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Biomedical subjects

C Caramelo

Publications and source records attributed to C Caramelo.

At least 55 records · Page 3Linked to original sources
PubMed1997

Concentrated ascitic fluid reinfusion in cirrhotic patients: a simplified method.

A new method for ascites filtration and reinfusion, which uses a single Cuprophan filter and is performed in the dialysis unit, is reported. Thirty-one procedures were performed in 17 patients with cirrhosis and massive ascites. A mean volume of 8.6 L of ascitic fluid was removed; from this volume, 5 L were ultrafiltered and a concentrated ascitic fluid was reinfused (x = 359.8 mL). The whole procedure was completed in a mean time of 248 minutes. No relevant method-related complications were detected. Moreover, no significant changes in blood urea nitrogen (BUN), creatinine, plasma and urinary electrolytes, or platelet count were found, even in the case of repeated procedures (two to nine times). The reinfused fluid contained a mean value of albumin of 4.7 g/dL and significant amounts of globulins and complement. The overall cost of the materials used in the procedure ($49.46) offered competitive advantages with respect to other types of frequently used methods. In conclusion, we present a safe, effective, and time- and cost-saving technique for ascites reinfusion that represents an advantageous alternative to more complicated and expensive methods or to the currently used medical therapy.

Ascites↗
PubMed1997

Role of nitric oxide in autocrine control of growth and apoptosis of endothelial cells.

Nitric oxide (NO) is a growth inhibitor for diverse cellular types. In the present study, we have found that the inhibition of NO production in bovine endothelial cells by an L-arginine competitive antagonist induces DNA replication and promotes the transition from prereplicative to replicative phases of the endothelial cell cycle and an increase in c-myc and c-fos oncogene-encoded protein expression. The inhibition of NO generation had, however, a markedly different outcome depending on the state of confluence of the cells, i.e., proliferation was found in subconfluent cells, whereas apoptosis occurred in confluent cells. Moreover, Western blot analysis revealed differences in the constitutive NO synthase expression in proliferating compared with growth-arrested cells. In conclusion, these results disclose an alternative mechanism of endothelial cell apoptosis at the confluent state, which is related to NO inhibition. Moreover, the fact that the apoptotic phenomenon occurred in the presence of growth factors indicates the existence of apoptotic mechanisms that do not require growth factor deprivation.

Animals↗
PubMed1997

Hepatitis B virus DNA in serum and blood cells of hepatitis B surface antigen-negative hemodialysis patients and staff.

Patients undergoing chronic hemodialysis, as well as dialysis staff members, are at high risk of infection with hepatitis B virus (HBV). We have analyzed by PCR the presence of HBV DNA in serum and peripheral blood mononuclear cells (PBMC) from 33 hepatitis B surface antigen (HBsAg)-negative hemodialysis patients and 24 dialysis unit staff members; eight of the 24 staff members had an acute hepatitis B resolved 13 to 21 yr before. HBV DNA was detected in serum of 19 (58%) patients (12 of 17 with and 7 of 16 without anti-HBV antibodies). HBV DNA was found in PBMC of 18 (54%) patients (13 of 17 with and 5 of 16 without anti-HBV antibodies). In the staff members, serum HBV DNA was found only in the individuals who suffered a previous acute hepatitis (P < 0.005). HBV DNA was detected in PBMC of four of six staff members (all with previous acute hepatitis). In two HBV DNA-positive PBMC samples, viral RNA was detected by reverse transcription-PCR. To ascertain whether the HBV DNA detected in serum was encapsulated, seven HBV DNA-positive serum samples were digested with DNase before PCR. After treatment, HBV DNA remained detectable in four cases. In conclusion, HBV DNA in serum and PBMC is detectable in a high proportion of HBsAg-negative hemodialysis patients and may persist several years after a resolved acute hepatitis B. The viral DNA is encapsulated and remains transcriptionally active in PBMC. In the anti-HBs-negative patients, HBV DNA is, at the present time, the only means for diagnosing a past HBV hepatitis.

Adult↗
PubMed1996

Aspirin-stimulated nitric oxide production by neutrophils after acute myocardial ischemia in rabbits.

