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Biomedical subjects

M A Delgado

Publications and source records attributed to M A Delgado.

At least 37 records · Page 2Linked to original sources
PubMed1997

[Septic shock and nitric oxide].

Refractory hypotension is the main cause of death of patients with septic shock. It has been shown that an excessive release of NO is responsible for the sepsis-induced hypotension and vascular hyporeactivity. Nitric oxide is produced under normal conditions by a constitutive enzyme present, among other cell types, in the endothelial cell, and is necessary for maintenance of normal organ perfusion. Under inflammatory or septic conditions, a new enzyme is expressed in phagocytic cells and vascular smooth muscle cells, giving rise to an uncontrolled NO production that is associated with cytotoxic effects and vasodilatation. Randomized clinical trials have shown that the administration of inhibitors of NO synthesis to patients with septic shock is associated with a greater incidence of shock resolution, without significant adverse effects. The recent discovery of the different biological functions of NO, both under normal and inflammatory conditions, has allowed the development of new concepts about the pathophysiology of septic shock, and has provided the bases to design novel therapeutic strategies for the treatment of septic shock, based on the inhibition of NO synthesis.

Arginine↗
PubMed1996

Effects of nitric oxide synthase inhibition on the cardiovascular response to low output shock.

OBJECTIVE: To study the role of nitric oxide in the cardiovascular response to a model of a low output syndrome. DESIGN: Prospective animal study. SETTING: Animal research laboratory. SUBJECTS: Sheep anesthetized with pentobarbital, mechanically ventilated, and monitored with pulmonary arterial and peripheral arterial catheters. INTERVENTIONS: A low output state was induced by inflating a balloon-tip catheter placed in the right atrium. Cardiac index was maintained at 1 L/min/m2 throughout the experiment in three groups of sheep: a) control (n=6) b)LNNA group (pretreated with the nitric oxide synthase inhibitor N omega-nitro-L-arginine [LNNA, 100 mg/kg, iv bolus, n=6); and c) dexamethasone group (pretreated with dexamethasone (6 mg/kg, intravenous bolus, n=6). Dexamethasone is an inhibitor of the induction of nitric oxide synthase. LNNA or dexamethasone were administered 15 mins before inducing the low output state. MEASUREMENTS AND MAIN RESULTS: Hemodynamic and oxygen transport variables, and plasma lactate and pyruvate concentrations, were measured at baseline and during the next 3 hrs. For a comparable decrease in cardiac index and oxygen delivery in all groups, the LNNA group had less hypotension and a more marked increase in systemic vascular resistance as compared with the control group. Oxygen consumption and oxygen extraction were higher in the LNNA group as compared with the control group at 30 and 60 mins. Plasma lactate concentration increased significantly less in the LNNA group than in the control and the dexamethasone groups during the observation period. CONCLUSIONS: Inhibition of nitric oxide synthesis during a severe low output state in sheep is associated with a better hemodynamic response, as evidenced by a greater vasoconstriction, and signs of less marked tissue hypoxia. It is likely that inhibition of nitric oxide synthesis in this model leads to an imbalance between the tonic relaxing action of nitric oxide and the influences of vasoconstrictor agents.

Analysis of Variance↗
PubMed1992

Mapping of the PCK1 gene encoding phosphoenolpyruvate carboxykinase on chromosome XI of Saccharomyces cerevisiae.

The gene PCK1 encoding phosphoenolpyruvate carboxykinase of Saccharomyces cerevisiae has been mapped on the right arm of chromosome XI, 12.7 centimorgans proximal to MAL4 and 20.1 centimorgans distal to MET1. In order to map the gene, hybridization of PCK1 DNA with separated yeast chromosomes and tetrad analysis of diploids with adequate markers were carried out.

Chromosome Mapping↗
PubMed1992

Frequency and prophylaxis of upper gastrointestinal hemorrhage in critically ill children: a prospective study comparing the efficacy of almagate, ranitidine, and sucralfate. The Gastrointestinal Hemorrhage Study Group.

