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Search Results: 1 - 10 of 351673 matches for " Paulo R. B. Evora "
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Endothelium-dependent relaxation in response to poly-L-arginine in canine coronary arteries: implications about hyperpolarization as a mechanism of vasodilatation
Evora, Paulo R. B.;Pearson, Paul J.;Rodrigues, Alfredo José;Viaro, Fernanda;Schaff, Hartzell V.;
Arquivos Brasileiros de Cardiologia , 2003, DOI: 10.1590/S0066-782X2003000600005
Abstract: objective: to study the mechanism by which poly-l-arginine mediates endothelium-dependent relaxation. methods: vascular segments with and without endothelium were suspended in organ chambers filled with control solution maintained at 37oc and bubbled with 95% o2 / 5% co2. used drugs: indomethacin, acetycholine, egta, glybenclamide, ouabain, poly-l-arginine, methylene blue, ng-nitro-l-arginine, and verapamil and ng-monomethyl-l-arginine. prostaglandin f2á and potassium chloride were used to contract the vascular rings. results: poly-l-arginine (10-11 to 10-7 m) induced concentration-dependent relaxation in coronary artery segments with endothelium. the relaxation to poly-l-arginine was attenuated by ouabain, but was unaffected by glybenclamide. l-noarg and oxyhemoglobin caused attenuation, but did not abolish this relaxation. also, the relaxations was unaffected by methylene blue, verapamil, or the presence of a calcium-free bathing medium. the endothelium-dependent to poly-l-arginine relaxation was abolished only in vessels contracted with potassium chloride (40 mm) in the presence of l-noarg and indomethacin. conclusion: these experiments indicate that poly-l-arginine induces relaxation independent of nitric oxide.
Endothelium-dependent relaxation in response to poly-L-arginine in canine coronary arteries: implications about hyperpolarization as a mechanism of vasodilatation
Evora Paulo R. B.,Pearson Paul J.,Rodrigues Alfredo José,Viaro Fernanda
Arquivos Brasileiros de Cardiologia , 2003,
Abstract: OBJECTIVE: To study the mechanism by which poly-L-arginine mediates endothelium-dependent relaxation. METHODS: Vascular segments with and without endothelium were suspended in organ chambers filled with control solution maintained at 37oC and bubbled with 95% O2 / 5% CO2. Used drugs: indomethacin, acetycholine, EGTA, glybenclamide, ouabain, poly-L-arginine, methylene blue, N G-nitro-L-arginine, and verapamil and N G-monomethyl-L-arginine. Prostaglandin F2á and potassium chloride were used to contract the vascular rings. RESULTS: Poly-L-arginine (10-11 to 10-7 M) induced concentration-dependent relaxation in coronary artery segments with endothelium. The relaxation to poly-L-arginine was attenuated by ouabain, but was unaffected by glybenclamide. L-NOARG and oxyhemoglobin caused attenuation, but did not abolish this relaxation. Also, the relaxations was unaffected by methylene blue, verapamil, or the presence of a calcium-free bathing medium. The endothelium-dependent to poly-L-arginine relaxation was abolished only in vessels contracted with potassium chloride (40 mM) in the presence of L-NOARG and indomethacin. CONCLUSION: These experiments indicate that poly-L-arginine induces relaxation independent of nitric oxide.
Curbing Inflammation
R. Clive Landis,Christopher D. Buckley,Paulo Roberto B. Evora,David A. Hart
International Journal of Inflammation , 2013, DOI: 10.1155/2013/468287
Abstract:
Coronary sinus iatrogenic lesion during repeated mitral valve replacement: case report of an immediate transmitral annulus repair
Evora, Paulo R. B.;Ribeiro, Paulo J. F.;Menardi, Antonio C.;Vicente, Walter V. A.;Rodrigues, Alfredo J.;
Revista Brasileira de Cirurgia Cardiovascular , 2003, DOI: 10.1590/S0102-76382003000200013
Abstract: we report a case and evolution of a patient in whom the coronary sinus was damaged and reconstructed through the mitral annulus. the surgical accident happened during a degenerated biological valve prosthesis instrumentation. an almost complete left circumflex coronary artery division was our first hypothesis. a coronary probe introduced through the vascular injury was distally detected inside the right atrium confirming a coronary sinus lesion. the surgical correction was performed using running polypropylene 7-0 sutures through the mitral ring. after fourteen months, a coronary sinus angiographic image was taking observing the venous phase of selective left coronary arteriography. the image demonstrated an acceptable narrowing of the local venous repair. in our opinion the single coronary sinus division or its repair, in this iatrogenic situation, is a matter of speculation.