BACKGROUND: In recent studies, it has been hypothesized that the protective anti-ischemic effects of aspirin outweigh the effects of inhibition of platelet thromboxane A2 synthesis. Recently, we have found that the antiaggregating effects of aspirin significantly affect nitric oxide (NO) generation by neutrophils. METHODS AND RESULTS: The present study used circulating neutrophils from myocardial ischemic rabbits to assess the effect of aspirin on the circulating neutrophil-derived NO production and, subsequently, on the modulation of platelet activation. Neutrophils were obtained after 60 minutes of coronary artery occlusion followed by 60 minutes of reperfusion. Sham-operated animals were used as controls. The results demonstrated that aspirin stimulated the production of NO by neutrophils obtained from both sham-operated rabbits and rabbits with myocardial ischemia. However, neutrophils isolated from animals with myocardial ischemia showed an enhanced ability to generate NO in the presence of aspirin. As a functional in vitro marker, we observed that neutrophils had a NO-dependent, platelet-antiactivating effect in the presence of aspirin. In the absence of aspirin, ischemic neutrophils did not modify platelet activation, even though they produced increased amounts of NO. An inhibitory role of superoxide anion on the neutrophil-related antiplatelet effect was suggested because superoxide dismutase induced significant platelet inhibition by myocardial ischemic neutrophils in the absence of aspirin. CONCLUSIONS: Our results show that myocardial ischemia/reperfusion stimulates production of NO by circulating neutrophils, an effect that was enhanced in the presence of aspirin. These results suggest a novel interpretation of the protective effect of aspirin on myocardial ischemia damage.

Animals↗
PubMed1996

Role of endothelin in the pathophysiology of renal ischemia-reperfusion in normal rabbits.

The present study addressed the acute effects of endothelin-1 on renal function and neutrophils accumulation in the setting of in vivo severe (60 min) acute ischemia/reperfusion. Ischemia/reperfusion decreased renal functional parameters and increased renal neutrophil accumulation and medullary congestion. All these parameters markedly improved with the intrarenal administration of anti-endothelin-1 antiserum. Comparatively, the intrarenal infusion of endothelin-1 decreased renal function and increased neutrophil accumulation. Abnormalities in renal histology were, however, less pronounced than with ischemia/ reperfusion. In experiments using rabbit isolated perfused kidneys, endothelin-1 induced the accumulation of labeled neutrophils. This accumulation was similar to that observed in kidneys obtained after 60 minutes of ischemia plus 60 minutes of reperfusion. Both endothelin and ischemia/ reperfusion effects were counteracted by an anti-endothelin antibody. In further in vitro studies, we found that endothelin-1-induced the expression of the CD18 antigens on the neutrophil surface. In subsequent experiments based on this effect of ET-1 on CD18 antigens, a blockade of both ischemia/reperfusion-induced and endothelin-1-induced neutrophil accumulation was obtained by infusion an anti-CD18 antibody. In conclusion, our experiments disclosed the critical role of endothelin-1 as a major promoter of early neutrophil accumulation after ischemia/reperfusion, which occurred through an integrin-mediated mechanism.

Animals↗
PubMed1996

Undiagnosed hepatitis C virus infection in hemodialysis patients: value of HCV RNA and liver enzyme levels.

