Sex steroid hormones, cardiovascular diseases and the metabolic syndrome.

The metabolic syndrome (MS) has become the new epidemic of this century. Although its associated pathologies may vary, the most common are hypertension, central obesity, dyslipidemia, low High Density Lipoproteins (HDL), high Low Density Lipoproteins (LDL), and type-2 diabetes. Several others can be present, such as hypertriglyceridemia, cardiopathies, atherosclerosis, altered levels of sex hormones, hypogonadism in men and nephropathy. Several factors such as gender, age, race, lifestyle and diet may contribute to modify its prevalence: men develop cardiovascular diseases at an earlier age than pre-menopausal women, who seem to be protected by the antioxidant properties of estrogens. The present review offers information, mostly from 2008 to the present, as well as our own work on a rat model of MS, which was developed by the administration of sucrose in drinking water. Sex steroid hormones play an important role in the appearance and development of the MS and of cardiovascular diseases. Variations in the levels of sex hormones, whether normal or pathological, may have significant influence in the onset of several diseases, metabolic syndrome components included, as well as in the behavior of tissues and organs. These are just some of the non-reproductive actions of sex hormones.

[The uncertain future of general surgery. A specialty in the process of extinction]. / El futuro incierto de la cirugía general. Una especialidad en proceso de extinción.

General surgery was the first specialty of medicine. Nowadays, it is fragmented a progressive number of specialties, and has lost many of its fields. What will be the future of general surgery? What will be its repercussion on teaching surgery? From the point of view of a professor of surgery, our specialty today has nothing like what it was in the middle of the past century. Every day, its field of action becomes more and more reduced. Probably in the future, training in surgery will be limited to 2 years of basic knowledge, before the resident goes into the specialty of his/her choice.

[Unnecessary operations in the exercise of surgery. A topic of our times with serious implications in medical ethics]. / Las operaciones innecesarias en el ejercicio de la cirugía. Un tema de nuestro tiempo con graves implicaciones en la ética médica.

Unnecessary operations represent between 20 and 25% of total surgical practice. This article analyses causes, history, enormous economic effects and their consequences as an iatrogenic harm. Looking for a solution to the problem of unnecessary operations is urgent because these surgeries have a direct effect on the field of ethics and morality in the practice of surgery.

Insulin-induced endothelin release and vasoreactivity in hypertriglyceridemic and hypertensive rats.

Insulin-elicited endothelin release in hypertriglyceridemic, hypertensive, hyperinsulinemic (HTG) rats was shown. Weanling male Wistar rats were given 30% sucrose in their drinking water for 20-24 wk. In vitro contractions of aorta and femoral arteries were elicited with 40 mM KCl. Endothelin release induced with KCl plus 50 microU/ml insulin resulted in increases in contractile responses: 41 +/- 5.9 and 57 +/- 6% for control and 65.5 +/- 6 and 95 +/- 9% for HTG aortas and femoral arteries, respectively. The endothelin ET(B)-receptor blocker BQ-788 decreased responses to KCl + insulin by 39 +/- 8 and 53 +/- 5% in control and 48 +/- 13 and 79 +/- 3.5% in HTG aortas and femoral arteries, respectively. The ET(A)-receptor antagonist PD-151242 inhibited these responses by 12 +/- 10 and 1 +/- 9% in control and by 51.5 +/- 9 and 58.5 +/- 1% in HTG aortas and femoral arteries, respectively. These results suggest that endothelin may contribute to the hypertension in this model.

[History of surgical treatment of gastroesophageal reflux]. / La historia de las operaciones para el tratamiento del reflujo gastroesofágico.

There exists, in our times, a great confusion concording the different techniques for the treatment of gastroesophageal reflux. Today, for instance, we use the name "fundoplication" for different operations that, in many occasions, have nothing to do with the original description of the technique. It can be said that there exists a great lack of knowledge of the historical origins and of the evolution of all of these operations. The authors of this article have done a large-scale review of the original publications, as they appeared, for the first time, in medical literature.

An approach to the historical evolution of surgical operations for the treatment of gastroesophageal reflux.

There exists great confusion concerning the different techniques for the treatment of gastroesophageal reflux. For instance, we apply the term fundoplication to different operations that often have nothing to do with the original description, and there is a serious lack of knowledge of the historical origins of many of these operations. This analysis is the result of a large review of the operations, and of the original papers as they were published.

Esophageal fibrovascular polyp protruding from the mouth.

A case of a 66-year-old woman with a giant fibrovascular polyp protruding from the mouth is presented. The polyp was successfully removed by a cervical esophagotomy.

[An operative primary health care services model including physicians and technicians]. / Un modelo operativo de servicios de atención primaria a la salud con médicos y técnicos.

The operative Model of Primary Health Care, was developed to offer health services to a population living under conditions of extreme poverty in the municipality of Chimalhuacán, State of México. This article describes the theorical framework, organization and operationalization of an innovative model, changing the current paradigm of clinical practice to include allied health personnel with and especial training. At the core of the model is the Basic Unit of Primary Care that includes one physician and five allied health technicians for each 15,000 habitants. This model offer an alternative to improve the utilization of available personnel and infrastructure. Finally this paper emphasizes the importance of the permanece, surveillance and evaluation of the model.

Regulation by glucose availability of tension development and electrical activity in fetal and neonatal rat hearts.

The aim of the present article was to study if changes in glucose availability modify the functional activity of the glucose-dependent developing heart. Our data indicate that a decrease in glucose availability increases tension development and action potential duration at early fetal stages. This fact could probably be explained by the enhancement of Ca2+ movements that regulate the number and turnover rate of membrane glucose transporters in muscle cells. The sensitivity to glucose availability decreases postnatally as the heart becomes fatty acid-dependent.

[The development of cardiac function and its relation to metabolism during the perinatal period]. / Desarrollo de la función cardíaca y su relación con el metabolismo durante el periodo perinatal.

Several aspects of heart development are reviewed such as development of excitability and electrical and mechanical activity of the heart. Special emphasis is made upon metabolic changes during heart development and its possible consequences on electrical and mechanical activity.

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)

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)

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)

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.