Efeitos dos componentes do vinho na função cardiovascular / Effects of wine components on cardiovascular function

Cardiovascular diseases are among the leading causes of death around the world. The prevention of these diseases is directly related to the consumption of certain foods, such as wine, which may bring benefits to the body and the cardiovascular system. Original articles and reviews were used in this essay which aims to investigate the effects of wine consumption, especially on the cardiovascular system. Wine is an alcoholic beverage obtained from the processing of organic grapes, it has substances called polyphenols which are the major compounds responsible for these beneficial effects. Among polyphenols, we can emphasize resveratrol, a substance which is mainly present in red grapes, reduces platelet aggregation and helps in the prevention of atherosclerosis. Like the wine, the grape juice also contains these substances, but the effects are not the same because of the difference in the absorption of these polyphenols. The types of grapes also contain different amounts of this substance. Studies high light that the Sangiovese, Merlot and Tannat varieties have higher concentrations of resveratrol and consequently a greater cardio-protective effect. The consumption of wine must be regular and moderate to avoid risks to health, though. In regular and moderate doses, wine can act beneficially in the body. The benefits of wine consumption to the cardiovascular system cannot be denied, but further studies must be conducted to clarify questions like which is the ideal amount of resveratrol recommended and what are other possible effects of its consumption.

Las enfermedades cardiovasculares están entre las principales causas de óbito en el mundo. El consumo de algunos alimentos esta directamente ligado a la prevención de estas enfermedades, como es el caso del vino, que puede producir efectos benéficos al organismo yal sistema cardiovascular. En este análisis fueran utilizados artículos originales y de revisión, y el objetivo fue pesquisar los efectos causados por el consumo de vino, principalmente en el sistema cardiovascular. El vino es una bebida alcohólica resultante de la transformación biológica de la uva, posee sustancias denominadas polifenoles que son los grandes responsables por los efectos benéficos. Entre los polifenoles se destacan el resveratrol, sustancia presente principalmenteen las uvas tintas y que actúa previniendo la ateroesclerosis por disminuir la agregación plaquetaria. Así como el vino, el jugo de uva posee estas sustancias, pero los efectos no son los mismos porque la absorción de los polifenoleses diferente. Los tipos de uvas también poseen diferentes cantidades de estas sustancias. Los estudios destacan las variedades Sangiovese, Merlot y Tannat con mayores concentraciones de resveratrol y, consecuentemente, mayor efecto en la protección cardiovascular. Pero el consumo de vino debe ser regular y moderado para que no traiga riesgos a la salud, en dosis regulares y moderadas el vino puede actuar benéficamente en el organismo. Son innegableslos beneficios del consumo de vino al sistema cardiovascular, pero más estudios deben serrealizados para aclarar las dudas acerca de la cantidad ideal recomendada de resveratrol asícomo otros efectos del consumo.

As doenças cardiovasculares estão entre as principais causas de morte no mundo. O consumo de alguns alimentos está diretamente ligado à prevenção dessas doenças, como é o caso do vinho, que pode produzir efeitos benéficos ao organismo e ao sistema cardiovascular. Neste levantamento bibliográfico, foram utilizados artigos originais e de revisão como objetivo de abordar os efeitos causados pelo consumo de vinho, principalmente ao sistema cardiovascular. O vinho é uma bebida alcoólica resultante da transformação biológicada uva. Possui substâncias denominadas polifenóis, responsáveis pelos efeitos benéficos.Entre os polifenóis destaca-se o resveratrol, substância presente principalmente nas uvas tintas e que age prevenindo a aterosclerosepor diminuir a agregação plaquetária. Assim,como o vinho, o suco de uva possui tais substâncias, porém os efeitos não são os mesmos, diferenciando-se na absorção dos polifenóis. Os tipos de uvas também possuem quantidades diferentes desta substância. Estudos destacam as variedades Sangiovese, Merlot e Tannat com maiores concentrações de resveratrol e, consequentemente, maior efeito cardioprotetor. O consumo de vinho deve ser regular e moderado para que não traga riscos para a saúde, dessa forma o vinho pode atuar beneficamente no organismo. São inegáveis os benefícios do consumo de vinho ao sistema cardiovascular, porém mais estudos devem ser realizados para esclarecer dúvidas em relação à quantidade ideal recomendada de resveratrol, assim como outros efeitos do seu consumo.

Tolbutamide blocks postsynaptic but not presynaptic effects of adenosine on hippocampal CA1 neurones.

