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1.
Microcirculation ; : e12608, 2020 Jan 28.
Artigo em Inglês | MEDLINE | ID: mdl-31991513

RESUMO

OBJECTIVE: We aimed to determine whether high-dose nitroglycerin, a nitric oxide donor, preserves erythrocyte deformability during cardiopulmonary bypass and examines the signaling pathway of nitric oxide in erythrocytes. METHODS: In a randomized and controlled fashion, forty-two patients undergoing cardiac surgery with hypothermic cardiopulmonary bypass were allocated to high-dose (N = 21) and low-dose groups (N = 21). During rewarming period, patients were given intravenous nitroglycerin with an infusion rate 5 and 1 µg·kg-1 ·min-1 in high-dose and low-dose groups, respectively. Tyrosine phosphorylation level of non-muscle myosin IIA in erythrocyte membrane was used as an index of erythrocyte deformability and analyzed using immunoblotting. RESULTS: Tyrosine phosphorylation of non-muscle myosin IIA was significantly enhanced after bypass in high-dose group (3.729 ± 1.700 folds, P = .011) but not low-dose group (1.545 ± 0.595 folds, P = .076). Phosphorylation of aquaporin 1, vasodilator-stimulated phosphoprotein, and focal adhesion kinase in erythrocyte membrane was also upregulated in high-dose group after bypass. Besides, plasma nitric oxide level was highly correlated with fold change of non-muscle myosin IIA phosphorylation (Pearson's correlation coefficient .871). CONCLUSIONS: High-dose nitroglycerin administered during cardiopulmonary bypass improves erythrocyte deformability through activating phosphorylation of aquaporin 1, vasodilator-stimulated phosphoprotein, and focal adhesion kinase in erythrocytes.

2.
J Chin Med Assoc ; 82(2): 120-125, 2019 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-30839502

RESUMO

BACKGROUND: The aim of the study was to evaluate the effects of high-dose nitroglycerine administered during cardiopulmonary bypass on the intraoperative cerebral saturation and postoperative serum creatinine concentration in cardiac surgery. METHODS: In a retrospective cohort study, a total of 239 patients undergoing cardiac surgery with cardiopulmonary bypass at a tertiary medical center were included. General anesthesia consisted of volatile anesthetic and either intravenous loading of high-dose nitroglycerin (infusion rate 10 to 20 mg·h with a total dose of ≥0.5 mg·kg) starting from rewarming of cardiopulmonary bypass throughout the end of the surgery (NTG group; N = 96) or without high-dose nitroglycerin (control group; N = 143). Data for intraoperative cerebral saturation and serum creatinine concentrations before and after cardiac surgery were collected. Propensity score method was used to adjust for potential confounders. RESULTS: Patients receiving high-dose nitroglycerin had significantly lower mean arterial pressure and hematocrit levels during and after cardiopulmonary bypass. The risk of intraoperative cerebral desaturation was left-sided 23.9% versus 38.5% (p = 0.023), right-sided 28.1% versus 35.7% in the NTG and control groups, respectively. The risk of new-onset stroke and postoperative dialysis was 2.1% versus 6.3% and 1.0% versus 3.5% in the NTG and control groups, respectively. CONCLUSION: An infusion of high-dose nitroglycerin initiating at rewarming of cardiopulmonary bypass and throughout the postbypass interval may induce hypotension and hemodilution in cardiac surgical patients. Cerebral saturation and renal function were well maintained without increasing the risk of stroke and renal replacement therapy after cardiac surgery with cardiopulmonary bypass.


Assuntos
Encéfalo/efeitos dos fármacos , Procedimentos Cirúrgicos Cardíacos , Nitroglicerina/farmacologia , Pontuação de Propensão , Adulto , Idoso , Pressão Arterial/efeitos dos fármacos , Encéfalo/metabolismo , Ponte Cardiopulmonar , Feminino , Humanos , Rim/efeitos dos fármacos , Rim/fisiologia , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos
3.
Am J Chin Med ; 45(7): 1421-1439, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28946769

RESUMO

Magnolol, a constituent of the bark of Magnolia officinalis, has been reported to decrease myocardial stunning and infarct size. In this study, we investigated whether magnolol can reduce renal ischemia and reperfusion (I/R) injury. Renal I/R, induced by a 60-min occlusion of bilateral renal arteries and a 24-h reperfusion, significantly increased blood urea nitrogen (BUN) and creatinine levels, and caused histological damage to the kidneys of rats. Apoptosis, as evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining and caspase-3 activation, was significantly increased in the kidneys. Furthermore, serum levels of tumor necrosis factor-[Formula: see text] (TNF-[Formula: see text]), interleukin-1ß (IL-1ß), and interleukin-6 (IL-6) were significantly elevated, while the interleukin-10 (IL-10) level was suppressed. However, intravenous pretreatment with magnolol at doses of 0.003[Formula: see text]mg/kg and 0.006[Formula: see text]mg/kg 10[Formula: see text]min before renal I/R significantly limited the increases of BUN, creatinine, the histological damage, and apoptosis in the kidneys. The increases in TNF-[Formula: see text], IL-1ß, and IL-6, and the decrease in IL-10 were also significantly inhibited. Additionally, magnolol increased Bcl-2 and decreased Bax in the kidneys. Phosphorylation of the prosurvival kinases, including Akt and extracellular signal-regulated kinases 1 and 2 (ERK1/2), was elevated, while phosphorylation of the pro-apoptotic mitogen-activated protein kinases, including p38 and c-Jun N-terminal kinase (JNK), was suppressed. In conclusion, magnolol reduces renal I/R injury. The underlying mechanisms for this effect might be related to the prevention of apoptosis, possibly via the inhibition of both extrinsic and intrinsic apoptotic pathways, including the reduction of TNF-[Formula: see text] production and the modulation of pro- and anti-apoptotic signaling elements.


