Astaxanthin Ameliorates Blood Pressure in Salt-Induced Prehypertensive Rats Through ROS/MAPK/NF-κB Pathways in the Hypothalamic Paraventricular Nucleus.

Astaxanthin (AST) has a variety of biochemical effects, including anti-inflammatory, antioxidative, and antihypertensive functions. The aim of the present study was to determine whether AST ameliorates blood pressure in salt-induced prehypertensive rats by ROS/MAPK/NF-κB pathways in hypothalamic paraventricular nucleus.To explore the central effects of AST on the development of blood pressure, prehypertensive rats were induced by a high-salt diet (HS, 8% NaCl) and its control groups were treated with normal-salt diet (NS, 0.3% NaCl). The Dahl salt-sensitive (S) rats with HS diet for 6 weeks received AST or vehicle by gastric perfusion for 6 weeks. Compared to those with NS diet, rats with HS diet exhibited increased mean arterial pressure (MAP) and heart rate (HR). These increases were associated with higher plasma level of norepinephrine (NE), interleukin 1ß (IL-1ß), and interleukin 6 (IL-6); elevated PVN level of reactive oxygen species (ROS), NOX2, and NOX4, that of IL-1ß, IL-6, monocyte chemotactic protein 1 (MCP-1), tyrosine hydroxylase (TH), phosphorylation extracellular-signal-regulated kinase (p-ERK1/2), phosphorylation Jun N-terminal kinases (p-JNK), nuclear factor-kappa B (NF-κB) activity; and lower levels of IL-10, superoxide dismutase (SOD), and catalase (CAT) in the PVN. In addition, our data demonstrated that chronic AST treatment ameliorated these changes in the HS but not NS diet rats. These data suggested that AST could alleviate prehypertensive response in HS-induced prehypertension through ROS/MAPK/NF-κB pathways in the PVN.

ECG de enero de 2018 / ECG, January 2018

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ECG de noviembre de 2017 / ECG, November 2017

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Hypotensive acute effect of photobiomodulation therapy on hypertensive rats.

The purpose of this study was to evaluate the acute effect of photobiomodulation therapy (PBM) on arterial pressure in hypertensive and normotensive rats with application in an abdominal region. Normotensive (2K) and hypertensive (2K-1C) wistar rats were treated with PBM. Systolic arterial pressure (SAP), diastolic arterial pressure (DAP), mean arterial pressure (MAP) and heart rate (HR) were measured before, during and after PBM application. The nitric oxide (NO) serum concentration was measured before and after PBM application. Vascular reactivity study was performed in isolated thoracic aortas. Aluminum gallium arsenide (GaAlAs) diode laser was used, at 660nm wavelength and 100mW optical output. The PBM application induced a decrease of SAP in 2K-1C rats. In 2K rats, the PBM application had no effect on SAP, DAP and MAP. Moreover, the magnitude of hypotensive effect was higher in 2K-1C than in 2K rats. The PBM application induced a decrease of HR in 2K-1C and 2K, with higher effect in 2K-1C rats. In 2K-1C, the hypotensive effect induced by PBM was longer than that obtained in 2K rats. PBM application induced an elevation of NO concentration in serum from 2K-1C and 2K rats, with higher effect in 2K-1C. In isolated aortic rings PBM effect is dependent of NO release, and is not dependent of nitric oxide synthase (NOS) activation. Our results indicate that the abdominal acute application of PBM at 660nm is able to induce a long lasting hypotensive effect in hypertensive rats and vasodilation by a NO dependent mechanism.

El cateterismo radial previo dificulta la monitorización invasiva durante la cirugía cardíaca / Previous radial artery catheterization complicates invasive monitoring during cardiac surgery

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Systematic understanding of acute effects of intravenous guanfacine on rat carotid sinus baroreflex-mediated sympathetic arterial pressure regulation.

AIMS: To assess the acute effects of intravenous guanfacine, an α2A-adrenergic agonist, on sympathetic outflow from the central nervous system and on sympathetic arterial pressure (AP) response. MAIN METHODS: In anesthetized Wistar Kyoto rats, carotid sinus baroreceptor regions were isolated. Changes in electrical sympathetic nerve activity (SNA) and AP in response to a baroreceptor pressure input were examined before and after an intravenous administration of a high dose (100µg/kg, n=7) or a low dose (20µg/kg, n=5) of guanfacine. KEY FINDINGS: The higher dose of guanfacine significantly narrowed the range of the AP response (86.8±6.4 to 38.4±12.9mmHg, P<0.01) but increased the minimum AP (79.3±7.5 to 93.2±8.7mmHg, P<0.05). In the neural arc, guanfacine reduced both the response range (90.4±2.3 to 33.4±10.7%, P<0.01) and the minimum SNA (11.4±1.9 to 2.6±1.5%, P<0.01). In the peripheral arc, guanfacine increased the intercept (67.6±7.1 to 92.8±8.5mmHg, P<0.01) without a significant effect on the slope. The lower dose of guanfacine weakened the effects on both the neural and peripheral arcs. SIGNIFICANCE: Guanfacine suppressed SNA without a significant reduction of AP, which may be attributable to the peripheral vasoconstrictive effect. Reducing the dose of acutely administered intravenous guanfacine does not aid in separating the central sympathoinhibitory effect from the peripheral vasoconstrictive effect on AP in anesthetized rats in vivo.