Extracellular recording in the CA1 pyramidal cell layer of rat hippocampal slices was used to examine the effect of the ATP-sensitive potassium channel blocker tolbutamide and the channel opener levcromakalim on responses to adenosine. Tolbutamide 1 mM blocked the inhibitory effect of adenosine on the size of orthodromic population spikes but had no effect on the inhibitory action of adenosine on field EPSPs. Tolbutamide also blocked the suppression by adenosine of repetitive antidromic spikes induced in calcium-free media with high magnesium but did not prevent the effects of baclofen. Levcromakalim 100 microM potentiated inhibitory effect of adenosine, but not baclofen, on orthodromic population spikes. The results show that at postsynaptic, but not presynaptic, sites adenosine may activate an ATP-sensitive potassium channel.

Adenosine A2 receptor-induced inhibition of leukotriene B4 synthesis in whole blood ex vivo.

1. Engagement of adenosine A2 receptors suppresses several leukocyte functions. In the present study, we examined the effect of adenosine on the inhibition of leukotriene B4 (LTB4) synthesis in heparinized human whole blood, pretreated with lipopolysaccharide (LPS) and tumour necrosis factor alpha (TNF-alpha) and stimulated with the chemotactic peptide, N-formyl-Met-Leu-Phe (FMLP). 2. The FMLP-induced synthesis of LTB4 in whole blood pretreated with LPS and TNF-alpha was dose-dependently inhibited by adenosine analogues in the following order of potency; 5'(N-ethyl)carboxamidoadenosine (NECA) approximately equal to CGS 21680 > 2-Cl-adenosine > N6-cyclopentyladenosine (CPA), indicating the involvement of the adenosine A2 receptor subtype. The IC50 values for NECA, CGS 21680, 2-Cl-adenosine, and CPA were 6 nM, 9 nM, 180 nM, and 990 nM, respectively. 3. Dipyridamole, an agent that blocks the cellular uptake of adenosine by red cells and causes its accumulation in plasma, also inhibited the synthesis of LTB4 in LPS and TNF-alpha-treated whole blood stimulated by FMLP; moreover, this inhibition was reversed upon addition of adenosine deaminase. 4. A highly selective antagonist of the adenosine A2 receptor, 8-(3-chlorostyryl)caffeine (CSC), reversed the inhibition of LTB4 synthesis by 2-Cl-adenosine and dipyridamole in LPS and TNF-alpha-treated whole blood, stimulated by FMLP. 5. LTB4 synthesis in whole blood originates predominantly from neutrophils and to a lesser extent from monocytes. 2-Cl-adenosine also inhibited the synthesis of LTB4 induced by FMLP in these isolated LPS and TNF-alpha-treated cells; however, 2-Cl-adenosine was a more potent inhibitor of LTB4 synthesis in neutrophils than monocytes. 6. The present data demonstrate that adenosine, acting through A2 receptors, exerts a potent inhibitory effect on the synthesis of LTB4 and thus contribute to the understanding of its anti-inflammatory properties.

Effects of ONO-1078, a leukotriene antagonist, on cardiovascular responses induced by vagal stimulation, capsaicin, and substance P in guinea pigs.

AIM: To determine the role of ONO-1078, 4-oxo-8 -[p-(4-phenylbutyloxy) benzoylamino]- 2-(tetrazol-5-yl) -4H-1-benzopyran hemihydrate, in cardiovascular responses induced by vagal stimulation, capsaicin, and substance P. METHODS: Evans blue extravasation in the atrium and ventricle, and mean arterial pressure (MAP) were observed. RESULTS: Electric stimulation of vagus (ESV, 10 Hz, 5 ms, 2 or 10 V, for 90 s) increased Evans blue extravasation in the hearts of atropine (1 mg.kg-1, i.v.)-pretreated guinea pigs. Capsaicin (0.05 mg.kg-1, i.v.) and substance P (1 microgram.kg-1, i.v.) enhanced the dye extravasation and elicited a drop in MAP. ONO-1078 (0.03 and 0.1 mg.kg-1, i.v.) inhibited ESV-induced response, especially at stimulation of 2 V. ONO-1078 (0.03 mg.kg-1) attenuated capsaicin-induced cardiac microvascular leakage and hypotensive response, but failed to inhibit substance P-induced responses. CONCLUSION: ONO-1078 can modulate the cardiovascular responses in neurogenic inflammation, possibly mediated by inhibiting sensory neuropeptide release.

