly and progressively increased up to 60 cm H2O in 3 minutes and kept stable for 20 minutes. Then either muzolimine 1.2 mg, or furosemide 4 mg, was injected i.v. together with 131I-Hypaque as a glomerular marker. Three minutes later the hydronephrosis was released in the left kidney by cutting the catheter, and urine collections were started simultaneously in both kidneys into 25 microliter glass capillaries, that were filled in continuous sequence and numbered progressively. In each urine sample from each glass capillary Na and 131I-Hypaque were measured. In 5 animals receiving furosemide, UNa rose in the left post-obstructed kidney and reached a plateau level by the 3rd to 5th sample. The rise in Na concentration, indicating delivery of urine whose Na reabsorption had been inhibited along the loop of Henle paralleled that in 131I-Hypaque, indicating that the diuretic and the glomerular marker had reached Henle's loop simultaneously, following filtration after the hydronephrosis had been discontinued.(ABSTRACT TRUNCATED AT 250 WORDS)
Experiments were performed on 26 rats to evaluate the effect of furosemide and muzolimine in an experimental model of acute renal failure (ARF). After control clearance measurements from both the left and the right kidney, an acute hydronephrosis was produced on the left side only, to completely interrupt urine flow rate. At the 17th minute of stop-flow, placebo (4 animals), furosemide (4 mg i.v. in 5 animals) or muzolimine (1.2 mg i.v. in 5 rats) were injected and three minutes later the renal arteries were clamped bilaterally for 20 minutes. The arterial clamps and the left hydronephrosis were removed at the 20th minute of ischemia and then 5 consecutive clearance periods were performed from either side to assess recovery from post-ischemic ARF. There was no difference in the entity of GFR depression and speed of recovery of either kidney between placebo, muzolimine and furosemide. The left, post-hydronephrotic kidney consistently exhibited a post-ischemic renal function more depressed than that measured in the contralateral side, although the speed of recovery was the same. The ATP content of the renal tissue was significantly larger in the right kidney compared to the contralateral side in the group receiving furosemide. In the animals treated with muzolimine ATP was significantly depressed in both kidneys. In the post-ischemic period the urinary Na excretion and the fractional water excretion rose significantly with either diuretic compared to placebo. However, this did not influence the recovery in GFR.(ABSTRACT TRUNCATED AT 250 WORDS)
The appearance of the gallbladder was monitored by serial ultrasound examinations in 36 women at various times during their normal pregnancy and postpartum. The gallbladder remained within normal limits in size, but there was a progressive increase in its longitudinal and transverse diameters. The contractibility of the gallbladder was also assessed and found to be satisfactory in most cases. However, the formation of sludge was demonstrated in several instances beyond the 20-25th weeks of pregnancy. Gallstones were detected in 2 patients, 1 of whom had initially normal findings on cholecystosonography during her first trimester.
The importance of prostaglandins (PG) in Na and water retention of liver cirrhosis was studied in rats with porta-cava shunt (PCS) compared to control, non-shunted animals. Balance studies were performed in metabolic cages with diets of high, normal and low Na. An experimental phase, during which the animals received either 5 mg X kg-1 of indomethacin daily or placebo, was preceded by a control period and followed by a post-indomethacin period identical to the control phase. In each diet, indomethacin, but non placebo, caused a positive Na balance, correlated with Na intake, which in overall pooled data amounted to -1453 +/- 255 muEq in PCS rats, significantly larger than that measured in controls, of -295 +/- 320 muEq (P less than 0.01). This was attended by a reverse change in K balance of -35.6 +/- 349 muEq versus -1566 +/- 582 muEq (P less than 0.01); glomerular filtration rate (GRF) was unchanged. These data demonstrate that PGs contribute to the control of Na homeostasis in the presence of PCS.