At present, routine screening for hepatitis C virus (HCV) infection is based on the detection of antiviral antibodies. Underdiagnosis of HCV infection by using HCV antibody tests, however, still occurs. Additional diagnostic means are provided by the polymerase chain reaction (PCR). The measurement of aminotransferase (ASAT and ALAT) has served as an auxiliary, less specific test. The present research aimed to design practical and low cost strategies to diminish underdiagnosis of HCV infection in dialysis patients. With this purpose in mind, we examined whether aminotransferases values in HCV antibody-negative patients could be related to undiagnosed HCV infection, by using HCV RNA testing by PCR as the gold standard. In 112 hemodialysis patients, we found 78 negative and 34 positive for HCV antibodies. A major finding was that 222 (28.2%) out of the 78 HCV antibodies-negative patients had positive HCV RNA by PCR. In repeated samples taken at six months follow-up from 19 out of these 22 patients, only one of them was positive for anti-HCV antibodies; moreover, a positive HCV RNA by PCR was confirmed in 13 (68.5%) of them. Within the HCV antibody-negative group, the mean values of ASAT, ALAT and gammaglutamiltransferase were higher (P < 0.001, P < 0.001 and P < 0.02, respectively) in the HCV PCR-positive versus the HCV PCR-negative patients. No significant differences were found in the liver enzyme values between the HCV antibody-negative, HCV RNA positive and the HCV antibody positive, HCV RNA positive individuals. Histological samples from two HCV RNA positive, HCV antibody-negative patients disclosed the presence of a mild liver disease. In conclusion, the present study demonstrates the critical importance of HCV RNA determination by PCR in hemodialysis patients who have no detectable circulating antibodies against the HCV. Furthermore, in conditions in which PCR technology is not readily available, we have established that the existence of a moderate increase of aminotransferases is a helpful clue to detect patients with absent HCV antibodies, and might represent an useful, low cost tool for HCV screening in dialysis patients.

Adult↗
PubMed1996

Acute renal failure due to sulphadiazine crystalluria in AIDS patients.

We report two AIDS patients who developed acute renal failure while receiving sulphadiazine for cerebral toxoplasmosis. Renal ultrasound revealed diffuse bilateral echogenic shadowing material. 'Sheaves of wheat' crystals, typical of sulphadiazine crystalluria, were present in the urine. One patient required a percutaneous nephrostomy. Hydration and urine alkalinisation resulted in rapid improvement of renal function and ultrasonographic findings. Sulphadiazine-induced crystalluria and acute renal failure is increasingly frequent. Awareness of its existence may lead to prevention and early conservative treatment.

AIDS-Related Opportunistic Infections↗
PubMed1996

Effect of dietary fat saturation on LDL oxidation and monocyte adhesion to human endothelial cells in vitro.

Forty-two healthy men and women were subjected to four consecutive dietary periods differing in the fat content of saturated fatty acids (SFAs), monounsaturated fatty acids (MUFAs), and polyunsaturated fatty acids (n-6) [PUFA(n-6)] and (n-3) [PUFA(n-3)]. Plasma lipids, vitamin E, and in vitro LDL oxidation were examined during each period. Adhesion of human monocytes to cultured human endothelial cells was used as a functional test to identify differences in the biological properties of LDL from each dietary period. Consumption of an SFA-rich diet resulted in higher LDL cholesterol (4.06 +/- 0.85 mmol/L, P < .05) than did consumption of MUFA- (3.59 +/- 0.75 mmol/L), PUFA(n-6)- (3.44 +/- 0.77 mmol/L), or PUFA(n-3)- (3.31 +/- 0.8 mmol/L) rich diets. HDL cholesterol was lower during both PUFA-rich diets (1.24 +/- 0.28 and 1.27 +/- 0.28 mmol/L for n-6 and n-3, respectively) than during the SFA-(1.32 +/- 0.36 mmol/L) and MUFA- (1.32 +/- 0.34 mmol/L) rich diets. LDL resistance to copper-induced oxidation, expressed as lag time, was highest during the MUFA-rich diet (55.1 +/- 7.3 minutes) and lowest during the PUFA(n-3)- (45.3 +/- 7 minutes) and SFA- (45.3 +/- 6.4 minutes) rich diets. LDL induction of monocyte adhesion to endothelial cells was lower during the MUFA-rich diet than the other periods. The highest monocyte adhesion was obtained during the PUFA(n-3) and SFA dietary periods. In conclusion, an MUFA-rich diet benefits plasma lipid levels compared with an SFA-rich diet. Furthermore, this diet results in an increased resistance of LDL to oxidation and a lower rate of monocyte adhesion to endothelial cells than the other dietary fats examined.

Adult↗
PubMed1996

Role of endothelium-related mechanisms in the pathophysiology of renal ischemia/reperfusion in normal rabbits.