The Effect of Extracellular pH Changes on Intracellular pH and Nitric Oxide Concentration in Endothelial and Smooth Muscle Cells from Rat Aorta
Verena K. Capellini, Carolina B. A. Restini, Lusiane M. Bendhack, Paulo R. B. Evora, Andréa C. Celotto
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0062887
Abstract: Aims It has been known for more than a century that pH changes can alter vascular tone. However, there is no consensus about the effects of pH changes on vascular response. In this study, we investigated the effects of extracellular pH (pHo) changes on intracellular pH (pHi) and intracellular nitric oxide concentration ([NO]i) in freshly isolated endothelial cells and cross sections from rat aorta. Main Methods The HCl was used to reduce the pHo from 7.4 to 7.0 and from 7.4 to 6.5; the NaOH was used to increase the pHo from 7.4 to 8.0 and from 7.4 to 8.5. The fluorescent dyes 5-(and-6)-carboxy SNARF-1, acetoxymethyl ester, acetate (SNARF-1) and diaminofluorescein-FM diacetate (DAF-FM DA) were employed to measure the pHi and [NO]i, respectively. The fluorescence intensity was measured in freshly isolated endothelial cells by flow cytometry and in freshly obtained aorta cross sections by confocal microscopy. Key Findings The endothelial and vascular smooth muscle pHi was increased at pHo 8.5. The extracellular acidification did not change the endothelial pHi, but the smooth muscle pHi was reduced at pHo 7.0. At pHo 8.5 and pHo 6.5, the endothelial [NO]i was increased. Both extracellular alkalinization and acidification increased the vascular smooth muscle [NO]i. Significance Not all changes in pHo did result in pHi changes, but disruption of acid-base balance in both directions induced NO synthesis in the endothelium and/or vascular smooth muscle.
Disfun??o endotelial após isquemia global e reperfus?o em cirurgia cardíaca com circula??o extracorpórea: estudo do papel do magnésio em artérias coronarianas caninas
VOLPE, Marco A.;CARNEIRO, Jo?o J.;MAGNA, Luiz Alberto;VIARO, Fernanda;ORIGUELA, Eliana Aparecida Lopes;EVORA, Paulo R. B.;
Revista Brasileira de Cirurgia Cardiovascular , 2002, DOI: 10.1590/S0102-76382002000300002
Abstract: introduction: hypomagnesemia and ischemia followed by reperfusion often occur in cardiac surgery. both of them are associated with endothelial dysfunction which interfers negatively with patient evolution. phisiopatology of these disturbances is similar and involves g-proteins dysfunction. objective: the present study focuses on the endothelial dysfunction consequent to the lesion resulting from global ischemia followed by reperfusion and the potential protective influence of magnesium on the endothelium functional integrity in isolated coronaries of dogs. method: segments of canine coronary arteries were suspended in organ chambers to measure isometric force. endothelial dysfunction was evaluated by the ability of these segments to produce nitric oxide changing the initial isometric force. four groups with six dogs in each one were selected: sem cec (control), cec (110 minutes of perfusion without ischemia), isq (45 minutes of ischemia), isq/rep (45 minutes of ischemia followed by 60 minutes of reperfusion). the magnesium action was evaluated in three different phases: i (organ chambers with magnesium), ii (organ chambers without magnesium) and iii (organ chambers with restored magnesium). three pharmacological agonists were used which represented the main steps involved in the nitric oxide production: the membrane receptor of the endothelial cell - acetylcholine (ach); transduction of the signal between the receptor and the intracellular processes through the g-protein - sodium fluoride (naf); liberation of intracellular stocks of calcium - calcium ionophore (a23187). the study of endothelial function was combined with the evaluation of smooth muscle activity dependent on gmpc - sodium nitroprusside (nps). results: the major findings of this investigation were as follows: 1) presence of magnesium in priming seemed to attenuate the endothelial dysfunction caused by global ischemia followed by reperfusion; 2) presence of magnesium in the organ chamber (phase i) was
The protective effect of cilostazol on isolated rabbit femoral arteries under conditions of ischemia and reperfusion: the role of the nitric oxide pathway