The segment of the nephron where carbohydrate deprivation depresses Na transport leading to natriuresis was sought by a new clearance technique designed to measure segmental reabsorption in each portion of the human renal tubule. Experiments were performed during maximal water diuresis before and 4 days after carbohydrate withdrawal. Proximal reabsorption had fallen from 70 +/- 4 to 60 +/- 5 ml X min-1, p less than 0.05, by the 4th day of sugar deprivation, accounting for the natriuresis and the associated weight loss of 1.8 kg. By the 4th day of fasting, when Na excretion had returned to control levels, GFR had fallen nonsignificantly from 99 +/- 6 to 95 +/- 5 ml X min-1, while Na reabsorption along distal segments had risen. In fact, Na transport, expressed by the equivalent volumes of solute free-water generated, rose from 17.4 +/- 3.4 to 23.6 +/- 2.1 along the ascending limb of Henle's loop, and from 8.1 +/- 0.8 to 9.2 +/- 1.3 ml X min-1 X GFR-1 X 100 along the distal tubule. Thus, analysis of segmental Na transport by this method discloses that starvation natriuresis is a proximal tubular event, progressively counterbalanced by enhanced Na reclamation in more distal sites. Volume contraction and the attendant fall in GFR concur to curb delivery out of the proximal tubule which is matched by enhanced distal Na reabsorption till a new steady-state excretion is attained.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Progressively increasing concentrations of potassium chloride in Evans blue saline were administered to patients affected with myotonic dystrophy and to healthy volunteers before and after parenteral treatment with taurine. Excitability changes of thenar eminence muscles were related to the venous potassium and chloride concentrations. The actual electrolyte concentrations were compared to those to be expected if no infused electrolytes had been transported into cells. The expected concentrations were calculated by means of Evans blue dilution. This method permitted quantification of changes of muscle-excitability in terms of the potassium chloride concentration capable of disturbing the electrical activity of the studied muscles. The method also provided an indirect evaluation of electrolyte movements across muscle membrane in vivo in humans. Dystrophic myotonic muscles appeared highly sensitive to extracellular potassium and, unlike normal muscles, were unable to accumulate potassium-induced muscle hyperexcitability and favored electrolyte accumulation in dystrophic myotonic muscles. The stabilizing effect of taurine is discussed in relation to its ability to increase intracellular potassium concentration, membrane conductance, or both.
An 18-year-old-woman, with dermatitis herpetiformis, acute glomerulonephritis, malabsorption and villous atrophy due to massive infiltration of IgA producing plasma cells was studied. By light microscopy, her renal biopsy specimen showed heavy immunofluorescence for IgA, a mixed proliferative and membranous lesion with occasional crescents and focal sclerosis. Electron microscopic examination revealed three main lesions: (1) swelling and bleb formation in endothelial cells, (2) extensive fusion of foot processes of podocytes, and (3) a dense quasi-linear, continuous deposition of immune complexes, encompassing several loops; they were characteristically located within the basement membrane at the boundary between the lamina densa and the lamina rara interna. At occasional points where the immune complexes had reached the outer aspects of the basement membrane, there was damage to the podocyte cytoplasm. This electron microscopic aspect supports the interpretation that these immune complexes, although non-complement fixing, exhibit a high damaging potential, leading to relentless disease progression.
1 The relative importance of the effect of prostaglandins on renal sodium and water reabsorption was assessed in rats. 2 Clearance experiments were performed on 24 anaesthetized rats divided into 3 groups. Each group was infused throughout either with Ringer solution at 9 ml/h (Protocol I), or at 3 ml/h (Protocol II) or with hypotonic fluid at 5 ml/h (Protocol III). Clearance periods were performed before and after intravenous injection of indomethacin (5 mg/kg) and then of aspirin (20 mg/kg). The natriuretic response to different degrees of volume expansion was not modified during the action of the inhibitors. 3 When baseline urine osmolality (Uosm) was high (Protocol II) no further increase occurred in the presence of prostaglandin inhibition. Conversely, Uosm rose from 771 +/- 134 to 1356 +/- 414 and from 575 +/- 245 to 841 +/- 407 mosm/kg (P less than 0.05) in Protocol I and Protocol III respectively, when antidiuretic hormone secretion was inhibited by the higher degree of volume expansion. 4 There was a significant correlation between the change in urine flow rate induced by cyclooxygenase inhibitors and the attendant variations in Na excretion, r = 0.42, n = 41, P less than 0.01. 5 Thus, prostaglandins affect Na loss during saline load as a side effect of their action on water permeability. They could play an important role in volume depletion by counterbalancing the large secretion rate of renal vasoconstrictors.