The present study addressed the effect of interventions aimed to increase NO in the setting of acute renal ischemia/reperfusion (I/R) in uninephrectomized rabbits. In the 60-minute post-I/R period, L-arginine+superoxide (O2.-) dismutase (SOD) synergistically improved the renal functional (69.4% versus 10.4% of the pre-I/R glomerular filtration rate with or without L-arginine+SOD, respectively; p < .01) and histological parameters (82.9% decrease of medullary congestion in L-arginine+SOD, P < .01 versus vehicle) and blocked the I/R-dependent neutrophil accumulation (89.3% reduction). In spite of these results over the short term, a second set of experiments disclosed that the protection by L-arginine+SOD was no longer present at 24 and 48 hours (plasma creatinine in vehicle-treated versus L-arginine+SOD-treated animals [mg/100 mL]: 24 hours after I/R, 9.4 +/- 1.9 versus 8.07 +/- 0.65; 48 hours after I/R, 11.6 +/- 3.6 versus 9.7 +/- 0.9; P = NS in all the cases). Additional experiments were conducted using a milder 30-minute ischemic model, which showed no significant functional or histological protection by using L-arginine+SOD. In conclusion, our experiments disclosed the following: (1) the critical importance of the interaction between NO and O2.- in the acute protective effect of L-arginine (this effect not only improved renal function and histology but also reduced neutrophil accumulation) and (2) the discordance existing between the immediate protection afforded by L-arginine+SOD and the lack of protection observed at 24 and 48 hours. This finding suggests that a punctual intervention on the NO system at the time of I/R is not sufficient to reduce renal damage over the long term.

Animals↗
PubMed1996

Influence of iron status in the response to the deferoxamine test.

The study presented here was carried out to evaluate the possible relationship between serum iron and iron transferrin saturation with the response to the deferoxamine test in 86 chronic renal failure patients undergoing hemodialysis. The deferoxamine test was performed as a diagnostic tool for aluminum intoxication. Basal serum aluminum levels correlated with: (1) serum aluminum levels after the infusion of deferoxamine (r = 0.45; P < 0.05); (2) serum iron levels (r = -0.26; P < 0.05), and; (3) iron transferrin saturation (r = -0.33; P < 0.05). The increase in serum aluminum levels after deferoxamine administration (DAI) showed a negative relationship with serum iron levels (r = -0.23; P < 0.05) and iron transferrin saturation (r = -0.26; P < 0.05). The correlations improved when analysis of this study included only those patients with high serum iron levels or high iron transferrin saturation (r = -0.55). Patients with low probability of having aluminum overload (serum iron levels < 40 micrograms/L and DAI < 150 micrograms/L) had significantly higher values of serum iron, iron transferrin saturation, and serum ferritin levels compared with those patients with a high probability of having aluminum overload (serum aluminum levels > 40 micrograms/L and DAI > 150 micrograms/L). The study presented here suggests that patients who have indicators of iron repletion would tend to have lower increases in serum aluminum levels after the challenge with deferoxamine and presumably a higher incidence of false negative results with the deferoxamine test. These findings indicate that iron measurements must be always taken into account when interpreting the deferoxamine test.

Aluminum↗
PubMed1996

Relationships between plasma ferritin and aminotransferase profile in haemodialysis patients with hepatitis C virus.

BACKGROUND: HCV infection is a major complication among patients undergoing dialysis therapy throughout the world. In the years prior to the use of human recombinant erythropoietin (rHuEpo), patients undergoing haemodialysis were subjected to an excessive iron load as a consequence of frequent blood transfusions. Recent data in the non-dialysis population have shown a positive correlation between iron deposits and the severity of HCV hepatitis and between iron deposition and an impaired response to interferon therapy. METHODS: One hundred and five haemodialysis patients were studied. Every patient was screened for HCV infection by ELISA II and HCV RNA. Serum biochemistries were analysed by SMAC20. Ferritin was measured by radioimmunoassay. RESULTS: The aminotransferase levels for the HCV positive (n = 39) and negative patients (n = 66) were below the normal levels for the general population. The mean values of aminotransferases and plasma ferritin were, however, higher in the HCV-positive patients than in the HCV-negative patients. A positive correlation between aminotransferases and plasma ferritin was evident in HCV-positive patients, which was absent in the HCV-negative individuals. The histological severity of liver disease (n = 7) was, however, not statistically related with the levels of either ferritin or aminotransferases. CONCLUSION: HCV infection is a relevant variable when estimating iron deposits by measuring plasma ferritin. Accordingly, a misinterpretation of the actual amount of iron deposits may occur in HCV-positive patients, which should be taken into account at the time of planning their iron reposition therapy. On the other hand, the level of iron deposits might have a significant role in the evolution of HCV-related liver disease.

