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Biomedical subjects

V Guarner

Publications and source records attributed to V Guarner.

At least 19 recordsLinked to original sources
PubMed1992

Effects of maternal protein-calorie malnutrition on the phospholipid composition of surfactant isolated from fetal and neonatal rat lungs. Compensation by inositol and lipid supplementation.

The effects of a maternal protein-calorie malnutrition during gestation and lactation were analyzed on fetal and postnatal lung growth and maturation, including a surfactant fraction isolated from lung tissue. There was a considerable reduction in body weight and in wet and dry lung weights of malnourished pups. Lung protein and DNA concentrations were similar in both groups except in late gestation (lung hyperplasia) and 2 and 15 d after delivery (hypocellularity). Lung glycogen breakdown was slowed down in malnourished newborns. Surfactant material was decreased the most perinatally and the reduction was more marked than for the nonsurfactant fraction of the lung. Disaturated phosphatidylcholine, the major surface active surfactant component, was decreased the most at birth (1.70 +/- 0.31 nmol/mg wet wt versus 3.68 +/- 0.17 nmol/mg in controls, n = 8) and on d 2 (5.04 +/- 0.53 nmol/mg versus 7.67 +/- 0.44 nmol/mg in controls, n = 8). There was an apparent recovery in the composition of surfactant in malnourished rats 5 d after delivery, due in fact to a decrease in controls, and an actual return to normal levels 15 to 20 d after birth. Postnatal lipid supplementation with Intralipid led to partial recovery on d 10. Inositol supplementation totally reverted the effects of malnutrition on surfactant phospholipids (8.36 +/- 0.94 nmol disaturated phosphatidylcholine/mg wet wt on d 2 versus 7.67 +/- 0.44 nmol/mg in controls and 5.55 +/- 0.62 nmol/mg in untreated malnourished rats, n = 10; 2.43 +/- 0.32 nmol disaturated phosphatidylcholine/mg wet wt on d 10 versus 3.26 +/- 0.32 nmol/mg in controls and 1.18 +/- 0.27 nmol/mg in untreated malnourished rats, n = 8).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Developmental changes in blood glucose and tissue carbohydrates in the fetal rat: effects of insulin and adrenaline.

The ontogeny of glucose regulation was studied in the rat by measuring the levels of plasma glucose, tissue glucose and tissue glycogen from fetal day 15 (E15) to adulthood. Since insulin and adrenaline are important glucose regulators in the adult, we also tested the effects of these hormones on above variables. The main findings are the following: 1) Umbilical blood glucose was very low (25 mg/100 ml) from E15 to E19, increasing to 66 mg/100 ml by E21 but still below maternal levels (110 mg/100 ml). 2) Umbilical venous-arterial (VEN-ART) glucose differences were very small (1 mg/100 ml) from E15 to E17, increased to 6 mg/100 ml by E19, but dropped again becoming negative (-15 mg/100 ml) just before birth when umbilical arterial blood glucose rose above venous blood glucose. 3) Glucose and glycogen concentrations rose drastically in liver towards the end of gestation. 4) Tissue glycogen and, to a much lesser degree, glucose, fell after birth to rise again in adulthood. 5) Insulin injection caused an increase in liver glycogen from E17 onwards, and also increased glycogen in brain and placenta on E19. However, insulin decreased glycogen in brain and kidney by E21. 6) Adrenaline caused an increase in the umbilical venous-arterial glucose difference at E15 and E17 with a concomitant increase in liver, brain and heart glycogen at E15. By E21 the response of liver glycogen to adrenaline was drastically reversed. Our data suggest that the mechanism regulating glucose homeostasis changes half way through fetal development. Tissue self-regulation is replaced with a centralized mechanism similar to that of the adult.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Changes in brain glucose retention produced by the stimulation of an insulin-sensitive reflexogenic zone in rats.

Although it has been reported that insulin decreases glucose efflux from the brain causing an increase in brain glucose retention, its mechanism of action is still unknown. The present results indicate that peripheral insulin may act through the stimulation of insulin-sensitive receptors localized in the region irrigated by the coeliac trunk and innervated by the vagus nerve. Stimulation of this zone in anaesthetized, artificially ventilated rats with a bolus millidose of insulin (50 mU) caused a significant increase in brain glucose retention as a result of decreased glucose efflux from the brain. The same dose of insulin injected 1-2 cm caudally in the abdominal aorta below the coeliac trunk failed to increase brain glucose retention. The effects of insulin above the coeliac trunk disappear when the vagus nerve is sectioned, suggesting that the vagus participates as the afferent pathway of this reflex.