Assuntos
Apoptose/efeitos dos fármacos , Compostos de Bifenilo/administração & dosagem , Compostos de Bifenilo/farmacologia , Isquemia/tratamento farmacológico , Rim/irrigação sanguínea , Rim/patologia , Lignanas/administração & dosagem , Lignanas/farmacologia , Fitoterapia , Traumatismo por Reperfusão/tratamento farmacológico , Animais , Nitrogênio da Ureia Sanguínea , Creatinina/sangue , Relação Dose-Resposta a Droga , Infusões Intravenosas , Interleucina-10/sangue , Interleucina-1beta/sangue , Interleucina-6/sangue , Isquemia/sangue , Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo , Rim/metabolismo , Masculino , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , Fosforilação/efeitos dos fármacos , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Ratos Sprague-Dawley , Traumatismo por Reperfusão/sangue , Transdução de Sinais/efeitos dos fármacos , Fator de Necrose Tumoral alfa/sangue , Proteína X Associada a bcl-2/metabolismo
4.
Am J Chin Med ; 45(4): 791-811, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-28521514

RESUMO

Baicalein is an active component of Scutellaria baicalensis Georgi, which has traditionally been used to treat cardiovascular diseases in China. In this study, we investigated if treatment with baicalein can attenuate the lung injury induced by myocardial ischemia and reperfusion (I/R). Myocardial I/R, induced by a 40-min occlusion of the left anterior descending coronary artery and a 3-h reperfusion, significantly increased histological damage and the wet-to-dry weight ratio of lungs in rats. The terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive nuclei and caspase-3 activation was significantly increased in the lungs. Serum and bronchoalveolar lavage fluid levels of tumor necrosis factor-[Formula: see text] (TNF-[Formula: see text]), interleukin-1[Formula: see text] (IL-1[Formula: see text]), and interleukin-6 (IL-6) were significantly elevated, as were TNF-[Formula: see text] levels in the lung. Intravenous administration with baicalein at doses of 3, 10, and 30[Formula: see text]mg/kg for ten minutes before myocardial I/R significantly reduced histological damage, the wet-to-dry weight ratio, and apoptosis in the lung. Baicalein also significantly inhibited the increase in levels of TNF-[Formula: see text], IL-1[Formula: see text], and IL-6. Moreover, baicalein increased Bcl-2 and decreased p53, Bax, and cytochrome [Formula: see text] in lungs. Phosphorylation of the prosurvival kinases, including Akt and extracellular signal-regulated kinases 1 and 2 (ERK1/2), was increased, while the phosphorylation of the pro-apoptotic mitogen-activated protein kinases, including p38 and c-Jun N-terminal kinase (JNK), was decreased. In conclusion, treatment with baicalein attenuates the lung injury induced by myocardial I/R. The mechanisms might be related to the limiting of apoptosis, possibly via the inhibition of both the extrinsic and intrinsic pathways of apoptosis, including the inhibition of TNF-[Formula: see text] production and modulation of pro- and anti-apoptotic signaling elements.


Assuntos
Apoptose/efeitos dos fármacos , Flavanonas/uso terapêutico , Pneumopatias/tratamento farmacológico , Pneumopatias/etiologia , Isquemia Miocárdica/complicações , Reperfusão Miocárdica/efeitos adversos , Fitoterapia , Scutellaria baicalensis/química , Animais , Apoptose/genética , Caspase 3/metabolismo , Citocinas/metabolismo , DNA Nucleotidilexotransferase/metabolismo , Nucleotídeos de Desoxiuracil/metabolismo , Flavanonas/administração & dosagem , Flavanonas/isolamento & purificação , Infusões Intravenosas , Pulmão/metabolismo , Pneumopatias/metabolismo , Pneumopatias/prevenção & controle , Masculino , Ratos Sprague-Dawley
5.
Am J Chin Med ; 44(3): 531-50, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27109160

