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1.
BMC Cardiovasc Disord ; 21(1): 350, 2021 07 22.
Artigo em Inglês | MEDLINE | ID: mdl-34294029

RESUMO

BACKGROUND: Primary aldosteronism (PA), as a cause of secondary hypertension, can cause more serious cardiovascular damage than essential hypertension. The aldosterone-to-renin ratio (ARR) is recommended as the most reliable screening method for PA, but ARR screening is often influenced by many factors. PA cannot be easily excluded when negative ARR. CASE PRESENTATION: We report the case of a 45-year-old Chinese man with resistant hypertension. Three years ago, he underwent a comprehensive screening for secondary hypertension, including the ARR, and the result was negative. After that, the patient's blood pressure was still poorly controlled with four kinds of antihypertensive drugs, the target organ damage of hypertension progressed, and hypokalaemia was difficult to correct. When the patient was hospitalized again for comprehensive examination, we found that aldosterone levels had significantly increased, although the ARR was negative. An inhibitory test with saline was further carried out, and the results suggested that aldosterone was not inhibited; therefore, PA was diagnosed. We performed a unilateral adenoma resection for this patient, and spironolactone was continued to control blood pressure. After the operation, blood pressure is well controlled, and hypokalaemia is corrected. CONCLUSION: When the ARR is negative, PA cannot be easily excluded. Comprehensive analysis and diagnosis should be based on the medication and clinical conditions of patients.


Assuntos
Adenoma/complicações , Neoplasias das Glândulas Suprarrenais/complicações , Aldosterona/sangue , Hiperaldosteronismo/sangue , Hipertensão/etiologia , Renina/sangue , Adenoma/sangue , Adenoma/diagnóstico , Adenoma/cirurgia , Neoplasias das Glândulas Suprarrenais/sangue , Neoplasias das Glândulas Suprarrenais/diagnóstico , Neoplasias das Glândulas Suprarrenais/cirurgia , Adrenalectomia , Anti-Hipertensivos/uso terapêutico , Biomarcadores/sangue , Pressão Sanguínea/efeitos dos fármacos , Humanos , Hiperaldosteronismo/diagnóstico , Hiperaldosteronismo/etiologia , Hipertensão/diagnóstico , Hipertensão/tratamento farmacológico , Hipertensão/fisiopatologia , Masculino , Pessoa de Meia-Idade , Resultado do Tratamento
2.
Medicine (Baltimore) ; 100(20): e25928, 2021 May 21.
Artigo em Inglês | MEDLINE | ID: mdl-34011065

RESUMO

ABSTRACT: Bilateral kidney damage in hypertensive patients is not parallel. Angiotensin-converting enzyme inhibitor/angiotensin receptor blocker (ACEI/ARB), as a commonly used antihypertensive drug, could protect kidney function and delay its deterioration. Most studies focused on overall renal function, but the researches on split renal function (SRF) are rare. We investigated the effects of ACEI/ARB on the SRF in patients with primary hypertension.Patients with primary hypertension (n = 429; male: 213; female: 216) admitted to our department between January 2014 and December 2016 were included in this study. The glomerular filtration rate (GFR) of split and total renal function were determined using diethylenetriaminepentaacetic acid tagged with 99mTc renal dynamic imaging method. For the same patient, the side with high GFR was considered as higher GFR kidney, whereas that with a low GFR was considered as lower GFR kidney. The split function score (Q value) was utilized to evaluate the differences of bilateral renal function. The patients were divided into 3 groups based on the Q values (Group 1, Q value <5%; Group 2, Q value of 5%-10%; Group 3, Q value ≥10%). All the patients received antihypertensive therapy based on ACEI/ARB. The renal dynamic imaging was performed in the 1-year follow-up to investigate the changes of the SRF.Compared with the baseline level, significant decline was noticed in the serum creatinine (Scr) in Group 2 and Group 3 (P < .05). The cystatin C in Group 3 showed significant decline (P < .05). Compared with the baseline, there was significant decline in the Q value in Group 2, whereas the GFR of lower GFR kidney showed significant increase (P < .05). No statistical differences were noticed in the Q value and split GFR in Group 1 and Group 3 (P > .05).In primary hypertension patients, ACEI/ARB therapy could improve the SRF of lower GFR kidney in the presence of certain differences between the SRF. As a result, the SRF difference was reduced. In case of Q value in a range of 5% to 10%, ACEI/ARB could improve the renal function effectively. It may be significant for the design of antihypertensive drugs.