[A mathematical analysis of the cardiac activity indices in patients with ischemic heart disease undergoing antianginal pharmacotherapy]. / Matematicheskii analiz pokazatelei serdechnoi deiatel'nosti u bol'nykh ishemicheskoi bolezn'iu serdtsa pri antianginal'noi farmakoterapii.

Taking into account various parameters of heart rhythm variability makes it possible to differentiate patients with ischemic heart disease by their response to antianginal pharmacotherapy. The cardiointervalographic method may be used to predict therapeutical effects in making clinical and pharmacological decisions.

Pharmacologic profile of cromakalim in the treatment of myocardial ischemia in isolated rat hearts and anesthetized dogs.

The detailed antiischemic pharmacology of the potassium channel activator cromakalim was determined in isolated globally ischemic rat hearts and a canine model of coronary occlusion and reperfusion. Cromakalim significantly improved reperfusion function in rat hearts starting at a concentration of 1 microM; this effect peaked at 7 microM. No cardiodepressant effects were observed in nonischemic tissue with cromakalim until a concentration of 100 microM was achieved, and this effect was reversed by glyburide. The antiischemic effect of 7 microM cromakalim was also completely reversed by glyburide and the novel ATP-sensitive potassium channel blocker sodium 5-hydroxydecanoate (5-HD). Glyburide did not reverse the antiischemic effects of 1 microM diltiazem. Cromakalim not only improved reperfusion contractile function in rat hearts, but improved the functional reserve and efficiency of O2 utilization. In anesthetized dogs, intracoronary cromakalim (0.1 micrograms/kg/min given throughout ischemia and reperfusion) significantly reduced infarct size in hearts subjected to 90-min coronary occlusion and 5-h reperfusion. Along with this reduced infarct size, the frequency of ectopic beats and the proportion of animals fibrillating during reperfusion were significantly reduced by cromakalim. In isolated globally ischemic and reperfused rat hearts, cromakalim was significantly profibrillatory. Thus, cromakalim is significantly cardioprotective, and may have the propensity for profibrillatory activity, although this is not true under all conditions.

Characteristics of cardiovascular reflexes originating from 5-HT3 receptors in the heart and lungs of unanaesthetized rabbits.

1. When phenylbiguanide (1-PBG) (6.25-400 micrograms) was injected into the left atrium, right atrium or pulmonary artery of unanesthetized rabbits it caused dose-dependent falls of heart rate and arterial pressure, and short-lived hypopnoea or apnoea. The threshold dose was 50-100 micrograms. Maximal falls of heart rate (86-108 beats/min) and arterial pressure (33-35 mmHg) occurred at a dose of 200 micrograms. The latency between injection and onset of the bradycardia was 2.2-2.6 s and did not depend on the route. Cardiac output fell transiently with heart rate, but at the time of the maximal fall of arterial pressure it had returned to normal. All effects were abolished by intrapericardial procaine. The haemodynamic effects were exaggerated by sino-aortic barodenervation. Intrapericardial 1-PBG (200-400 micrograms) was without effect. Injection of 1-PBG (greater than 50-100 micrograms) into the aortic arch caused a variable increase in heart rate and arterial pressure. 2. When both cervical vagus nerves were crushed the depressor effects of atrial 1-PBG were reduced by only 76-84%. 3. The dose-response curves for left atrial and pulmonary artery injection of 1-PBG were shifted successively to the right by intravenous infusion of the 5-HT3 antagonist MDL72222 (0.1 and 1.0 mg/kg). 4. We conclude that in unanesthetized rabbits left atrial 1-PBG selectively excites myocardial afferents, whereas right atrial or pulmonary artery 1-PBG excites afferents that originate close to the pulmonary vasculature. In each case 1-PBG acts through pharmacologically specific 5-HT3 receptors. The afferents run mainly, but not exclusively, in the vagus nerves. The reflex fall of arterial pressure is accounted for almost entirely by a decrease in peripheral resistance.

Iloprost-induced writhing in mice and its suppression by morphine.

Intraperitoneally (i.p.) administered iloprost produced a writhing response indicating nociception. This effect induced by 4 micrograms/kg iloprost was dose dependently protected by morphine with an ED50 (95% confidence limits) value of 0.039 (0.0018-0.067) mg/kg. On the other hand, indomethacin had no effect on iloprost-induced writhing. Thus, this effect of iloprost seems to be relatively more sensitive than other irritants-induced responses on determining the analgesic potency of narcotic drugs.