RESUMO

Baicalein is a component of the root of Scutellaria baicalensis Georgi, which has traditionally been used to treat liver disease in China. In the present study, we investigated baicalein' ability to reduce the liver injury induced by myocardial ischemia and reperfusion (I/R). Myocardial I/R was induced in this experiment by a 40[Formula: see text]min occlusion of the left anterior descending coronary artery and a 3[Formula: see text]h reperfusion in rats. The induced myocardial I/R significantly increased the serum levels of aspartate transaminase (AST) and alanine transaminase (ALT), indicating the presence of liver injury. Hepatic apoptosis was significantly increased. The serum levels of tumor necrosis factor-[Formula: see text] (TNF-[Formula: see text]), interleukin-1[Formula: see text] (IL-1[Formula: see text]), and interleukin-6 (IL-6) were significantly elevated, as was the TNF-[Formula: see text] level in the liver. Intravenous pretreatment with baicalein (3, 10, or 30[Formula: see text]mg/kg) 10[Formula: see text]min before myocardial I/R significantly reduced the serum level increase of AST and ALT, apoptosis in the liver, and the elevation of TNF-[Formula: see text], IL-1[Formula: see text], and IL-6 levels. Moreover, baicalein increased Bcl-2 and decreased Bax in the liver. Phosphorylation of the prosurvival kinases, including Akt and extracellular signal-regulated kinases 1 and 2 (ERK1/2), was also increased. In conclusion, we found that baicalein can reduce the liver injury induced by myocardial I/R. The underlying mechanisms are likely related to the inhibition of the extrinsic and intrinsic apoptotic pathways, possibly via the inhibition of TNF-[Formula: see text] production, the modulation of Bcl-2 and Bax, and the activation of Akt and ERK1/2. Our findings may provide a rationale for the application of baicalein or traditional Chinese medicine containing large amounts of baicalein to prevent liver injury in acute myocardial infarction and cardiac surgery.


Assuntos
Flavanonas/uso terapêutico , Hepatopatias/tratamento farmacológico , Hepatopatias/etiologia , Isquemia Miocárdica/complicações , Traumatismo por Reperfusão Miocárdica/complicações , Fitoterapia , Alanina Transaminase/sangue , Animais , Apoptose , Aspartato Aminotransferases/sangue , Biomarcadores/sangue , Modelos Animais de Doenças , Flavanonas/administração & dosagem , Flavanonas/isolamento & purificação , Flavanonas/farmacologia , Infusões Intravenosas , Interleucina-1beta/sangue , Interleucina-6/sangue , Hepatopatias/diagnóstico , Hepatopatias/patologia , Masculino , Proteína Quinase 3 Ativada por Mitógeno , Extratos Vegetais/química , Proteínas Proto-Oncogênicas c-bcl-2 , Ratos Sprague-Dawley , Fator de Necrose Tumoral alfa/sangue
6.
Planta Med ; 82(3): 181-9, 2016 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-26550790

RESUMO

Acute kidney injury is a common and severe complication of acute myocardial infarction and cardiac surgery. It results in increased mortality, morbidity, and duration of hospitalization. Baicalein is a component of the root of Scutellaria baicalensis, which has traditionally been used to treat cardiovascular and liver diseases in Asia. In this study, we investigated whether baicalein can attenuate kidney injury induced by myocardial ischemia and reperfusion in rats. Myocardial ischemia and reperfusion, induced by a 40-minute occlusion and a 3-hour reperfusion of the left anterior descending coronary artery, significantly increased blood urea nitrogen and creatinine levels in addition to causing histological changes in the kidneys. Kidney apoptosis was also significantly increased. Furthermore, myocardial ischemia and reperfusion significantly increased the serum levels of tumor necrosis factor-α, interleukin-1, and interleukin-6 as well as the tumor necrosis factor-α levels in the kidneys. Intravenous pretreatment with baicalein (in doses of 3, 10, or 30 mg/kg), however, significantly reduced the increases in the creatinine level, renal histological damage, and apoptosis induced by myocardial ischemia and reperfusion. In addition, the increases in the serum levels of tumor necrosis factor-α, interleukin-1, and interleukin-6, and of tumor necrosis factor-α in the kidneys were significantly reduced. Western blot analysis revealed that baicalein significantly increased Bcl-2 and reduced Bax in the kidneys. The phosphorylation of Akt and extracellular signal-regulated kinases 1 and 2 was also significantly increased. In conclusion, baicalein significantly attenuates kidney injury induced by myocardial ischemia and reperfusion. The underlying mechanisms might be related to the inhibition of apoptosis, possibly through the reduction of tumor necrosis factor-α production, the modulation of Bcl-2 and Bax, and the activation of Akt and extracellular signal-regulated kinases 1 and 2.


Assuntos
Lesão Renal Aguda/prevenção & controle , Flavanonas/uso terapêutico , Traumatismo por Reperfusão Miocárdica/prevenção & controle , Extratos Vegetais/uso terapêutico , Scutellaria baicalensis/química , Animais , Apoptose/efeitos dos fármacos , Masculino , Proteína Quinase 1 Ativada por Mitógeno/metabolismo , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , Proteínas Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Ratos , Ratos Sprague-Dawley , Proteína X Associada a bcl-2/metabolismo
7.
J Chin Med Assoc ; 78(8): 460-8, 2015 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-26071976