Assuntos
Antagonistas de Receptores de Angiotensina/administração & dosagem , Inibidores da Enzima Conversora de Angiotensina/administração & dosagem , Hipertensão/tratamento farmacológico , Rim/efeitos dos fármacos , Insuficiência Renal/prevenção & controle , Idoso , Idoso de 80 Anos ou mais , Meios de Contraste/administração & dosagem , Creatinina/sangue , Cistatina C/sangue , Feminino , Seguimentos , Taxa de Filtração Glomerular/efeitos dos fármacos , Taxa de Filtração Glomerular/fisiologia , Humanos , Hipertensão/sangue , Hipertensão/complicações , Rim/diagnóstico por imagem , Rim/fisiopatologia , Masculino , Pessoa de Meia-Idade , Insuficiência Renal/sangue , Insuficiência Renal/diagnóstico , Insuficiência Renal/etiologia , Tomografia Computadorizada de Emissão de Fóton Único/métodos , Resultado do Tratamento
3.
BMC Cardiovasc Disord ; 21(1): 194, 2021 04 20.
Artigo em Inglês | MEDLINE | ID: mdl-33879070

RESUMO

BACKGROUND: Circulating monocytes and tissue macrophages play complex roles in the pathogenesis of hypertension and the resulting target organ damage. In this study, we observed alterations in the monocyte phenotype and inflammatory state of hypertensive patients with left ventricular hypertrophy (LVH) and studied the effects of irbesartan in these patients. This study might reveal a novel mechanism by which irbesartan alleviates LVH, and it could provide new targets for the prevention and treatment of hypertensive target organ damage. METHODS: CD163 and CD206 expression on monocytes and IL-10 and TNF-α levels in the serum of hypertensive patients with or without LVH and of healthy volunteers were detected. Furthermore, we treated monocytes from the LVH group with different concentrations of irbesartan, and then, CD163, CD206, IL-10 and TNF-α expression was detected. RESULTS: We found, for the first time, that the expression of CD163, CD206 and IL-10 in the LVH group was lower than that in the non-LVH group and healthy control group, but the TNF-α level in the LVH group was significantly higher. Irbesartan upregulated the expression of CD163 and CD206 in hypertensive patients with LVH in a concentration-dependent manner. Irbesartan also increased the expression of IL-10 and inhibited the expression of TNF-α in monocyte culture supernatants in a concentration-dependent manner. CONCLUSIONS: Our data suggest that inflammation was activated in hypertensive patients with LVH and that the monocyte phenotype was mainly proinflammatory. The expression of proinflammatory factors increased while the expression of anti-inflammatory factors decreased. Irbesartan could alter the monocyte phenotype and inflammatory status in hypertensive patients with LVH. This previously unknown mechanism may explain how irbesartan alleviates LVH. Trail registration The study protocols were approved by the Ethical Committee of the Second Affiliated Hospital of Dalian Medical University. Each patient signed the informed consent form.


Assuntos
Anti-Inflamatórios/farmacologia , Anti-Hipertensivos/farmacologia , Hipertensão/tratamento farmacológico , Hipertrofia Ventricular Esquerda/prevenção & controle , Irbesartana/farmacologia , Monócitos/efeitos dos fármacos , Idoso , Antígenos CD/sangue , Antígenos de Diferenciação Mielomonocítica/sangue , Pressão Sanguínea , Estudos de Casos e Controles , Células Cultivadas , Feminino , Humanos , Hipertensão/sangue , Hipertensão/complicações , Hipertensão/fisiopatologia , Hipertrofia Ventricular Esquerda/sangue , Hipertrofia Ventricular Esquerda/etiologia , Hipertrofia Ventricular Esquerda/fisiopatologia , Interleucina-10/sangue , Masculino , Glicoproteínas de Membrana/sangue , Pessoa de Meia-Idade , Monócitos/metabolismo , Fenótipo , Receptores de Superfície Celular/sangue , Receptores Imunológicos/sangue , Fator de Necrose Tumoral alfa/sangue , Função Ventricular Esquerda , Remodelação Ventricular
5.
Med Sci Monit ; 26: e924748, 2020 Aug 28.
Artigo em Inglês | MEDLINE | ID: mdl-32855380