Santos, Mariana R.G.A.;Celotto, Andréa C.;Capellini, Verena K.;Evora, Paulo R. B.;Piccinato, Carlos E.;Joviliano, Edwaldo E.;
Clinics , 2012, DOI: 10.6061/clinics/2012(02)13
Abstract: objectives: the clinical significance of ischemia/reperfusion of the lower extremities demands further investigation to enable the development of more effective therapeutic alternatives. this study investigated the changes in the vascular reactivity of the rabbit femoral artery and nitric oxide metabolites under partial ischemia/ reperfusion conditions following cilostazol administration. methods: ischemia was induced using infrarenal aortic clamping. the animals were randomly divided into seven groups: control 90 minutes, ischemia/reperfusion 90/60 minutes, control 120 minutes, ischemia/reperfusion 120/90 minutes, cilostazol, cilostazol before ischemia/reperfusion 120/90 minutes, and ischemia 120 minutes/cilostazol/ reperfusion 90 minutes. dose-response curves for sodium nitroprusside, acetylcholine, and the calcium ionophore a23187 were obtained in isolated femoral arteries. the levels of nitrites and nitrates in the plasma and skeletal muscle were determined using chemiluminescence. results: acetylcholine-and a23187-induced relaxation was reduced in the ischemia/reperfusion 120/90 group, and treatment with cilostazol partially prevented this ischemia/reperfusion-induced endothelium impairment. only cilostazol treatment increased plasma levels of nitrites and nitrates. an elevation in the levels of nitrites and nitrates was observed in muscle tissues in the ischemia/reperfusion 120/90, cilostazol/ischemia/reperfusion, and ischemia/ cilostazol/reperfusion groups. conclusion: hind limb ischemia/reperfusion yielded an impaired endothelium-dependent relaxation of the femoral artery. furthermore, cilostazol administration prior to ischemia exerted a protective effect on endotheliumdependent vascular reactivity under ischemia/reperfusion conditions.
The role of G-proteins in the pathophysiology of the cardiovascular diseases
Evora Paulo Roberto B.,Nobre Fernando
Arquivos Brasileiros de Cardiologia , 1999,
Abstract:
Atrial infarction is a unique and often unrecognized clinical entity
Mendes, Rosana G. G.;Evora, Paulo Roberto B.;
Arquivos Brasileiros de Cardiologia , 1999, DOI: 10.1590/S0066-782X1999000300007
Abstract: a patient with heart failure and acute atrial fibrillation received the final diagnosis of atrial infarction associated with ventricular infarction based on clinical findings of ischemia in association with atrial fibrillation and heart failure (mechanisms probably involved: contractile dysfunction and loss of atrial contribution). although a transesophageal echocardiography, which could refine the diagnosis of anatomic abnormalities, was not performed, all evidence led to the diagnosis of atrial involvement. electrocardiographic findings were consistent with liu's major criterion 3. therapy with digitalis, quinidine and angiotensin-converting enzyme inhibitors was chosen, as the patient had acute pulmonary edema. the use of beta-blockers and verapamil was restricted. no other complications, such as thrombo-embolism or atrial rupture, were noted.
Atrial infarction is a unique and often unrecognized clinical entity
Mendes Rosana G. G.,Evora Paulo Roberto B.
Arquivos Brasileiros de Cardiologia , 1999,
Abstract: A patient with heart failure and acute atrial fibrillation received the final diagnosis of atrial infarction associated with ventricular infarction based on clinical findings of ischemia in association with atrial fibrillation and heart failure (mechanisms probably involved: contractile dysfunction and loss of atrial contribution). Although a transesophageal echocardiography, which could refine the diagnosis of anatomic abnormalities, was not performed, all evidence led to the diagnosis of atrial involvement. Electrocardiographic findings were consistent with Liu's major criterion 3. Therapy with digitalis, quinidine and angiotensin-converting enzyme inhibitors was chosen, as the patient had acute pulmonary edema. The use of beta-blockers and verapamil was restricted. No other complications, such as thrombo-embolism or atrial rupture, were noted.
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