RESUMO

BACKGROUND: Ischemic preconditioning has been reported to protect the myocardium against ischemia and reperfusion injury. The underlying mechanisms have been extensively investigated but are not fully elucidated. In this study, we investigated the role of apoptosis in ischemic preconditioning protection and the signal pathways involved. METHODS: Myocardial ischemia and reperfusion were induced in anesthetized male Sprague-Dawley rats by a 40-minute occlusion and a 3-hour reperfusion of the left anterior descending coronary artery. Ischemic preconditioning was elicited by two 10-minute coronary artery occlusions and two 10-minute reperfusions. RESULTS: The myocardial infarct size, expressed as the percentage of area at risk, was significantly decreased in the ischemic preconditioning group (16.8 ± 2.0% and 27.9 ± 2.7% in the ischemia and reperfusion groups, respectively, p < 0.001). Additionally, ischemic preconditioning significantly reduced apoptosis, as evidenced by the decrease in the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive nuclei, DNA laddering, and caspase-3 activation. Western blot analysis revealed that ischemic preconditioning significantly reduced myocardial tumor necrosis factor-α levels. Bcl-2 was increased, whereas Bax was decreased in the myocardium. Phosphorylation of the prosurvival kinases, including Akt and extracellular signal-regulated kinases 1 and 2, was significantly increased. Hemodynamics, area at risk, and mortality did not differ significantly among the groups. CONCLUSION: Ischemic preconditioning reduces apoptosis induced by myocardial ischemia and reperfusion. The underlying mechanisms might be related to inhibition of both the extrinsic and the intrinsic apoptotic pathway via inhibition of production of tumor necrosis factor-α, modulation of expression of Bcl-2 and Bax, and activation of the prosurvival kinases.


Assuntos
Apoptose , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Precondicionamento Isquêmico Miocárdico , Miocárdio/patologia , Proteínas Proto-Oncogênicas c-akt/metabolismo , Animais , Hemodinâmica , Marcação In Situ das Extremidades Cortadas , Masculino , Fosforilação , Ratos , Ratos Sprague-Dawley , Transdução de Sinais/fisiologia , Fator de Necrose Tumoral alfa/biossíntese
8.
J Chin Med Assoc ; 78(9): 506-12, 2015 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-26074368

RESUMO

BACKGROUND: We have previously reported that brief pressure overload of the left ventricle reduced myocardial infarct (MI) size. However, the role of protein kinase C (PKC) remains uncertain. In this study, we investigated whether pressure overload reduces MI size by activating PKC. METHODS: MI was induced by a 40-minute occlusion of the left anterior descending coronary artery and a 3-hour reperfusion in anesthetized Sprague-Dawley rats. MI size was determined using triphenyl tetrazolium chloride staining. Brief pressure overload was achieved by two 10-minute partial snarings of the ascending aorta, raising the systolic left ventricular pressure 50% above the baseline value. Ischemic preconditioning was elicited by two 10-minute coronary artery occlusions and 10-minute reperfusions. Dimethyl sulfoxide (vehicle) or calphostin C (0.1 mg/kg, a specific inhibitor of PKC) was administered intravenously as pretreatment. RESULTS: The MI size, expressed as the percentage of the area at risk, was significantly reduced in the pressure overload group and the ischemic preconditioning group (19.0 ± 2.9% and 18.7 ± 3.0% vs. 26.1 ± 2.6% in the control group, where p < 0.001). Pretreatment with calphostin C significantly limited the protection by pressure overload and ischemic preconditioning (25.2 ± 2.4% and 25.0 ± 2.3%, where p < 0.001). Calphostin C itself did not significantly affect MI size (25.5 ± 2.4%). Additionally, the hemodynamics, area at risk, and mortality were not significantly different. CONCLUSION: Brief pressure overload of the left ventricle reduced MI size. Since calphostin C significantly limited the decrease of MI size, our results suggested that brief pressure overload reduces MI size via activation of PKC.


Assuntos
Infarto do Miocárdio/terapia , Proteína Quinase C/fisiologia , Animais , Ativação Enzimática , Ventrículos do Coração , Hemodinâmica , Precondicionamento Isquêmico Miocárdico , Masculino , Infarto do Miocárdio/mortalidade , Infarto do Miocárdio/fisiopatologia , Naftalenos/farmacologia , Pressão , Ratos , Ratos Sprague-Dawley
9.
Eur J Cardiothorac Surg ; 48(3): 382-91, 2015 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-25475946