RESUMO

BACKGROUND Chronic hypertension changes the function and structure of the heart and blood vessels. This study aimed to explore the role of the NOD1/Rip2 (nucleotide-binding oligomerization domain 1/receptor-interacting protein 2) signaling pathway in myocardial remodeling in spontaneously hypertensive rats (SHRs). MATERIAL AND METHODS Blood pressure was measured using a tail cuff. The cardiac structure was observed using echocardiography. Slices of the myocardium were stained with hematoxylin and eosin. The expression of NOD1 and Rip2 was detected using real-time polymerase chain reaction, western blot, and immunohistochemistry. The content and distribution of collagen in the myocardium were observed using Van Gieson staining. Enzyme-linked immunosorbent assay was used to detect the interleukin-1 (IL-1) concentrations. SHRs were treated with the NOD1 agonist iE-DAP and NOD1 inhibitor ML130. RESULTS The NOD1 agonist increased blood pressure in SHRs, and the NOD1 inhibitor decreased blood pressure; the interventricular septum thickness (IVST) and left ventricular posterior wall thickness (LVPWT) of the agonist-treated group were thicker than those of the control group, and the antagonist exerted the opposite effects. The levels of the NOD1 and Rip2 mRNAs and proteins, serum IL-1 concentration, and myocardial collagen volume fraction (CVF%) increased in SHRs in the NOD1 agonist group, but the levels of NOD1 and Rip2, serum IL-1 concentration, and myocardial collagen volume fraction (CVF%) decreased in SHRs in the NOD1 inhibitor group. CONCLUSIONS NOD1/Rip2 expression increased during the progression of myocardial remodeling in SHRs. The NOD1 agonist increased NOD1 expression and promoted myocardial remodeling, while the NOD1 antagonist reduced NOD1/Rip2 expression and protected against myocardial remodeling.


Assuntos
Proteína Adaptadora de Sinalização NOD1/metabolismo , Proteína Serina-Treonina Quinase 2 de Interação com Receptor/metabolismo , Transdução de Sinais , Remodelação Ventricular , Animais , Pressão Sanguínea/efeitos dos fármacos , Masculino , Proteína Adaptadora de Sinalização NOD1/agonistas , Proteína Adaptadora de Sinalização NOD1/antagonistas & inibidores , Ratos , Ratos Endogâmicos SHR , Ratos Endogâmicos WKY , Reação em Cadeia da Polimerase em Tempo Real
6.
Biomed Pharmacother ; 129: 110364, 2020 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-32531678

RESUMO

Cardiac hypertrophy and remodeling are among the major health challenges facing countries around the world today. Neohesperidin plays an important role in influencing cell apoptosis, cell growth, tumorigenesis and tumor microenvironment, but the mechanism and role of Neohesperidin in cardiac hypertrophy and remodeling caused by Angiotensin II has not been fully elucidated. This study used Angiotensin II to induce cardiac hypertrophy and cardiac remodeling in mice. Echocardiography was used to evaluate cardiac function, H&E and Masson trichrome staining were used to detect myocardial histological changes. Cardiac cell size was determined by WGA staining. The protein content of the signaling pathway was detected by Western blot, and the mRNA expression of fibrosis and hypertrophy markers was detected by qPCR. DHE staining was used to detect oxidative stress. We also observed the effect of Neohesperidin on Ang II-induced NRCMs. The results showed that neohesperidin can significantly inhibit Ang II-induced myocardial contractile dysfunction, cardiac hypertrophy, myocardial fibrosis, myocardial oxidative stress and inflammation. These results suggest that Neohesperidin can alleviate cardiac hypertrophy and remodeling caused by Ang II, and its mechanism may be related to the inhibition of multiple signaling pathways.


Assuntos
Angiotensina II , Hesperidina/análogos & derivados , Hipertrofia Ventricular Esquerda/prevenção & controle , Miócitos Cardíacos/efeitos dos fármacos , Função Ventricular Esquerda/efeitos dos fármacos , Remodelação Ventricular/efeitos dos fármacos , Animais , Células Cultivadas , Modelos Animais de Doenças , Fibrose , Regulação da Expressão Gênica , Hesperidina/farmacologia , Hipertrofia Ventricular Esquerda/metabolismo , Hipertrofia Ventricular Esquerda/patologia , Hipertrofia Ventricular Esquerda/fisiopatologia , Mediadores da Inflamação/metabolismo , Masculino , Camundongos Endogâmicos C57BL , Miócitos Cardíacos/metabolismo , Miócitos Cardíacos/patologia , Estresse Oxidativo/efeitos dos fármacos , Ratos Sprague-Dawley , Transdução de Sinais
7.
Sci Prog ; 103(1): 36850419878065, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-31829866