Aged↗
PubMed1995

Effects of aspirin on platelet-neutrophil interactions. Role of nitric oxide and endothelin-1.

BACKGROUND: In recent studies, the hypothesis has been raised that the mechanisms by which aspirin acts as a protective anti-ischemic agent exceed the inhibition of platelet thromboxane A2 synthesis. Recently, new data have been obtained disclosing a platelet-antiaggregating effect by neutrophils, which occurs through a nitric oxide (NO)/cGMP-dependent pathway. METHODS AND RESULTS: The present study, using platelets and neutrophils from normal subjects, was undertaken to assess the putative effect of aspirin on the neutrophil-mediated, platelet-inactivating effect. Aspirin facilitated the inhibitory effect of neutrophils on platelet activation by thrombin, ADP, or epinephrine. This effect was equally evident in vitro and in blood samples of normal individuals taking aspirin. A significant stimulation of NO-mediated mechanisms in the presence of aspirin was disclosed by different methods, as follows: (1) the increased metabolism of arginine to citrulline, (2) the increase of cGMP in the platelet/neutrophil system, and (3) the inhibitory action of the L-arginine (L-Arg)-competitive analogue L-NMMA, which was reversed by L-Arg. The effect of aspirin appeared to be related to cyclooxygenase inhibition, since it was reproduced by using indomethacin. The vasoconstricting peptide endothelin-1 (ET-1) reversed the effect of aspirin through the endogenous production of platelet-activating factor (PAF) by neutrophils, as judged by the marked inhibitory effect of the PAF antagonist BN-52021. CONCLUSIONS: Our results show that a significant part of the effect of aspirin on platelet activation involves a neutrophil-mediated, NO/cGMP-dependent mechanism. The presence of ET-1 counterbalances these effects of neutrophils on platelet activation, therefore acting as an indirect proactivating agent. These results add new elements for interpreting the effects of aspirin on the interactions between blood cells, with special reference to high endothelin states (for example, ischemia/reperfusion processes).

Animals↗
PubMed1995

[The reversibility of pulmonary hypertension associated with autoimmune hyperthyroidism].

We report the case of a 28-year-old woman in a chronic hemodialysis program, who developed moderate pulmonary hypertension (eco-Doppler assumed pulmonary systolic pressure of 62 mmHg), with right ventricular dilatation (49 mm) in coincidence with a fully symptomatic autoimmune hyperthyroidism. The improvement of thyroid function resulted in a significant regression of pulmonary hypertension (45 mmHg) and normalization of right ventricular size (35 mm). The appearance and reversibility of pulmonary hypertension associated to autoimmune hyperthyroidism have not been described before and, in our patient, it is probably facilitated by other coincident factors that increase cardiac output and, subsequently, pulmonary flow, i.e. anemia and the arteriovenous fístula for hemodialysis.

Adult↗
PubMed1994

Effects of nitric oxide on red blood cells: changes in erythrocyte resistance to hypotonic hemolysis and potassium efflux by experimental maneuvers that decrease nitric oxide.

To determine the role of nitric oxide (NO)-dependent mechanisms on erythrocyte properties, we exposed red cells to L-arginine competitive analogues, 8Br-cyclic guanosine monophosphate (8Br-cGMP) and neutrophil-eliminating filters. These treatments significantly decreased hypotonic hemolysis, increased potassium efflux and caused a spiculate change in erythrocyte morphology. These effects were related to a decrease of NO caused by the three types of treatments.

Adult↗