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C Caramelo

Publications and source records attributed to C Caramelo.

120 records · Page 7Linked to original sources

Mechanisms of the impaired diuretic and natriuretic responses to a sustained and moderate saline infusion in rats with experimental cirrhosis.

Kidney function and tubular handling of water and sodium by superficial nephrons, packed cell volume, total plasma proteins and albumin distribution space were studied in control and cirrhotic rats before and after a moderate and sustained saline infusion (3% body weight per 30 min + reposition of urinary losses). Tubular fluid samples were obtained from late proximal, early distal and late distal convolutions of superficial nephrons using micropuncture. Protein distribution was assessed by intravenous injection of 0.5 muCi of (125I)-albumin. In basal conditions, both groups of rats showed similar glomerular filtration rate and renal plasma flow, but cirrhotic animals had lower sodium excretion (fractional excretion of sodium = 0.04 +/- 0.01% vs. 0.22 +/- 0.02%, p less than 0.05) and urinary volume (4.31 +/- 0.41 vs. 7.57 +/- 0.53 microliter per min; p less than 0.05). After saline infusion, total plasma proteins decreased more in cirrhotic than in control rats (-18.5 +/- 2.7 vs. -12.9 +/- 2.2%, p less than 0.05). The opposite was observed for albumin distribution space (34.5 +/- 6.1 vs. 22.1 +/- 3.5%, p less than 0.05). Fractional sodium excretion increased to 2.98 +/- 0.15% in control rats but only to 0.61 +/- 0.080% in cirrhotic rats. The ratio single nephron glomerular filtration rate/glomerular filtration rate increased from 19.6 +/- 0.7 to 21.2 +/- 1.0 (X10(-6), p less than 0.005) in control animals but did not change in cirrhotic rats. These animals were unable to decrease adequately fractional fluid reabsorption in the proximal tubule and the loop of Henle.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effect of volume expansion on hemodynamics, capillary permeability and renal function in conscious, cirrhotic rats.

General and splanchnic hemodynamics (radioactive microspheres), renal function, spontaneous and histamine-mediated vasopermeability and albumin distribution space were studied in conscious control and nonascitic cirrhotic rats, before and after a moderate and sustained saline infusion (3% of body weight per 30 min + repletion of urinary losses). In basal conditions, cirrhotic rats showed lower fractional sodium excretion than did control rats (0.09 +/- 0.01 vs. 0.15 +/- 0.01%, p less than 0.005). In addition, cirrhotic animals showed higher cardiac output (161.4 +/- 12.8 ml per min) and lower total peripheral resistance (0.63 +/- 0.05 mm Hg . min per ml) and mean arterial pressure (102.9 +/- 3.9 mm Hg) than did control rats (cardiac output: 89.0 +/- 7.6; total peripheral resistance: 1.31 +/- 0.11; mean arterial pressure: 117.5 +/- 5.11; p less than 0.005). No differences in portal-systemic shunt rate or vasopermeability between both groups were observed. After saline infusion, fractional sodium excretion increased to 4.31 +/- 0.16% in controls but only 2.11 +/- 0.02% in cirrhotic animals. In this group, cardiac output decreased by 49.6 +/- 5.1% whereas mean arterial pressure and total peripheral resistance increased by 7.1 +/- 0.6 and 112 +/- 10%, respectively. In control rats, no significant hemodynamic changes were observed. Blood gases did not change after expansion in any group. Saline infusion induced an increase in histamine-mediated vasopermeability in cirrhotic rats but not in control rats. Also albumin distribution space increased more in cirrhotic than in control animals. Heart weight was higher in cirrhotic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Disruption of cadherin-related junctions triggers autocrine expression of vascular endothelial growth factor in bovine aortic endothelial cells : effects on cell proliferation and death resistance.