RESUMO

The stagnant region often appears in front of the tool cutting edge, which is caused by mechanical inlay and excessive pressing in plastic metal cutting with large negative rake angle tools at a low speed. It results in the change of the effective negative rake angle which can affect the flow characteristics of material, the quality of machined surface and the abrasion loss of cutting tools. However, the critical negative rake angle model based on the existence of the stagnant region has not been reported yet. Therefore, in order to investigate the critical negative rake angle value considering the stagnant region, a critical negative rake angle model based on the principle of minimum required energy is established, and the correctness of the theoretical model is verified by orthogonal cutting experiments. At the same time, the influence of the critical value of the large negative rake angle tool on the machined surface quality is studied through different cutting experiments. These experimental results show that the deviations of both experimental and theoretical critical negative rake angle are less than 5% during the orthogonally cutting of the aluminium (AL1060) and copper (T2) materials by the negative rake angle tool. Meanwhile, the critical negative rake angle is related to the adhesive friction coefficient of tool-workpiece contact surface. The analysis of friction characteristics shows that the deviation values of both theoretical and experimental critical negative rake angle are proportional to the coefficient of adhesive friction and the thickness of the stagnant region. Critical negative rake angle has a significant effect on roughness and residual stress of the machined surface.

8.
Arterioscler Thromb Vasc Biol ; 39(1): 48-62, 2019 01.
Artigo em Inglês | MEDLINE | ID: mdl-30580569

RESUMO

Objective- Hypoxic pulmonary hypertension (HPH) is characterized by proliferative vascular remodeling. Abnormal pulmonary artery smooth muscle cells proliferation and endothelial dysfunction are the primary cellular bases of vascular remodeling. AQP1 (aquaporin-1) is regulated by oxygen level and has been observed to play a role in the proliferation and migration of pulmonary artery smooth muscle cells. The role of AQP1 in HPH pathogenesis has not been directly determined to date. To determine the possible roles of AQP1 in the pathogenesis of HPH and explore its possible mechanisms. Approach and Results- Aqp1 knockout mice were used, and HPH model was established in this study. Primary pulmonary artery smooth muscle cells, primary mouse lung endothelial cells, and lung tissue sections from HPH model were used. Immunohistochemistry, immunofluorescence and Western blot, cell cycle, apoptosis, and migration analysis were performed in this study. AQP1 expression was upregulated by chronic hypoxia exposure, both in pulmonary artery endothelia and medial smooth muscle layer of mice. Aqp1 deficiency attenuated the elevation of right ventricular systolic pressures and mitigated pulmonary vascular structure remodeling. AQP1 deletion reduced abnormal cell proliferation in pulmonary artery and accompanied with accumulation of HIF (hypoxia-inducible factor). In vitro, Aqp1 deletion reduced hypoxia-induced proliferation, apoptosis resistance, and migration ability of primary cultured pulmonary artery smooth muscle cells and repressed HIF-1α protein stability. Furthermore, Aqp1 deficiency protected lung endothelial cells from apoptosis in response to hypoxic injury. Conclusions- Our data showed that Aqp1 deficiency could attenuate hypoxia-induced vascular remodeling in the development of HPH. AQP1 may be a potential target for pulmonary hypertension treatment.


Assuntos
Aquaporina 1/fisiologia , Hipertensão Pulmonar/etiologia , Hipóxia/complicações , Animais , Aquaporina 1/genética , Células Cultivadas , Ciclina D1/fisiologia , Hipertensão Pulmonar/fisiopatologia , Subunidade alfa do Fator 1 Induzível por Hipóxia/fisiologia , Masculino , Camundongos , Camundongos Knockout , Músculo Liso Vascular/citologia , Miócitos de Músculo Liso/fisiologia , Remodelação Vascular
9.
Artigo em Inglês | MEDLINE | ID: mdl-28884091