Animals↗
PubMed1990

Compensation by fetal erythrocytes of plasma glucose changes in rats.

Changes in plasma glucose and glucose and glycogen content in fetal erythrocytes (FRBCs) were studied in rats between days 15 and 21 of gestation and in adult rats. Plasma and FRBC glucose concentrations increased during fetal life and were higher in erythrocytes than in plasma. Glycogen was higher in FRBCs than in adult erythrocytes and tended to decrease from day 15 to 19 of gestation and to increase again on day 21. When FRBCs were incubated in vitro in different glucose concentrations to study their capacity to compensate for changes in plasma glucose concentration, younger cells showed better glucose-buffering capacities. Glucose and glycogen levels in FRBCs increased when they were incubated in high-glucose medium, and the glycogen concentration reached was higher in the early fetal stage than by the end of gestation. Nevertheless, adult erythrocytes accumulated more glycogen in high-glucose medium than cells from any of the fetal-aged erythrocytes. When glucose was injected intraperitoneally into fetuses of different ages, there was an increase of 3.7 microM/ml in glucose concentration in blood from the umbilical artery and 2.5 microM/ml in blood from the umbilical vein. FRBCs buffered some of this change, as evident by an increase in glycogen content. Again, buffering capacity was greater for erythrocytes in younger fetuses. Epinephrine diminished glycogen concentration in venous FRBCs on days 19 and 21 of gestation even in hyperglycemia. Insulin diminished glucose concentration in arterial plasma on days 17 and 21 of gestation, but there were no changes in glucose and glycogen in FRBCs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

The posterior fundoplasty in the treatment of gastroesophageal reflux.

The fundoplasty in the treatment of gastroesophageal reflux is essentially a modification of the Nissen fundoplication with the same percentage of effectiveness in the control of reflux but with a lower rate of undesirable side effects. The procedure is easy to perform. The author has performed this procedure more than 1,500 times within the last 20 years with very satisfactory results.

Esophagus↗
PubMed1989

Erythrocytes and glucose homeostasis in rats.

The capacity of erythrocytes to modify their glycogen stores to compensate for changes in glucose concentration in plasma was studied. Experiments in vitro and in vivo demonstrated that erythrocytes absorbed and incorporated glucose into their glycogen stores when glucose concentration in the medium was high and liberated it when the concentration was low. Epinephrine administration inhibited glucose absorption by erythrocytes, and in its presence, erythrocytes liberated glucose from their glycogen stores, being unable to compensate for this rise in glucose concentration in plasma. Similar results were obtained when endogenous secretion of epinephrine was enhanced by carotid sinus-chemoreceptor stimulation. Insulin had no effect on the capacity of erythrocytes to absorb glucose. These data suggest a role for erythrocytes in the transport of glucose to different regions in the organism's circulation and in the regulation of glucose concentration in plasma.

Animals↗
PubMed1979

[Gastrin].

Explore the source record for details and available documents.

Gastrins↗
PubMed1975

A new antireflux procedure at the esophagogastric junction: experimental and clinical evaluation.

In posterior fundoplasty, a derivative of Nissen fundoplication, the fundus is passed behind the abdominal esophagus and fixed to the anterior aspect of the stomach, thus modifying the angle of entrance of the esophagus, creating a posterior gastric reservoir relatively inaccessible to the cardia. In dogs, it was a successful as a Nissen fundoplication in reversing esophagitis caused by reflux and daily administration of histamine. In another group of dogs, a cylindrical resection of the last 4 or 6 cm of the esophagus and a posterior fundoplasty were performed simultaneously. In spite of the daily administration of 30 mg of histamine, none of the dogs developed esophagitis. Posterior fundoplasty has proved effective in 14 patients with hiatal hernia observed for three years. In five patients undergoing a Heller myotomy for achalasia, it was used successfully to prevent postoperative regurgitation.

Adolescent↗