The mechanisms involved in the blockade of proliferation in confluent endothelial cells are insufficiently understood. In this regard, the continuity of intercellular junctions appears to be critical to the regulation of endothelial monolayer cell growth. The present study examined the hypothesis that the disruption of the intercellular adherens junctions will trigger both endothelial cell proliferation and autocrine production of growth factors. With this purpose, we assessed the changes in growth, death resistance, and expression of vascular endothelial growth factor (VEGF) under conditions of disruption of the intercellular junctions between endothelial cells. Disruption of cell junctions was produced by means of a specific anti-vascular endothelial cadherin monoclonal antibody, EGTA, or cytochalasin D. Our results disclosed that these maneuvers induce an increase in VEGF mRNA production, with transcription of the 121-, 165-, and 189-amino acid isoforms of VEGF. Further evidence of the relationship between endothelial cells monolayer continuity and VEGF protein expression was obtained by the demonstration of an increase in VEGF protein, as determined by Western blot, induced by the aforementioned maneuvers, as well as by immunocytochemical detection of increased VEGF staining in the areas surrounding a mechanical endothelial injury and in endothelial cells at subconfluence. In functional terms, the autocrine expression of VEGF was associated with growth-promoting and cytoprotective effects, as assessed by [(3)H]thymidine uptake, (51)Cr release, and flow cytometry. In conclusion, our results reveal that disruption of homophilic interendothelial junctions induces VEGF expression. Under these conditions, autocrine VEGF appears to have a relevant role in death inhibition and proliferation of endothelial cells.

Animals↗

[Why do ambulatory hemodialysis patients go to hospital emergency services?

UNLABELLED: An important number of Hospital admissions (HA) occurs through Hospital Emergency Departments (HED). This is a indicator of quality and have to be lower than 50%. However there are almost no data available on the causes of emergency consultation by outpatient hemodialysis patients (HD). For this reason, we prospectively examined a population of 83 outpatient HD patients dialyzed in a peripheral unit under the surveillance of a University Hospital. OBJECTIVES: 1) To know the diagnosis of HED and days of hospitalization for which HD patients came to the HED in 1998. 2) To know the possible risk factors associated with the patients with frequent assistance in HED. 3) To compare the number and causes of emergency consultation in 1998 with a group of patients treated in the same Unit in 1991 (n = 39). RESULTS: The percentage of patients who used the HED in 1998 was 66.3% (55/83). The total number of emergency episodes in 1998 was 118 (mean of 55 patients 2.27 +/- 1.51). Fifty one percent of the emergency episodes were due to patients initiative. The 4 more frequent diagnoses of HED in 1998 were infectious, 19.5% (23/118); traumatologic emergencies, 15.3% (18/118); digestive disease 15.3% (18/118); relationed problem vascular access, 11.9% (14/118). Thirty percent (36/118) of the emergency consultations needed HA leading to a mean hospitalitation of 10.2 +/- 9.3 days. The infectious disease were the highest percentage of HA (36.1%) and the longest days of hospitalitation (12.7 +/- 11.2 days). The risk factors for repeated emergency consultation (more than 3 times) were: age (68.9 vs 61.4), lower hematocrit (31.6 vs 34.4%), lower hemoglobin (10.2 vs 11), high EPO dose (166.3 vs 109.7 unit/kg/week) and lower Kt/V (0.99 vs 1.11). If we compare these results with 1991 the percentage that used the HED was similar 66.2% (pNS); the number of emergency episodes was higher (mean 2.99 +/- 1.96) than 1998 (p < 0.006) and there are a significant differences in the diagnoses of HED between 1998 and 1991: acute pulmonary edema 1.7 vs 11.2% (p < 0.003); hiperkalemia 0.8 vs 7.9% (p < 0.009); gastrointestinal disease 15.3% vs 4.5% (p < 0.008) and infectious 19.5% vs 7.9% (p < 0.01). In conclusion our study provides data previously not available on the epidemiology of Emergency Consultation by outpatient HD patients treated in the same peripheral unit. The data obtained albeit limited because of the number provide information of potential protocol usefulness for the possible reduction in the frequency of Hospital Emergency Consultations by outpatient HD patients.