RESUMO

OBJECTIVES: Acute kidney injury is a common and serious complication of cardiac surgery. Because its underlying mechanisms are unclear, there is no specific therapy to prevent or treat it. A regional transient ischaemia and reperfusion (I/R) may provide protection to distant tissue or organs, a phenomenon known as remote preconditioning. In this study, we investigated whether myocardial preconditioning (MPC) would reduce kidney injury and apoptosis induced by myocardial I/R, as well as the mechanisms involved. METHODS: Myocardial I/R was induced by a 40-min occlusion of the left anterior descending artery and a 3-h reperfusion in anaesthetized Sprague-Dawley rats. MPC was elicited by two 10-min coronary artery occlusions and two 10-min reperfusions. A sham group received the same surgical procedures without coronary artery occlusion and reperfusion. RESULTS: Compared with the sham group, myocardial I/R significantly increased the serum creatinine levels (1.15 ± 0.44 vs 0.54 ± 0.23 mg/dl, P < 0.05, mean ± standard deviation) and renal histological damage, indicating increased kidney injury. Kidney apoptosis was also significantly increased, as evidenced by the increase in the terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate (dUTP) nick-end labelling (TUNEL)-positive nuclei, clear DNA laddering and increased caspase-3 activation. Serum levels of tumour necrosis factor-α (TNF-α), interleukin-1 (IL-1) and interleukin-6 (IL-6) were significantly elevated, as were TNF-α levels in the kidneys. MPC significantly decreased myocardial infarct size (18.5 ± 3.1 vs 25.6 ± 2.1% of area at risk, P < 0.001). Additionally, MPC significantly reduced the serum creatinine level (0.65 ± 0.19 mg/dl, P < 0.05), renal histological damage and apoptosis. The increase in the serum levels of TNF-α, IL-1 and IL-6, and of TNF-α in the kidneys, was significantly inhibited. Western blot analysis found that MPC significantly increased Bcl-2 and decreased Bax in the kidneys. Phosphorylation of Akt and extracellular signal-regulated kinases 1 and 2 (ERK1/2) was significantly increased. Haemodynamics, area at risk and mortality did not differ significantly among the groups. CONCLUSIONS: MPC significantly reduces kidney injury and apoptosis induced by myocardial I/R. The underlying mechanisms might be related to inhibition of both the extrinsic and intrinsic pathways of apoptosis, possibly via inhibition of TNF-α production, modulation of Bcl-2 and Bax and activation of Akt and ERK1/2.


Assuntos
Lesão Renal Aguda/prevenção & controle , Apoptose/fisiologia , Precondicionamento Isquêmico Miocárdico , Isquemia Miocárdica/complicações , Traumatismo por Reperfusão Miocárdica/complicações , Lesão Renal Aguda/patologia , Animais , Caspase 3/análise , Interleucina-1/sangue , Interleucina-6/sangue , Rim/química , Rim/patologia , Masculino , Proteínas Proto-Oncogênicas c-akt/análise , Proteínas Proto-Oncogênicas c-bcl-2/análise , Ratos , Ratos Sprague-Dawley , Fator de Necrose Tumoral alfa/análise , Fator de Necrose Tumoral alfa/sangue , Proteína X Associada a bcl-2/análise
10.
J Formos Med Assoc ; 114(8): 756-63, 2015 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-24076271

RESUMO

BACKGROUND/PURPOSE: Brief pressure overload of the left ventricle reduced myocardial infarct (MI) size in rabbits has been previously reported. Its effects in other species are not known. This study investigates effects of pressure overload and the role of adenosine in rats in this study. METHODS: MI was induced by 40-minute occlusion of the left anterior descending coronary artery followed by 3-hour reperfusion. MI size was determined by triphenyl tetrazolium chloride staining. Brief pressure overload was induced by two 10-minute episodes of partial snaring of the ascending aorta. Systolic left ventricular pressure was raised 50% above the baseline value. Ischemic preconditioning was elicited by two 10-minute coronary artery occlusions. RESULTS: The MI size (mean ± standard deviation), expressed as percentage of area at risk, was significantly reduced in the pressure overload group as well as in the ischemic preconditioning group (17.4 ± 3.0% and 18.2 ± 1.5% vs. 26.6 ± 2.4% in the control group, p < 0.001). Pretreatment with 8-(p-sulfophenyl)-theophylline (SPT), an inhibitor of adenosine receptors, did not significantly limit the protection by pressure overload and ischemic preconditioning (18.3 ± 1.5% and 18.2 ± 2.0%, respectively, p < 0.001). SPT itself did not affect the extent of infarct (25.4 ± 2.0%). The hemodynamics, area at risk and mortality were not significantly different among all groups of animals. CONCLUSION: Brief pressure overload of the left ventricle preconditioned rat myocardium against infarction. Because SPT did not significantly alter MI size reduction, our results did not support a role of adenosine in preconditioning by pressure overload in rats.


Assuntos
Adenosina/farmacologia , Ventrículos do Coração/efeitos dos fármacos , Hemodinâmica/efeitos dos fármacos , Precondicionamento Isquêmico Miocárdico , Infarto do Miocárdio/fisiopatologia , Animais , Modelos Animais de Doenças , Ratos , Ratos Sprague-Dawley
11.
J Surg Res ; 194(1): 34-42, 2015 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-25466518

RESUMO

BACKGROUND: Both apoptosis and necrosis contribute to cell death after myocardial ischemia and reperfusion. We previously reported that brief left ventricular pressure overload (LVPO) decreased myocardial infarct (MI) size. In this study, we investigated whether brief pressure overload reduces apoptosis and the mechanisms involved. MATERIALS AND METHODS: MI was induced by a 40-min occlusion of the left anterior descending coronary artery and 3-h reperfusion in male anesthetized Sprague-Dawley rats. Brief LVPO was achieved by two 10-min partial snarings of the ascending aorta, raising the systolic left ventricular pressure 50% above the baseline value. Ischemic preconditioning was elicited by two 10-min coronary artery occlusions and 10-min reperfusions. RESULTS: Brief LVPO and ischemic preconditioning significantly decreased MI size (P < 0.001). Brief pressure overload significantly reduced myocardial apoptosis, as evidenced by the decrease in the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive nuclei (P < 0.001), little or no DNA laddering, and reduced caspase-3 activation (P < 0.01). Moreover, brief pressure overload significantly increased Bcl-2 (P < 0.001) and decreased Bax (P < 0.001) and p53 (P < 0.01). Akt phosphorylation was significantly increased by brief pressure overload (P < 0.001), whereas c-Jun N-terminal kinase phosphorylation was significantly decreased (P < 0.001). Hemodynamics, area at risk, and mortality did not differ significantly among groups. CONCLUSIONS: Brief left LVPO significantly reduces myocardial apoptosis. The underlying mechanisms might be related to modulation of Bcl-2 and Bax, inhibition of p53, increased Akt phosphorylation, and suppressed c-Jun N-terminal kinase phosphorylation.


