ABSTRACT
En esta segunda parte de nuestra revisión se propone a la solución polarizante como una alternativa más, además de otras ya existentes, para el mantenimiento de las células cardíacas durante un infarto, apoyado en el cambio metabólico cardíaco durante la hipoxia.
Based on the cardiac metabolic changes during hypoxia, in this second part of our review we propose, the polarizing solution as an alternative for the maintenance of the cardiac cells during an infarction, in conjunction with other alternative therapies.
Subject(s)
Animals , Humans , Rats , Hypoxia/metabolism , Glucose/therapeutic use , Insulin/therapeutic use , Monosaccharide Transport Proteins/therapeutic use , Myocardial Ischemia/metabolism , Myocardium/metabolism , Potassium/therapeutic use , Clinical Trials as Topic , Myocardial Ischemia/drug therapyABSTRACT
The protective role of estrogens against peripheral vascular and coronary disease in women is well documented; however, it is not present in diabetic women. Estrogens reduce tension development through non-genomic mechanisms that include changes in calcium concentrations in endothelial and smooth muscle cells, and regulation of nitric oxide synthase (NOS) in endothelial cells. Insulin increases endothelin-1 (ET-1) release from endothelial cells modulating smooth muscle calcium levels and elevating force generated by femoral and coronary arteries. This paper examines whether 17/β-estradiol (E2β) modulates changes in femoral and coronary artery contractility induced by insulin. Femoral and coronary arteries were obtained from male Wistar rats, placed in isolated tissue baths for in vitro studies, perfused with different solutions, and the contractile response to KCl 40 mmol/L was measured. Insulin increased arterial contraction induced by KCl. This increase was not present when the endothelium was removed. In the presence of E2β, we observed a dose dependent reduction in the tension developed and this effect disappeared when the endothelium was removed. The insulin-induced contraction was significantly reduced in presence of E2β. These data indicate that the effect of insulin on femoral and coronary vascular contractility is modulated by E2β.
Los estrógenos protegen a la mujer contra enfermedades vasculares periféricas y centrales; sin embargo, su papel se pierde con la diabetes. Los estrógenos reducen la tensión en las arterias mediante cambios en el calcio intracelular en células endoteliales y musculares lisas y la regulación de la óxido nítrico sintasa en células endoteliales. La insulina incrementa la liberación de endotelina-1 (ET-1) en células endoteliales aumentando la fuerza generada por las arterias. En este estudio se examina si el 17/β-estradiol (E2β) modula los cambios en la contractilidad inducidos por insulina en las arterias femorales y coronarias. Las arterias se obtuvieron de ratas Wistar macho y se colocaron en cámaras para tejido aislado para perfundirse in vitro con distintas concentraciones de insulina y estrógenos estimulando la contracción con KCl 40 mmol/L. La insulina elevó la fuerza de la contracción inducida por KCl. Este incremento desapareció cuando se eliminó el endotelio. El E2β disminuyó la tensión desarrollada por las arterias conforme se aumentó la dosis y el efecto desapareció al quitar el endotelio. El incremento en la tensión por insulina disminuyó con E2β. En conclusión el efecto de la insulina sobre las arterias femorales y coronarias se encuentra modulado por el E2β.(Arch Cardiol Mex 2003; 73:254-260).
Subject(s)
Animals , Male , Rats , Estradiol/physiology , Insulin/pharmacology , Muscle Contraction/drug effects , Muscle Contraction/physiology , Muscle, Smooth, Vascular/drug effects , Muscle, Smooth, Vascular/physiology , Rats, WistarABSTRACT
El propósito de esta revisión es analizar las diferentes rutas metabólicas utilizadas por el corazón en momentos del desarrollo y situaciones como la hipoxia y la enfermedad, para tratar de comprenderlas y utilizarlas para restablecer las condiciones normales en células que se encuentran comprometidas durante un infarto.
We describe different metabolic states of the heart, during developmental stages, hypoxia and illness, to understand and use them to try to reestablish the normal conditions. (Arch Cardiol Mex 2003; 73:218-229).
Subject(s)
Adult , Animals , Humans , Myocardium/metabolism , Biological Evolution , Cell Hypoxia/physiology , Ischemia/metabolismSubject(s)
Humans , Adolescent , Adult , Middle Aged , Calcium-Transporting ATPases , Calcium/metabolism , Diabetes Mellitus/diagnosis , Diabetes Mellitus/metabolism , Hypertension/diagnosis , Hypertension/metabolism , Homeostasis/physiology , Hyperinsulinism/enzymology , Receptor, Insulin/metabolism , Cohort Studies , Cross-Sectional StudiesSubject(s)
Humans , Animals , Cardiovascular System/cytology , Cardiovascular System/drug effects , Protein Kinase C/analysis , Protein Kinase C/drug effects , Protein Kinase C/physiology , Protein-Tyrosine Kinases/antagonists & inhibitors , Protein-Tyrosine Kinases/drug effects , Protein-Tyrosine Kinases/physiology , Signal Transduction , Signal Transduction/physiology , Cell Division , Cell Division/physiology , Enzyme Inhibitors/pharmacology , ras Proteins , ras Proteins/physiologyABSTRACT
Se revisan distintos aspectos del desarrollo del corazón como son el desarrollo de la excitabilidad y de las actividad eléctrica y mecánica del corazón. Se hace especial énfasis en los cambios que ocurren en el metabolismo del corazón en desarrollo y sus posibles consecuencias sobre la actividad eléctrica y mecánica
Subject(s)
Humans , Fetal Heart/metabolism , Heart/physiology , Heart Rate/physiologyABSTRACT
La desnutrición puede ser una causa o consecuencia de deficiencias ventilatorias en el pulmón perinatall. La desnutrición disminuye el metablosimo oxidativo del pulmón y los procesos anabólicos incluyendo la síntesisla secreción del surfactante. En el presente trabajo se analizan los cmbios inducidos por una dieta materna hipoprotéica e hipocalórica durante la gestación y la lactancia, en la composición química de las fracciones surfactante y residual, aisladas del pulmón de ratas recién nacidas. Se estudian también los efectos de la suplementación de la dieta materna durante la lactancia con inositol y los efectos de inyecciones intraperitoneal de triglicéridos a los recién nacidos
Subject(s)
Animals , Rats , Phospholipids/metabolism , Inositol , Protein-Energy Malnutrition/diet therapy , Pulmonary Surfactants/metabolism , TriglyceridesABSTRACT
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/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 (-l5 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. This occurs just before birth as the liver becomes a reservoir for carbohydrates and responsive to insulin and adrenaline