Adult↗

[Increase of tubular secretion of creatinine by L-arginine: mechanism of practical significance in the assessment of renal function based on creatinine clearance].

BACKGROUND: Tubular secretion of creatinine is increased by meat meals. This increment has been attributed to the formation of new creatinine from creatine contained in the cooked meals. However, no studies are available using amino acid infusions containing no creatine, which allow to further investigate the putative causes of increment in tubular creatinine secretion. METHODS: We performed a prospective, interventional study involving 34 individuals with normal renal function participating in a protocol on arterial hypertension. A continuous infusion of L-arginine (6%, i.v., in four 30 min periods at 50, 100, 200 and 300 ml/h) was administered. Creatinine (CCr) and inulin (CIn) clearances were determined at baseline and during L-arginine infusion. We analyzed the effects of L-arginine on tubular secretion by comparing CCr and CIn and calculated tubular secretion of creatinine (TSCr). RESULTS: L-arginine infusion induced a significant increase in both CCr and CIn. CCr and CIn were respectively 117.9 +/- 22.7 and 107.5 +/- 23, before and 170.3 +/- 23 and 144.2 +/- 47.8 after the infusion of L-arginine (both p < 0.01). This increase was simultaneous with an increment in TSCr from 1.12 +/- 0.4 to 1.43 +/- 0.6 (p < 0.01). CCr correlated significantly with CIn at baseline and at 60 min of infusion (r = 0.365, p = 0.031 and r = 0.368, p = 0.038, respectively), but not at 120 min (r = 0.130, p = 0.412), a time corresponding to the maximum increase in CIn and TSCr. CONCLUSIONS: L-arginine induces a substantial increase of CCr, which exceeds that expected from the increase in glomerular filtration rate measured by CIn and corresponds to an increment in TSCr. This phenomenon adds a new interpretation of the effect of amino acids on tubular handling of creatinine and has practical implications in the evaluation of renal function by means of creatinine clearance.

Adult↗

[Can we increase phosphate removal with conventional hemodialysis?].

BACKGROUND: The aim of the present study was to investigate the effect of different dialysate buffer and glucose concentrations, membrane surface (S) bigger than 2 m2 and increased dialysate flow (Qd) in phosphate (P) removal. METHODS: A. First phase (5 patients): the following variations in dialysate composition were introduced. A: glucose 1.60 g/L, bicarbonate: 39 mEq/L, acetate 4 mEq/L, B: glucose 1.5 g/L bicarbonate 17 mEq/L, acetate 10 mEq/L; C: glucose 0, bicarbonate: 39 mEq/L, acetate 4 mEq/L; and D: glucose 0, bicarbonate 17 mEq/L, acetate 10 mEq/L. B. Second phase (14 patients): variations in S and Qd were: 1. Qd: 500 mL/min + Hemophan 2 m2, 2. Qd: 500 mL/min + Hemophan 2.6 m2, 3. Qd: 750 mL/min + Hemophan 2 m2, 4. Qd: 750 mL/min + Hemophan 2.6 m2. RESULTS: Comparing HDs performed with low bicarbonate (B and D) respect to current buffer formulations (A and C), total P removal was 997.3 (+/- 237.3) vs 882 (+/- 216.1) mg (p NS). No differences were found by grouping the sessions according to glucose concentration. There were no significant differences in total phosphate removal between the two different S or Qd. The most important predictive factor of total P removal was the initial P and 2 hours serum P concentration, and PTH concentration. CONCLUSIONS: i) Removal of P is better predicted by pre-dialysis P serum concentration; ii) P removal was not affected by the changes in bicarbonate and glucose concentration in the dialysate; iii) the increase of the dialyzer area between 2 and 2.6 m2 augments Kt/V, but without influencing P elimination; iv) a higher Qd does not determine significant differences in P removal and v) higher PTH is associated with a higher P elimination.

Adult↗