Search

PURPOSE: The aim of this study was to identify, assess, and reach a consensus on the professional competencies that optometrists must acquire during their undergraduate training at the University of Valladolid. The results obtained may be useful in the revision of the current curriculum. METHODS: A three round Delphi study was carried out with the participation of 116 participants grouped in 7 panels. In the first round, competencies were identified through an open-ended question and their frequency calculated. In the successive 2nd and 3rd rounds, the consensus and stability of each competency was established. RESULTS: A total of 56 professional competencies were identified, with 43 of them (77%) achieving a consensus among participants, of which the highest scores were obtained by the competencies that correspond to health functions of primary visual care. Out of the 13 competencies without consensus, for 11 of them this was due to the significant differences in assessment among the consulted participants; for 8 competencies (14%) response stability was found, while neither consensus nor stability were reached in 5 (9%) of the identified competencies. CONCLUSIONS: The results obtained with this Delphi study provide a set of relevant competencies for updating the curriculum of the university Degree in Optics and Optometry at the University of Valladolid, improving its suitability to current and future professional reality.

The molecular mechanisms underlying O

Guinea pigs (GP), originally from the Andes, have absence of hypoxia-driven carotid body (CB) reflex. Neonatal mammals have an immature CB chemo reflex and respond to hypoxia with metabolic changes arising from direct effects of hypoxia on adrenal medulla (AM). Our working hypothesis is that adult GP would mimic neonatal mammals. Plasma epinephrine (E) has an AM origin, while norepinephrine (NE) is mainly originated in sympathetic endings, implying that specific GP changes in plasma E/NE ratio, and in blood glucose and lactate levels during hypoxia would be observed. Experiments were performed on young adult GP and rats. Hypoxic ventilation (10% O

Resumen del trabajo presentado al European Respiratory Society (ERS) International Congress, celebrado en Paris (Francia) del 15 al 19 de septiembre de 2018., [Rationale & Aim]: Experimental evidences indicate a correlation among chronic intermittent hypoxia (CIH), increased carotid body (CB) activity, enhanced sympatho-respiratory coupling and arterial hypertension. The recurrent hypoxia/reoxygenation episodes in CIH models produce CB sensitization increasing secretory response and chemoreceptor input to the brainstem, exaggerating the sympathetic reflex. CIH effect in the guinea pig CB, with a hypofunctional CB and lack of ventilatory responses to hypoxia, has not been studied., [Methods]: Guinea pigs were exposed to CIH (21%O2-80s / 5%O2-40s 8h/day; 30 days) and CB secretory response, pletismographic parameters, systemic arterial pressure and sympathetic activity were measured and compared to control animals., [Results]: Ventilatory data showed that only intense hypoxia induced significant increase of minute ventilation in both groups of animals. CB response to hypoxia (catecholamine (CA) secretion or Ca2+i changes) were not observed in C or CIH animals. Plasma CA, heart rate and mean arterial blood pressure were significantly increased in CIH guinea pigs., [Conclusion]: CIH induced hypoxic activation of the sympathetic system non-dependent of CB chemoreceptors, promoting cardiovascular adjustments. Guinea pigs can be a model to study the CB-dependent and nondependent effects induced by CIH., Spanish Ministry of Economy and Competitiveness, MINECO/FEDER, UE (BFU2015-70616-R) and CIBERES, ISCiii (CB06/06/0050).

Resumen del trabajo presentado al European Respiratory Society (ERS) International Congress, celebrado en Paris (Francia) del 15 al 19 de septiembre de 2018., [Rationale & Aim]: Chronic sustained hypoxia (CSH) initiates physiological adaptations to maintain oxygen levels but also has deleterious effects as pulmonary hypertension (PH). Chronic intermittent hypoxia (CIH), as found in obstructive sleep apnea, is associated with the development of systemic hypertension and cardiovascular pathologies. Our aim was to compare systemic and pulmonary hypertension and endothelial dysfunction development in rats exposed to CSH vs. CIH., [Methods]: We exposed male rats to sustained hypoxic atmosphere (10%O2; pO2≈70 mmHg, 14 days) or intermittent hypoxia (5%O2 40s, 21%O2 80s, 8h/day, 21 days). We measured pulmonary artery (PA) pressure by right heart catheterization, Fulton index, vasomotor responses in PA using small vessels myography and L- arginine-NO metabolism., [Results]: Systemic and pulmonary hypertension, besides left ventricular hypertrophy, occurs in response to CIH exposure in rats, preserving pulmonary artery endothelial integrity, but decreasing NO production and eNOS protein expression. Conversely, CSH exposure triggers CB mediated respiratory chemoreflex, PH and right ventricular hypertrophy, besides blunted pulmonary vascular relaxation to carbachol and reduced plasma L-arginine: asymmetric dimethyl arginine (ADMA) ratio., [Conclusion]: CSH and CIH point to different targets and different mechanisms to produce endothelial dysfunction and systemic and pulmonary hypertension in the rat., Spanish Ministry of Economy and Competitiveness, MINECO/FEDER, UE (BFU2015-70616-R); CIBER Enfermedades Respiratorias, ISCiii (CIBERES, CB06/06/0050).