RESUMO

Introduction: Human gut microbiota is believed to be directly or indirectly involved in cardiovascular diseases and hypertension. However, the identification and functional status of the hypertension-related gut microbe(s) have not yet been surveyed in a comprehensive manner. Methods: Here we characterized the gut microbiome in hypertension status by comparing fecal samples of 60 patients with primary hypertension and 60 gender-, age-, and body weight-matched healthy controls based on whole-metagenome shotgun sequencing. Results: Hypertension implicated a remarkable gut dysbiosis with significant reduction in within-sample diversity and shift in microbial composition. Metagenome-wide association study (MGWAS) revealed 53,953 microbial genes that differ in distribution between the patients and healthy controls (false discovery rate, 0.05) and can be grouped into 68 clusters representing bacterial species. Opportunistic pathogenic taxa, such as, Klebsiella spp., Streptococcus spp., and Parabacteroides merdae were frequently distributed in hypertensive gut microbiome, whereas the short-chain fatty acid producer, such as, Roseburia spp. and Faecalibacterium prausnitzii, were higher in controls. The number of hypertension-associated species also showed stronger correlation to the severity of disease. Functionally, the hypertensive gut microbiome exhibited higher membrane transport, lipopolysaccharide biosynthesis and steroid degradation, while in controls the metabolism of amino acid, cofactors and vitamins was found to be higher. We further provided the microbial markers for disease discrimination and achieved an area under the receiver operator characteristic curve (AUC) of 0.78, demonstrating the potential of gut microbiota in prediction of hypertension. Conclusion: These findings represent specific alterations in microbial diversity, genes, species and functions of the hypertensive gut microbiome. Further studies on the causality relationship between hypertension and gut microbiota will offer new prospects for treating and preventing the hypertension and its associated diseases.


Assuntos
Bactérias/classificação , Disbiose/microbiologia , Microbioma Gastrointestinal/genética , Trato Gastrointestinal/microbiologia , Hipertensão/microbiologia , Bactérias/genética , Bactérias/isolamento & purificação , Fezes/microbiologia , Feminino , Humanos , Masculino , Metagenoma/genética , Pessoa de Meia-Idade , Sequenciamento Completo do Genoma
10.
J Nutr Biochem ; 36: 81-88, 2016 10.
Artigo em Inglês | MEDLINE | ID: mdl-27596528

RESUMO

Hypoxia-induced oxidative stress and excessive proliferation of pulmonary artery smooth muscle cells (PASMCs) play important roles in the pathological process of hypoxic pulmonary hypertension (HPH). Grape seed procyanidin extract (GSPE) possesses antioxidant properties and has beneficial effects on the cardiovascular system. However, the effect of GSPE on HPH remains unclear. In this study, adult Sprague-Dawley rats were exposed to intermittent chronic hypoxia for 4 weeks to mimic a severe HPH condition. Hemodynamic and pulmonary pathomorphology data showed that chronic hypoxia significantly increased right ventricular systolic pressures (RVSP), weight of the right ventricle/left ventricle plus septum (RV/LV+S) ratio and median width of pulmonary arteries. GSPE attenuated the elevation of RVSP, RV/LV+S, and reduced the pulmonary vascular structure remodeling. GSPE also increased the levels of SOD and reduced the levels of MDA in hypoxia-induced HPH model. In addition, GSPE suppressed Nox4 mRNA levels, ROS production and PASMCs proliferation. Meanwhile, increased expression of phospho-STAT3, cyclin D1, cyclin D3 and Ki67 in PASMCs caused by hypoxia was down-regulated by GSPE. These results suggested that GSPE might potentially prevent HPH via antioxidant and antiproliferative mechanisms.


Assuntos
Antioxidantes/uso terapêutico , Suplementos Nutricionais , Extrato de Sementes de Uva/uso terapêutico , Hipertensão Pulmonar/prevenção & controle , Músculo Liso Vascular/metabolismo , Estresse Oxidativo , Proantocianidinas/uso terapêutico , Traumatismo por Reperfusão/prevenção & controle , Animais , Antioxidantes/efeitos adversos , Antioxidantes/metabolismo , Biomarcadores/metabolismo , Proliferação de Células , Células Cultivadas , Suplementos Nutricionais/efeitos adversos , Regulação Enzimológica da Expressão Gênica , Extrato de Sementes de Uva/efeitos adversos , Extrato de Sementes de Uva/metabolismo , Hipertensão Pulmonar/dietoterapia , Hipertensão Pulmonar/metabolismo , Hipertensão Pulmonar/patologia , Peroxidação de Lipídeos , Pulmão/irrigação sanguínea , Pulmão/metabolismo , Pulmão/patologia , Masculino , Músculo Liso Vascular/enzimologia , Músculo Liso Vascular/patologia , NADPH Oxidase 4 , NADPH Oxidases/antagonistas & inibidores , NADPH Oxidases/genética , NADPH Oxidases/metabolismo , Proantocianidinas/efeitos adversos , Proantocianidinas/metabolismo , Artéria Pulmonar/metabolismo , Artéria Pulmonar/patologia , Distribuição Aleatória , Ratos Sprague-Dawley , Espécies Reativas de Oxigênio/antagonistas & inibidores , Espécies Reativas de Oxigênio/metabolismo , Traumatismo por Reperfusão/dietoterapia , Traumatismo por Reperfusão/metabolismo , Traumatismo por Reperfusão/patologia , Mucosa Respiratória/irrigação sanguínea , Mucosa Respiratória/metabolismo , Mucosa Respiratória/patologia , Remodelação Vascular
11.
ScientificWorldJournal ; 2012: 607157, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-22997500