Assuntos
Apoptose , Miocárdio/patologia , Pressão Ventricular/fisiologia , Animais , Caspase 3/metabolismo , Fragmentação do DNA , Proteínas Quinases JNK Ativadas por Mitógeno/metabolismo , Masculino , Fosforilação , Proteínas Proto-Oncogênicas c-akt/metabolismo , Ratos , Ratos Sprague-Dawley , Proteína Supressora de Tumor p53/análise
12.
J Chin Med Assoc ; 76(9): 497-503, 2013 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-23769879

RESUMO

BACKGROUND: We previously reported that pressure overload of the left ventricle reduced myocardial infarct (MI) size in rabbits. The threshold of pressure overload was investigated in this study. METHODS: Pressure overload of the left ventricle was induced by partial snare of the ascending aorta in anesthetized, open-chest rabbits. Systolic left ventricular pressure (SLVP) was elevated 50% or 30% above baseline value by varying the degree of partial snaring. Different duration of pressure overload, including 10 minutes, 5 minutes, 3 minutes, or 2 minutes, was applied to determine the threshold of protective effects. Ischemic preconditioning was elicited by two 10-minute coronary artery occlusions and reperfusions. Ten minutes after different pretreatment, 1 hour occlusion of the left anterior descending coronary artery followed by 3 hours reperfusion was done to induce MI. The size of area at risk and MI were determined by blue dye injection and triphenyl tetrazolium chloride staining after experiments. RESULTS: Pressure overload increase of SLVP 50% above baseline value for 10 minutes, 5 minutes, and 3 minutes significantly reduced MI size (18.5 ± 3.6%, 21.4 ± 1.9% and 21.6 ± 1.7%, respectively, vs. 26.6 ± 1.0% in the control group, mean ± standard deviation, p < 0.01). A 30% increase of SLVP by pressure overload for 10 minutes, 5 minutes and 3 minutes also significantly decreased MI size (20.5 ± 2.5%, 21.6 ± 2.3%, and 21.5 ± 2.3%, p < 0.01). Ischemic preconditioning significantly decreased MI size (19.9 ± 2.8%, p < 0.001). Pressure overload to elevate SLVP 50% or 30% above baseline value for 2 minutes did not significantly alter MI size (25.0 ± 2.3% and 26.0 ± 1.7%, p = 0.122 and p = 0.457). Two episodes of 2 minutes pressure overload did not significantly decrease MI size (25.0 ± 2.2% and 25.5 ± 2.2%, p = 0.118 and p = 0.281). The hemodynamics, area at risk, and mortality were not significantly different among all groups of animals. CONCLUSION: Pressure overload to raise SLVP either 50% or 30% above baseline value reduced MI size. A minimum duration of 3 minutes was necessary to induce the protective effects.


Assuntos
Precondicionamento Isquêmico Miocárdico/métodos , Infarto do Miocárdio/prevenção & controle , Animais , Ventrículos do Coração , Pressão , Coelhos
13.
PLoS One ; 8(2): e56440, 2013.
Artigo em Inglês | MEDLINE | ID: mdl-23437133

RESUMO

A length polymorphism of GT repeats in the promoter region of the human heme oxygenase-1 (HO-1) gene modulates its gene transcription to protect against myocardial injury. The present study investigated the association between HO-1 promoter polymorphisms and the outcomes of catheter ablation of atrial fibrillation (AF). The allelic frequencies of GT repeats in the HO-1 gene promoter were screened in 205 random individuals who underwent catheter ablation for drug refractory AF.In the patients who received catheter ablation, those with AF recurrence had fewer GT repeats (53.4±7.1 vs. 56.1±6.5, p = 0.004), a lower incidence of hyperlipidemia, more non-paroxysmal AF, and a larger left atrial diameter. After conducting a multivariate logistic analysis, the number of GT repeats (Odds ratio: 0.94, 95% CI 0.90-0.99, p = 0.01) and the diameter of the left atrium (Odds ratio: 1.08, 95% CI 1.02-1.15, p = 0.01) remained independent predictors. The carriers of GT repeats, which were <29 in both alleles, were associated with a lower sinus maintenance rate after catheter ablation (38.5% vs. 60.1%, p = 0.003). The patients were divided into paroxysmal and non-paroxysmal AF groups; the number of GT repeats was associated with AF recurrence only in the patients with paroxysmal AF. The number of GT repeats, combined with LAD, was significant for predicting AF recurrence after catheter ablation (p = 0.01). The number of GT repeats was not found to be associated with differences in the left atrial diameter, the biatrial voltage, or the levels of bilirubin, ferritin, iron, C-reactive protein, or von-Willibrand factor. In conclusions, HO-1 gene promoter polymorphisms were associated with AF recurrence after catheter ablation.


