[Mortality by COVID-19 in Spain. Approximation through public health expenditure by autonomous communities.] / Mortalidad por COVID-19 en España durante la primera oleada de la pandemia. Aproximación a través del gasto público sanitario por comunidades autónomas.

OBJECTIVE: The irruption of SARS-CoV-2 and its different incidence on the regional mortality rate could be revealing the effects of the change in the paradigm of health justice, initiated in Spain in 2010 and applied, more or less enthusiastically, by the different autonomous communities. The objective of this work was to look for if the socio-economic conditions and the policy of budgetary expenditure followed by the different Spanish autonomous communities have incidence, by themselves, on the mortality rate caused by the SARS-CoV-2. METHODS: Econometric research based on Multiple Linear Regression to determine the direct cause-effect relationship between the dependent variable, mortality associated with COVID-19, with explanatory variables of the health budget and socio-economic type. RESULTS: The number of deaths caused by COVID-19 has a positive relationship with the rate of GDP per capita and inversely with expenditure on hospital and specialized services, teaching and IRMs and with the resources allocated to health over the last nine years. A reduction in any of these health budget variables leads to an increase in mortality caused by COVID-19. CONCLUSIONS: The COVID-19 mortality rate has hit the wealthiest autonomous communities hardest but, above all, has hit those that, although richer, applied more restrictive budgetary measures in the period 2010-2018.

OBJETIVO: La irrupción del SARS-CoV-2 y su desigual incidencia sobre la tasa de mortalidad autonómica podría estar desvelando los efectos del cambio de paradigma de justicia sanitaria, iniciado en España durante 2010 y aplicado, de forma más o menos entusiasta, por las distintas comunidades autónomas. El objetivo de este trabajo fue buscar si las condiciones socio-económicas y la política de gasto presupuestario seguido por las distintas comunidades autónomas españolas tienen incidencia, por sí solas, sobre la tasa de mortalidad causada por el SARS-CoV-2. METODOS: Utilizando como fuente los datos proporcionados por el Instituto Nacional de Estadística y el Ministerio de Sanidad se elaboró un panel de datos de las diecisiete comunidades autónomas desde 2010 hasta 2018. Mediante una Regresión Lineal Múltiple, se determinó la relación causa-efecto entre la variable dependiente: la mortalidad asociada a la COVID-19, con variables explicativas de tipo presupuestarias sanitarias y socio-económicas. RESULTADOS: La tasa de mortalidad causada por COVID-19 tienen una relación positiva y directa con la tasa del PIB per Cápita e inversa con los gastos en servicios hospitalarios y especializados, en docencia y MIR y con los recursos destinados a salud pública durante los últimos nueve años. CONCLUSIONES: Una reducción en cualquiera de las variables presupuestarias sanitarias provoca un aumento en la mortalidad causada por COVID-19. La mortalidad por COVID-19 ha castigado más a las comunidades autónomas más ricas, pero sobre todo, ha castigado más a aquellas que, aun siendo más ricas, aplicaron medidas presupuestarias más restrictivas en el período 2010-2018.

Hypothalamic mediated action of free fatty acid on growth hormone secretion in sheep.

Experimental data suggest that elevated FFA levels play a leading role in the impaired GH secretion in obesity and may therefore contribute to the maintenance of overweight. GH has a direct lipolytic effect on adipose tissue; in turn, FFA elevation markedly reduces GH secretion. This suggests the existence of a classical endocrine feedback loop between FFA and GH secretion. However, the FFA mechanism of action is not yet understood. The involvement of somatostatin (SRIH) is controversial, and in vitro experiments suggest a direct effect of FFA on the pituitary. In sheep it is possible to collect hypophysial portal blood and quantify SRIH secretion in hypophysial portal blood under physiological conscious and unstressed conditions. In this study we determined the effects of FFA (Intralipid and heparin) infusion on peripheral GH and portal SRIH levels in intact rams chronically implanted with perihypophysial cannula and in rams actively immunized against SRIH to further determine SRIH-mediated FFA effects on GH axis. Immediately after initiation of Intralipid infusion, we observed a marked increase in the FFA concentration (2160 +/- 200 vs. 295 +/- 28 nmol/ml; P < 0.01) as well as a significant decrease in basal GH secretion (1.8 +/- 0.1 vs. 2.5 +/- 0.3 ng/ml; P < 0.05) and a drastic reduction of the GH response to i.v. GH-releasing hormone injection (4.8 +/- 0.7 ng/ml in FFA group vs. 35.8 +/- 9.7 ng/ml in saline group; P < 0.01). No change in plasma insulin-like growth factor I levels was observed. During the first 2 h of infusion, the GH decrease observed was concomitant with a significant increase in portal SRIH levels (22.1 +/- .2 vs. 13 +/- 1.6 pg/ml; P < 0.01). In rams actively immunized against SRIH, the effect of FFA on basal GH secretion was biphasic. During the first 90 min of infusion, the decrease in GH induced by FFA was significantly blunted in rams actively immunized against SRIH (57 +/- 9% for immunized rams vs. 23.5 +/- 2.5% for control rams). This corresponds to the period of increased SRIH portal levels. After this first 90-min period, no difference was seen between control and immunized rams. Our results show that FFA exert their inhibitory action on the GH axis at both pituitary and hypothalamic levels, the latter mainly during the first 90 min, through increased SRIH secretion.

Endotoxin injection increases growth hormone and somatostatin secretion in sheep.

Endotoxin has been shown to stimulate GH secretion in human and sheep. However, changes in hypothalamic neurohormones involved in the GH regulation by endotoxin have never been studied in vivo. In sheep it is possible to collect hypophysial portal blood (HPB) and quantify GH-releasing hormone (GHRH) and somatostatin (SRIH) secretion under physiological conditions. The purpose of this study was to determine the effect of an acute i.v. endotoxin administration on the secretion of these peptides in sheep. Endotoxin induced a sustained increase of GH (x6.2 +/- 1.3) in intact rams. This stimulation was delayed and less marked when compared with the hypothalamic-pituitary-adrenal axis. Surprisingly, the GH increase was associated with an important rise of jugular (x10.6 +/- 2.4) and portal (x7.9 +/- 3) SRIH levels, without a significant GHRH increase. To determine if the portal SRIH increase was a consequence of an increased short feedback of GH, we studied GH response to endotoxin after a previous GHRH injection to deplete the pituitary pools of GH. In that case, despite the absence of increase of GH after endotoxin treatment, SRIH levels was markedly increased. For the first time we have observed an experimental situation in sheep with a simultaneous and closed amplitude increase in jugular and portal SRIH. The source of jugular SRIH is likely the gastrointestinal tract and the increased jugular SRIH release in systemic circulation might be in part responsible for the increase of hypophysial portal SRIH. Ultimately our results show that endotoxin induced a complex reaction at multiple levels with a specific increase in both portal and peripheral SRIH levels. The surprising association of a lack of change in GHRH release and an increased secretion of SRIH with the increase of GH suggests that the effect of endotoxin on GH axis is mainly a pituitary one. The selective blockade of somatostatin should be useful for a better knowledge of the role of SRIH stimulation in the physiopathology of septic shock.