Efectos de dos métodos de termoterapia sobre la respuesta vascular aguda y parámetros hemodinámicos en un grupo de sujetos sanos / Effects of two methods of heat therapy on the acute vascular response and hemodynamics in healthy subjects

Objetivo. Recientemente determinados recursos no farmacológicos, como el paquete caliente (PC) y los ultrasonidos (US), son utilizados en el alivio del dolor con alto grado de aceptación en la práctica clínica. Sin embargo, la evidencia experimental que apoye los posibles mecanismos por los que se producen estos beneficios es escasa. El objetivo de este estudio fue comprobar los efectos de dos métodos de termoterapia (PC y US) sobre la respuesta vascular aguda y parámetros hemodinámicos en sujetos sanos. Materiales y métodos. Estudio experimental en 20 sujetos sanos (10 hombres y 10 mujeres; edad media, 22,54±1,70 años). Se aplicaron dos intervenciones de forma aleatoria: a) PC (n=10): 15min a 60°C, y b) US (n=10): 15min a 1Mhz, y se realizaron mediciones vasculares mediante ecografía doppler con transductor de 7Mhz, antes y después de cada intervención. Parámetros vasculares: distensibilidad arterial (Da), módulo elástico (Ep), índice beta de rigidez (β), diámetro arterial sistólico y diastólico, velocidad del flujo sistólico (Vfs) y diastólico (Vfd), relación sístole/diástole (RSD), índice de resistencia (IR) e índice de pulsatilidad (IP) en la arteria braquial, y monitorización hemodinámica de la frecuencia cardiaca y de las presiones arteriales sistólica, diastólica y media. Resultados. Se encontraron diferencias en la Vfd y en el IP (p<0,05), en la intervención con PC, mientras que la intervención con US mostró cambios en la Vfd, la RSD, el IR y la Da (p<0,05). No se encontraron cambios en los parámetros hemodinámicos. Conclusiones. La fisiología del sistema vascular se modifica por la aplicación del PC y los US, sin afectar los parámetros hemodinámicos en sujetos sanos(AU)

Objective. Recently, non-pharmacological resources to relieve pain like hot packs and ultrasound (US) have become common in clinical practice. However, little experimental evidence is available about the possible mechanisms through which these methods bring about pain relief. We aimed to determine the effects of hot packs and US on the acute vascular response and on hemodynamic parameters in healthy subjects. Materials and methods. We conducted an experimental study in 20 healthy subjects (10 men and 10 women; mean age, 22.54±1.70 years). The two interventions were randomly applied: a) hot packs (n=10): 15min at 60°C and b) US (n=10): 15min at 1Mhz. Before and after each intervention, the following vascular parameters were measured in the brachial artery using Doppler ultrasonography with a 7MHz probe: arterial compliance, elastic modulus, beta stiffness index, systolic and diastolic arterial diameters, systolic flow velocity and diastolic flow velocity, systolic/diastolic ratio, resistance index, and pulsatility index. The following hemodynamic parameters were monitored: heart rate and blood pressure (systolic, diastolic, and mean). Results. After the application of hot packs, we observed changes in diastolic flow velocity and in the pulsatility index (P<05). After the application of US, we observed changes in diastolic flow velocity, systolic/diastolic ratio, resistance index, and arterial compliance (P<05). No changes in hemodynamic parameters were observed after either intervention. Conclusions. Applying hot packs or US modifies the physiology of the vascular system but does not affect hemodynamic parameters in healthy subjects(AU)

The relationship between aortic stiffness and left ventricular dyssynchrony in hypertensive patients with preserved left ventricular systolic function.

Left ventricular (LV) dyssynchrony is often seen in patients with hypertension, even without heart failure. Arterial stiffness is well accepted as an important factor of increasing blood pressure and influencing ventricular function. The purpose of this study was to determine the relationship between aortic stiffness and LV dyssynchrony in hypertensive patients with preserved LV systolic function. Eighty hypertensive patients with preserved LV systolic function (LV ejection fraction > 50%) and 30 controls were studied. The LV systolic and diastolic dyssynchrony indices were determined as the standard deviation of the time interval from onset of the QRS complex to peak myocardial systolic velocity (Ts-SD) and to early diastolic velocity (Te-SD) and the maximal differences in Ts (Ts-Max) and Te (Te-Max) in 12 LV segments. Aortic stiffness index was calculated from aortic diameters in the systolic and diastolic phases, as measured by echocardiography and blood pressure. No relationship was observed between LV systolic and diastolic dyssynchrony indices (r = 0.057, P = .61). In simple regression, aortic stiffness parameter was related to left ventricular mass index (LVMI), E/A ratio, and LV diastolic dyssynchrony index. But using multiple linear regression, Te-Max remained as a single variable related to aortic strain and aortic stiffness index (r = -0.271, P = .008 and r = 0.269, P = .008). LVMI was related to aortic distensibility using multiple linear regression (r = -0.239, P = .02). Aortic stiffness index was related to LV diastolic dyssynchrony index and LVMI. These findings suggest that LV diastolic dyssynchronous changes may be caused by increased LV mass and arterial stiffness.