OBJECTIVE: To determine the occurrence of upper gastrointestinal hemorrhage in critically ill children, and the efficacy of prophylaxis with almagate (antacid), ranitidine, and sucralfate. DESIGN: Prospective, randomized, controlled trial. SETTING: Pediatric ICU of a tertiary care pediatric hospital. PATIENTS: During a 2-yr study period, 165 patients with one or more upper gastrointestinal hemorrhage risk factors were randomized into one of four groups. Twenty-five patients were excluded because of protocol violations. A total of 140 patients completed the study, with 35 patients in each group. INTERVENTIONS: Patients received no treatment in the control group. The antacid group received almagate 0.25 to 0.5 mL/kg every 2 hrs by nasogastric tube. The ranitidine group received 1.5 mg/kg every 6 hrs iv. The sucralfate group received 0.5 to 1 g every 6 hrs by nasogastric tube. METHODS: Gastric pH and macroscopic bleeding were determined every 2 hrs in all patients until the end of the study. Macroscopic bleeding was classified as nonhemorrhage, slight, or important. Microscopic gastric bleeding was researched with guaiac testing in 72 patients (680 samples). The severity of illness was evaluated by using the Therapeutic Intervention Scoring System, Physiologic Stability Index, and the Multiorgan System Failure scores. The risk of upper gastrointestinal hemorrhage was evaluated by the Zinner and Tryba indices, and was modified for children. MEASUREMENTS AND MAIN RESULTS: The occurrence rate of important upper gastrointestinal hemorrhage was higher (by 20%) in the control group than in the rest of the groups (5.7%), p less than .01. There were no differences between the other groups (almagate 5.7%, ranitidine 8.5%, and sucralfate 2.8%). There was a statistically significant correlation between the occurrence rate of important upper gastrointestinal hemorrhage, the scores of severity of illness indices (Therapeutic Intervention Scoring System, Physiologic Stability Index, and the Multiorgan System Failure scoring system), the risk of upper gastrointestinal hemorrhage indices (Zinner and Tryba), and mortality rate. The Zinner index better classified the patients in relation to the onset of important upper gastrointestinal hemorrhage (sensitivity 76.9%, specificity 85.8%). CONCLUSIONS: Upper gastrointestinal hemorrhage is an important complication in critically ill children. Prophylaxis with almagate, ranitidine, or sucralfate reduces the occurrence rate of clinically important gastrointestinal hemorrhage.

Aluminum Hydroxide↗
PubMed1992

Plasma and gastric juice levels of prostaglandins in critically ill children.

The levels of prostaglandin (PG) E2 and 6-keto-PGF1 alpha (stable metabolite of prostacyclin) in plasma and gastric juice were determined in 113 critically ill children and adolescent, and compared to those registered in a plasma control group of 24 children and a gastric juice control group of 15. The gastric juice concentration of PGE2 is our patients [9.2 +/- 3.1 (SEM) pg/ml] was significantly lower (p = 0.001) than in the control group [81.1 +/- 18.1 (SEM) pg/ml]. There were no differences in plasma levels of PGE2 and plasma gastric juice levels of 6-keto-PGF1 alpha between the patients and the control groups. Children who died had lower plasma levels of PGE2 [6.2 +/- 2.2 (SEM) pg/ml] and gastric juice levels of PGE2 [2.3 +/- 0.8 (SEM) pg/ml] than the survivors (p less than 0.05). The gastric juice concentration of PGE2 was also lower in children who suffered important upper gastrointestinal bleeding, although the difference did not reach statistical significance.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Inhibition by different amino acids of the aspartate kinase and the homoserine kinase of the yeast Saccharomyces cerevisiae.

In this paper, we describe a simple method to measure the yeast homoserine kinase and aspartate kinase activities, independently but in the same extract. With this method, we have determined some kinetic parameters for the physiological substrates of both enzymes, and investigated the inhibition exerted by different amino acids on these activities. Of all natural amino acids tested, only threonine inhibits effectively both enzymatic activities, although to a different degree. We did not find the reported inhibition by L-homoserine over the aspartate kinase. Altogether the data point to the aspartate kinase and to the threonine as the key factors in the regulation of this route.

Amino Acids↗
PubMed1991

Developmental expression of cathepsin L and c-rasHa in the mouse placenta.