Assuntos
Fibrilação Atrial/genética , Fibrilação Atrial/terapia , Ablação por Cateter/métodos , Heme Oxigenase-1/genética , Fibrilação Atrial/patologia , Proteína C-Reativa/genética , Proteína C-Reativa/metabolismo , Feminino , Seguimentos , Estudos de Associação Genética , Humanos , Masculino , Repetições de Microssatélites/genética , Prognóstico , Regiões Promotoras Genéticas , Recidiva , Resultado do Tratamento , Fator de von Willebrand/genética , Fator de von Willebrand/metabolismo
14.
J Chin Med Assoc ; 75(12): 630-4, 2012 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-23245478

RESUMO

BACKGROUND: Less invasive cardiac surgery is widely adopted nowadays. Upper or lower partial sternotomy is an approach for less invasive cardiac surgery. We report results of less invasive cardiac surgery via partial sternotomy. METHODS: From August 1, 2009 to September 30, 2010, 35 patients underwent cardiac surgery via upper or lower partial sternotomy. The preoperative characteristics, operative variables, mortality, and morbidity were reviewed retrospectively. RESULTS: Thirty-five patients underwent cardiac surgery via partial sternotomy during the study period. Eleven patients (31%) were female. The mean age was 66 ± 11 years (range 38 to 88). Seven patients underwent aortic valve replacement via upper partial sternotomy. Simultaneous mitral valve replacement was done in one patient. Lower partial sternotomy was done in 28 patients. Sixteen patients received mitral valve replacement. Three patients underwent mitral valve repair. Concomitant tricuspid valve repair was done in eight patients. Two patients received aortic valve replacement. One patient had replacement of aortic and mitral valve replacement. One patient had repair of tricuspid valve. Two patients received LIMA anastomosis to the LAD. Two patients underwent emergent repair of the right ventricle. One patient had resection of myxoma in the left atrium. Direct cannulation of the aorta and right atrium was used for cardiopulmonary bypass in 15 patients (48%). Both antegrade and retrograde administration of cardioplegia solution was used routinely for myocardial protection. There was no mortality. Two patients developed respiratory failure. One patient suffered unstable sternum. One patient required conversion to full sternotomy. No patient suffered mediastinitis or groin wound infection. CONCLUSION: Upper or lower partial sternotomy provides adequate exposure for various kind of cardiac surgery. Conventional cardiopulmonary bypass and cardioplegia solution administration can be used. The immediate preliminary outcome was acceptable.


Assuntos
Procedimentos Cirúrgicos Cardíacos/métodos , Esternotomia/métodos , Adulto , Idoso , Idoso de 80 Anos ou mais , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Estudos Retrospectivos
16.
J Air Waste Manag Assoc ; 62(1): 87-91, 2012 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-22393813

RESUMO

This study has investigated numerically the influence of particle location on the number of charges per charged particle in the 10-40 nm size range at the outlet of a needle charger by simulating flow field, electric field, particle charging, and particle trajectory at various conditions. The results show that the total (i.e., diffusion + field charging) number of charges per particle increase with decreasing ratio values of radial location at the outlet of the charger due to the particle position close to the needle tip. It has also been shown that in the outlet region of the charger there is a critical radial location at which the number of charges per particle is a maximum; this critical radial location represents the point at which the charged particle trajectory becomes closest to the needle electrode. The maximum value of number of charges increases with increasing Reynolds number and slightly increases with decreasing applied voltage for particle diameter larger than 20 nm. The maximum number of charges per charged nanoparticle increases with increasing particle diameter. In addition, the minimum ratio value of radial particle location decreases with increasing Reynolds number for various particle diameters.


Assuntos
Poluentes Atmosféricos/química , Eletroquímica , Nanopartículas , Material Particulado/química , Eletricidade Estática , Monitoramento Ambiental/instrumentação
17.
Ann Thorac Surg ; 92(5): 1727-32, 2011 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-21945226

RESUMO

BACKGROUND: We previously reported brief pressure overload of the left ventricle reduced myocardial infarct size. The role of adenosine receptors was investigated in this study. METHODS: Pressure overload was achieved by two 10-minute partial snaring of the ascending aorta. Systolic left ventricular pressure was raised 50% above baseline value. Ischemic preconditioning was elicited by two 10-minute coronary artery occlusions. Ten minutes after different pretreatments, 60-minute occlusion of the left anterior descending coronary artery followed by 3-hour reperfusion was done to induce infarction. The area at risk and myocardial infarct size were determined by Evans blue dye injection and triphenyltetrazolium chloride staining. RESULTS: Myocardial infarct size (mean ± standard deviation), expressed as percentage of area at risk, was significantly reduced in the pressure overload group (19.3 ± 2.5 %, p < 0.001) and in the ischemic preconditioning group (18.3 ± 1.8 %, p < 0.001) versus the control group (27.3 ± 3.3 %). Pretreatment with 8-(p-sulfophenyl)-theophylline, an adenosine receptor antagonist, limited the protection by ischemic preconditioning (26.8 ± 3.7%), but not that by pressure overload (19.2 ± 2.5%, p < 0.001). The 8-(p-sulfophenyl)-theophylline did not significantly affect the extent of infarct (26.4 ± 5.4%). The hemodynamics prior to treatment, area at risk, and mortality were not significantly different among all groups of animals. CONCLUSIONS: Brief pressure overload of the left ventricle preconditioned rabbit myocardium against infarction. Because 8-(p-sulfophenyl)-theophylline had no significant effect on this response, the results are consistent with the hypothesis that the underlying mechanism does not depend on activation of adenosine receptors.