RESUMO

OBJECTIVE: To investigate the expression of NOD2 in human VSMCs, its role in the production of inflammatory cytokines in VSMC and the possible interaction of NOD2-mediated signaling pathway with those mediated by TLR2 and TLR4. METHODS: Human coronary artery smooth muscle cells were stimulated with NOD2 agonist MDP alone or in combination with either TLR2 agonist PAM3 or TLR4 agonist LPSs. The mRNA expression of NOD2 and FGF-2 were measured by RT-PCR. The concentration of IL-8 and TNF-α in the culture supernatants was determined by ELISA. VSMC proliferation ability was analyzed by MTT assay. RESULTS: MDP up regulated the expression of NOD2 mRNA in VSMC in a time-dependent manner, up regulated the expression of FGF-2 mRNA in VSMC, induced the production of IL-8 and TNF-α, and promoted the proliferation of VSMC. Additionally, MDP synergied with LPS and PAM3 to promote the proliferation of VSMC and induce the production of IL-8 and TNF-α. CONCLUSION: The activation of NOD2-mediated innate immune signaling pathway can increase the proliferation ability of VSMC and induce the production of inflammatory cytokines in VSMC. It is also shown a synergistic effect with TLR2- and TLR4-mediated signaling pathways in this process.


Assuntos
Músculo Liso Vascular/citologia , Miócitos de Músculo Liso/imunologia , Proteína Adaptadora de Sinalização NOD2/agonistas , Receptor 2 Toll-Like/agonistas , Receptor 4 Toll-Like/agonistas , Acetilmuramil-Alanil-Isoglutamina/farmacologia , Proliferação de Células , Células Cultivadas , Vasos Coronários/citologia , Vasos Coronários/imunologia , Meios de Cultura/metabolismo , Sinergismo Farmacológico , Ensaio de Imunoadsorção Enzimática , Fator 2 de Crescimento de Fibroblastos/genética , Fator 2 de Crescimento de Fibroblastos/imunologia , Humanos , Imunidade Inata , Interleucina-8/imunologia , Lipopeptídeos/farmacologia , Lipopolissacarídeos/farmacologia , Músculo Liso Vascular/imunologia , Miócitos de Músculo Liso/citologia , Miócitos de Músculo Liso/efeitos dos fármacos , Proteína Adaptadora de Sinalização NOD2/genética , Proteína Adaptadora de Sinalização NOD2/imunologia , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Transdução de Sinais , Fatores de Tempo , Receptor 2 Toll-Like/imunologia , Receptor 4 Toll-Like/imunologia , Fator de Necrose Tumoral alfa/imunologia
12.
Hypertens Res ; 25(2): 191-5, 2002 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-12047034

RESUMO

To evaluate the alteration of myocardial contractility in hypertensive patients with different left ventricular geometric patterns by the end-systolic stress-midwall fractional shortening relation. Echocardiography was applied to study the left ventricular geometry and cardiac function among 117 cases of essential hypertension, with 45 normal cases as control(s). Left ventricular mass index (LVMI) and relative wall thickness (RWT) were calculated using echocardiographic data. All patients were divided into four kinds of left ventricular geometry pattern based on LVMI and RWT. Patients of the eccentric hypertrophy group suffered the most serious damage of left ventricular systolic function. Myocardial contractility shown by end-systolic stress-midwall fractional shortening relation was significantly decreased in the concentric remodeling group, eccentric hypertrophy group and concentric hypertrophy group, and those with concentric hypertrophy showed the worst contractility. The degree of myocardial contractility damage was different in patients with different left ventricular geometric patterns. Geometric changes may have compensated for the reduction of myocardial contractility in some phases in order to maintain the normal pump function.


Assuntos
Ecocardiografia , Hipertensão/diagnóstico por imagem , Hipertensão/fisiopatologia , Função Ventricular Esquerda , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Contração Miocárdica , Estresse Mecânico , Sístole
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