ABSTRACT
La adaptación al medio extrauterino incluye un aumento considerable de la PaO2, que induce especialmente cambios estructurales y vasoactivos en la circulación pulmonar, que llevarán a una circulación previamente pobremente irrigada, a recibir ∼100% del gasto cardíaco del recién nacido, permitiendo el normal intercambio gaseoso. La regulación local de la circulación arterial pulmonar neonatal basal, es mantenida por un delicado equilibrio entre agentes vasoconstrictores y vasodilatadores. Este equilibrio, permite mantener la circulación pulmonar como un territorio de gran flujo sanguíneo y baja resistencia. La acción de los vasoconstrictores permite la formación de las interacciones entre actina y la cadena liviana de la miosina, esta es inducida en la célula muscular lisa principalmente por dos vías: a) dependiente de calcio, que consiste en aumentar el calcio intracelular, facilitando finalmente la unión de actina y miosina, y b) independiente de calcio, la cual a través de consecutivas fosforilaciones logra sensibilizar a las proteínas involucradas promoviendo la unión de actina y miosina. Estas acciones son mediadas por agonistas generados principalmente en el endotelio pulmonar, como endotelina-1 y tromboxano, o por agonistas provenientes de otros tipos celulares como la serotonina. Los agentes vasodilatadores regulan la respuesta vasoconstrictora, principalmente inhibiendo la señalización que induce la vasocontricción independiente de calcio, a través de la activación de proteínas quinasas que inhibirán la función de la ROCK quinasa, uno de los últimos efectores de la vasocontricción antes de la formación de la unión de actina y miosina. Esta revisión describe estos mecanismos de primordial importancia en las primeras horas de nuestra vida como individuos independientes.
The extrauterine-milieu adaptation includes a considerable increase in PaO2, that specifically induces structural and vasoactive changes at pulmonary circulation. Such changes transform a poor irrigated circulation into a circulation that receive ∼100% of neonatal cardiac output, supporting the normal alveolar-capillary gas exchange. Local regulation of basal neonatal pulmonary circulation is maintaining by a delicate equilibrium between vasoconstrictor and vasodilator agents. This equilibrium, allows to maintain the pulmonary circulation as an hemodynamic system with a high blood flow and a low vascular resistance. Vasocontrictors action allows actin and light-chain myosin interaction. Two main pathways induced this effect in smooth muscle cell: a) a calcium dependent pathway, that increases intracellular calcium, facilitating actin - myosin binding, and b) the independent calcium pathway, which achieves through consecutive phosphorylation reactions sensitize the proteins involved, promoting the binding of actin and light-chain myosin. These actions are mediated by agonists produced mainly in the pulmonary endothelium, such as endothelin-1 and thromboxane, or by agonists from other cell types such as serotonin. Vasodilator agents regulate the vasoconstrictor response, mainly by inhibiting signals that induce calcium-independent vasoconstriction, through activation of protein kinases, which in turn will inhibit the function of ROCK kinase, one of the last effectors of vasoconstriction before formation of the actin and light-chain myosin binding. This review will focus on describing these mechanisms of primal importance in the first hours of our lives as independent individuals.
Subject(s)
Humans , Infant, Newborn/physiology , Pulmonary Circulation/physiology , Lung/blood supply , Vascular Resistance , Vasoconstriction/physiology , Vasoconstrictor Agents/antagonists & inhibitors , Vasodilation/physiology , Vasodilator Agents/antagonists & inhibitors , Adaptation, Physiological , Serotonin/physiology , Thromboxanes/physiology , Calcium , Endothelin-1/physiologyABSTRACT
Group A Streptococcal (GAS) infections have increased in frequency and severity worldwide. During April 1996, a nosocomial outbreak associated to GAS infections affected seven patients admitted to a pediatric burn unit. The causative organism was likely disseminated from the source patient to another child in the emergency room before he was transferred to the burn unit. Patients developed burn infections or invasive disease. One of them died due to a toxic shock syndrome and 3 other lost their skin grafts. Perineal and nasal microbiological surveillance of 42 related health care workers identified only one of them as carrier of S pyogenes. Aim: To report a molecular analysis of an apparently clonal outbreak. Material and methods: The available isolates were analyzed by molecular methods including random amplified polymorphic DNA analysis (RAPD) with 4 different primers, Sma-I pulsed field gel electrophoresis (PFGE) analysis, and speA, speB and speC detection by polymerase chain reaction (PCR). Results: Two phylogenetically distant and sequentially isolated bacterial groups were identified either by RAPD analysis with selected primers or by Smal-PFGE analysis. The first group involved isolates identified in two patients that included the lethal case. The second bacterial group comprised 5 clinical isolates and the perineal and nasal isolates obtained from a health care worker. Only strains belonging to the first group harbored the speA gene and were associated with invasive disease. The second group could be split further in two subgroups according to their speB profile. Conclusions: RAPD analysis with selected primers can reproduce the PFGE-discriminating ability on the epidemiological analysis of GAS infections