Adult animals that have been perinatally exposed to oxygen-rich atmospheres (hyperoxia), recalling those used for oxygen therapy in infants, exhibit a loss of hypoxic pulmonary vasoconstriction, whereas vasoconstriction elicited by depolarizing agents is maintained. Loss of pulmonary hypoxic vasoconstriction is not linked to alterations in oxygen-sensitive K(+) currents in pulmonary artery smooth muscle cells. Loss of hypoxic vasoconstriction is associated with early postnatal oxidative damage and corrected by an antioxidant diet. Perinatal hyperoxia damages carotid body chemoreceptor cell function and the antioxidant diet does not reverse it. The hypoxia-elicited increase in erythropoietin plasma levels is not affected by perinatal hyperoxia. The potential clinical significance of the findings in clinical situations such as pneumonia, chronic obstructive pulmonary disease or general anaesthesia is considered.Adult mammalians possess three cell systems that are activated by acute bodily hypoxia: pulmonary artery smooth muscle cells (PASMC), carotid body chemoreceptor cells (CBCC) and erythropoietin (EPO)-producing cells. In rats, chronic perinatal hyperoxia causes permanent carotid body (CB) atrophy and functional alterations of surviving CBCC. There are no studies on PASMC or EPO-producing cells. Our aim is to define possible long-lasting functional changes in PASMC or EPO-producing cells (measured as EPO plasma levels) and, further, to analyse CBCC functional alterations. We used 3- to 4-month-old rats born and reared in a normal atmosphere or exposed to perinatal hyperoxia (55-60% O2 for the last 5-6 days of pregnancy and 4 weeks after birth). Perinatal hyperoxia causes an almost complete loss of hypoxic pulmonary vasoconstriction (HPV), which was correlated with lung oxidative status in early postnatal life and prevented by antioxidant supplementation in the diet. O2 -sensitivity of K(+) currents in the PASMC of hyperoxic animals is normal, indicating that their inhibition is not sufficient to trigger HPV. Perinatal hyperoxia also abrogated responses elicited by hypoxia on catecholamine and cAMP metabolism in the CB. An increase in EPO plasma levels elicited by hypoxia was identical in hyperoxic and control animals, implying a normal functioning of EPO-producing cells. The loss of HPV observed in adult rats and caused by perinatal hyperoxia, comparable to oxygen therapy in premature infants, might represent a previously unrecognized complication of such a medical intervention capable of aggravating medical conditions such as regional pneumonias, atelectases or general anaesthesia in adult life.

The views presented in this article are the fruit of reflections and discussion with my colleagues at Valladolid and with the members of the Sleep Apnea Hypopnea Syndrome Group of the CIBERES (Spain). We have assembled the article in three sections. In the first one we provide a mechanistic description of obstructive sleep apnea (OSA) and all of its components, including the repetitive episodes of upper airways (UA) obstruction and accompanying hypoxic hypoxia, the respiratory efforts to fight and overcome the obstruction, and the sleep fragmentation due to the hypoxia-triggered arousal reactions, all events occurring during sleep hours with frequencies that might reach up40-50 episodes/sleep hour. When OSA is accompanied by some of the elements of a big cohort of associated pathologies (vascular, metabolic, and neuropsychiatric) it conforms the obstructive sleep apnea syndrome (OSAS). The high frequency of OSAS in adults (35 years old) and the costs in every regard of the treatment makes the syndrome a primary importance socio-sanitary problem. In the second section, we describe the experimental models of OSAS, basically the episodic repetitive hypoxic model described by Fletcher and coworkers in 1992, today named in short intermittent hypoxia (IH). From these lines, we want to call for some kind of consensus among researchers to lessen the dispersion of IH protocols. Finally, in the last section we intend to share our optimism with all ISAC members. The optimism is based on the recognition that carotid body (CB) chemoreceptors are critical elements of one of the main pathophysiologic loops in the genesis of OSAS. Therefore, we believe that all of us, as ISAC members, are well qualified to contribute in multidisciplinary research teams with well defined translational interests.

The views presented in this article are the fruit of reflections and discussion with my colleagues at Valladolid and with the members of the Sleep Apnea Hypopnea Syndrome Group of the CIBERES (Spain). We have assembled the article in three sections. In the first one we provide a mechanistic description of obstructive sleep apnea (OSA) and all of its components, including the repetitive episodes of upper airways (UA) obstruction and accompanying hypoxic hypoxia, the respiratory efforts to fight and overcome the obstruction, and the sleep fragmentation due to the hypoxia-triggered arousal reactions, all events occurring during sleep hours with frequencies that might reach up >40–50 episodes/sleep hour. When OSA is accompanied by some of the elements of a big cohort of associated pathologies (vascular, metabolic, and neuropsychiatric) it conforms the obstructive sleep apnea syndrome (OSAS). The high frequency of OSAS in adults (>35 years old) and the costs in every regard of the treatment makes the syndrome a primary importance socio-sanitary problem. In the second section, we describe the experimental models of OSAS, basically the episodic repetitive hypoxic model described by Fletcher and coworkers in 1992, today named in short intermittent hypoxia (IH). From these lines, we want to call for some kind of consensus among researchers to lessen the dispersion of IH protocols. Finally, in the last section we intend to share our optimism with all ISAC members. The optimism is based on the recognition that carotid body (CB) chemoreceptors are critical elements of one of the main pathophysiologic loops in the genesis of OSAS. Therefore, we believe that all of us, as ISAC members, are well qualified to contribute in multidisciplinary research teams with well defined translational interests., Supported by the MICINN grant (BFU2007-61848) and Accion Integrada PT2009-0172 and ICiii-CIBERES CB06/06/0050.