Assuntos
Precondicionamento Isquêmico Miocárdico , Infarto do Miocárdio/prevenção & controle , Receptores Purinérgicos P1/fisiologia , Animais , Precondicionamento Isquêmico Miocárdico/métodos , Coelhos , Função Ventricular Esquerda
18.
BMC Infect Dis ; 11: 152, 2011 May 26.
Artigo em Inglês | MEDLINE | ID: mdl-21612672

RESUMO

BACKGROUND: Emergence of daptomycin-nonsusceptible (DNS) Staphylococcus aureus is a dreadful problem in the treatment of endocarditis. Few current therapeutic agents are effective for treating infections caused by DNS S. aureus. CASE PRESENTATION: We describe the emergence of DNS S. aureus. in a patient with implantable cardioverter-defibrillator (ICD) device -related endocarditis who was priorily treated with daptomycin. Metastatic dissemination as osteomyelitis further complicated the management of endocarditis. The dilemma was successfully managed by surgical removal of the ICD device and combination antimicrobial therapy with high-dose daptomycin and fosfomycin. CONCLUSIONS: Surgical removal of intracardiac devices remains an important adjunctive measure in the treatment of endocarditis. Our case suggests that combination therapy is more favorable than single-agent therapy for infections caused by DNS S. aureus.


Assuntos
Antibacterianos/uso terapêutico , Farmacorresistência Bacteriana , Endocardite Bacteriana/tratamento farmacológico , Fosfomicina/uso terapêutico , Infecções Estafilocócicas/tratamento farmacológico , Staphylococcus aureus/fisiologia , Adulto , Daptomicina , Quimioterapia Combinada , Endocardite Bacteriana/microbiologia , Feminino , Humanos , Testes de Sensibilidade Microbiana , Infecções Estafilocócicas/microbiologia , Staphylococcus aureus/efeitos dos fármacos
19.
Heart ; 97(8): 648-54, 2011 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-21330312

RESUMO

BACKGROUND: Obesity has numerous adverse effects on general, and especially, cardiovascular health. Plasma adiponectin, an adipokine, is inversely related to adipose tissue mass, and also the prognosis of heart failure and coronary artery disease (CAD). Coronary artery bypass grafting (CABG) surgery is usually the treatment of choice for patients with complex CAD. OBJECTIVE: To investigate the impact of body mass index (BMI) and the associated biomarkers on clinical outcomes after CABG. METHODS: Patients with CAD who underwent CABG by a single cardiac surgeon team were prospectively enrolled and followed for up to 5 years after CABG. RESULTS: Among the 234 consecutive patients (aged 70.4 ± 10.5 years, BMI 24.68 ± 3.27 kg/m(2), 84.6% men), there were 76 mortalities during follow-up. BMI was negatively correlated with adiponectin (r=-0.203, p=0.003), high-sensitivity C-reactive protein (hsCRP; r=-0.176, p=0.009), and N-terminal pro-brain natriuretic peptide (NT-proBNP; r=-0.271, p<0.001). Patients of normal weight (BMI <25 kg/m(2)) had a decreased event free survival when compared with overweight or obese patients (BMI ≥25 kg/m(2)). After accounting for age, sex, manifest acute coronary syndrome, glomerular filtration rate, and left ventricular ejection fraction, BMI remained correlated with cardiovascular mortality in the study population. (HR and 95% CI per 1 kg/m(2): 0.912 (0.833 to 0.998)). However, adiponectin, hsCRP, and NT-proBNP would abolish the prognostic impact of BMI. In addition, risk-stratified subgroup analysis showed that adiponectin, hsCRP and NT-proBNP predicted mortality in patients with normal weight, rather than in overweight or obese patients. CONCLUSIONS: BMI was inversely associated with the prognosis of CABG. Such association may be linked to the baseline mechanisms related to metabolic disorder (adiponectin) and systemic inflammation (hsCRP). Future pathophysiological validation is indicated.


Assuntos
Índice de Massa Corporal , Ponte de Artéria Coronária/mortalidade , Doença da Artéria Coronariana/cirurgia , Obesidade/complicações , Adiponectina/sangue , Idoso , Idoso de 80 Anos ou mais , Biomarcadores/sangue , Proteína C-Reativa/metabolismo , Doença da Artéria Coronariana/sangue , Doença da Artéria Coronariana/complicações , Métodos Epidemiológicos , Feminino , Humanos , Masculino , Peptídeo Natriurético Encefálico/sangue , Prognóstico
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