An investigation is described of the expression of the cysteine proteinase cathepsin L during placental development. In addition, whether cathepsin L expression is linked to c-rasHa expression in development, as it is in metastatic cells, is examined. Large amounts of cathepsin L and its transcript are present in the mouse placenta, more than six times more than in adult kidney and liver. Throughout gestation, cathepsin L and its transcript are located in the giant cells and spongiotrophoblasts of the placenta. Several forms of different mobility on denaturing gels are found in the placenta. Their apparent molecular weights, as determined from the gels, are 43,000, 39,000, 29,000, and 20,000. The 39-kDa form is procathepsin L. The 29-kDa and 20-kDa forms are lysosomal cathepsin Ls. The 39-kDa procathepsin L and the 20-kDa mature cathepsin L are the most abundant species in the placenta and are present in about equal amounts throughout gestation. At any time during gestation, placental minces synthesize and secrete only procathepsin L. The amniotic fluid of the fetus contains the 43-kDa form of cathepsin L and procathepsin L, but no detectable amounts of mature cathepsin L. By contrast, serum from nonpregnant or pregnant mice contains three forms of cathepsin L (i.e., the 43-kDa form, procathepsin L, and mature cathepsin L). Cathepsin L and the rasHa oncogene are expressed in two coincident waves corresponding to periods during which the placenta is invasive and just before parturition. The presence of large amounts of cathepsin L in the placenta suggests that the proteinase has a significant function there. Expression of cathepsin L in the placenta is potentially under the control of the ras gene product p21; both are under developmental control.

Animals↗
PubMed1989

Continuous arteriovenous haemofiltration in children.

Continuous arteriovenous haemofiltration (CAVH) was used in 7 critically ill children: a premature neonate with hypervolaemia secondary to hydrops foetalis and six children aged 9 days to 7 years with acute oliguric renal failure. Biospal 0.5 m2, Renaflo 0.25 m2, Gambro 0.15 m2 and Amicon 0.015 m2 filters were used according to the weights and ages of the patients. Adequate removal of water and solutes was obtained in 6 patients. One of the patients with the smallest filter needed a change to a filter with a larger surface area to improve water and solute removal. Haemofiltration was maintained for between 17 hours and 31 days and was well tolerated. CAVH was discontinued because of recovery of renal function in three patients, improvement of the hypervolaemic state in one, death in three, and transfer to continuous ambulatory peritoneal dialysis because of chronic renal failure in one patient. CAVH is a useful technique for the treatment of acute renal failure and hypervolaemia in critically ill children.

Acute Kidney Injury↗
PubMed1989

Dosage of nifedipine in hypertensive crises of infants and children.

Eight hypertensive crises (HC) were treated with 2.5 mg of sublingual nifedipine in three children with weights below 10 kg (group A); 16 HC in 6 children between 10 and 20 kg with 5 mg (group B); and 40 HC in 10 children over 20 kg with 10 mg of nifedipine (group C). The relative decrease in both systolic and diastolic blood pressure was similar in all groups. The decrease was more rapid in groups A and B when the contents were extracted from the capsule and given directly. The hypotensive effect lasted 4 h. There were no side effects. The effective and safe single dose of nifedipine has been established to be 2.5 mg for children weighing less than 10 kg, and 5 mg for children weighing between 10 and 20 kg.

Acute Disease↗
PubMed1984

Isolation and characterization of a mutant from Saccharomyces cerevisiae lacking fructose 1,6-bisphosphatase.

Mutants lacking fructose 1,6-bisphosphatase activity have been isolated from Saccharomyces cerevisiae and genetically purified. Mutants were unable to grow on gluconeogenic carbon sources. Revertants that grew on glycerol have regained the fructose 1,6-bisphosphatase activity, showing that there is no bypass in yeast for this enzymatic step. No significant differences were found in the growth of the mutants and the parental strains in other carbon sources. Other mutants lacking fructose 1,6-bisphosphatase activity but pleiotropically affected in the derepression of several enzymes sensitive to catabolite repression were also isolated. All the mutants isolated were of nuclear origin and defined three complementation groups.

Fructose-Bisphosphatase↗