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1.
Scientific Journal of Iranian Blood Transfusion Organization Research Center [The]. 2011; 8 (3): 195-206
in Persian | IMEMR | ID: emr-118286

ABSTRACT

Coagulation system activation in response to physical activity is already to some extent determined and known, but the effect of eccentric contraction exercise on its activation is not specified. The purpose of this study was to investigate the effect of a single session eccentric resistance exercise on some coagulation factors of inactive males. Twelve male students volunteered to participate in this study and were divided randomly to experimental and control groups. Experimental group performed a controlled return movement from elbow flexion exercise as eccentric contraction. Blood sampling was implemented 30 min before, and immediately after exercise test; it was also done 2 and 24 h after the exercise test. Statistical analysis revealed that plasma fibrinogen elevated significantly over 24 h after test [pre: 2.56 +/- 0.23 and 24h post: 2.84 +/- 0.24]. Prothrombin time did not change significantly but significant decrease was found over 24 h after test for activated partial thromboplastin time [pre: 43.05 +/- 3.33 and 24h post: 26.65 +/- 0.61]. Platelet counts and its indices did not change significantly. Eccentric exercise as defined in our research somehow caused a blood coagulation increase and this activation is probably accomplished through intrinsic pathways and not extrinsic ones. It showed a decrease in activated partial thromboplastin time, without any change in prothrombin time. Insignificant changes in plasma fibrinogen, platelet and its morphologic indices could be related to both inclusion of low volume of muscles and eccentric type of contraction


Subject(s)
Humans , Male , Blood Coagulation Factors , Prothrombin Time , Partial Thromboplastin Time , Fibrinogen/physiology
2.
Pakistan Journal of Pharmaceutical Sciences. 2009; 22 (4): 355-359
in English | IMEMR | ID: emr-102254

ABSTRACT

Effect of evening primrose oil [EPO] was assessed on coagulation parameters following 30 and 60 days administration of 90, 180 and 360 micro l/kg oil to healthy rabbits of either sex. There was significant increase in all assays except Fibrinogen time. These effects might be due to inactivation or inhibition of factors affecting coagulation. The intake of evening primrose oil also significantly decreased platelet count. Results of this study suggest that evening primrose oil shows considerable anti-anticoagulant and anti-platelet activity in animals and has potential to reduce cardiovascular morbidity and mortality


Subject(s)
Female , Animals , Plant Oils , Anticoagulants , gamma-Linolenic Acid/pharmacology , Warfarin/pharmacology , Partial Thromboplastin Time , Fibrinogen/physiology , Prothrombin Time , Platelet Count , Plants, Medicinal , Oleic Acid , Rabbits , Vitamin E , Palmitic Acid , Stearic Acids
3.
Arch. cardiol. Méx ; 76(supl.4): S158-S172, oct.-dic. 2006.
Article in Spanish | LILACS | ID: lil-568123

ABSTRACT

Endothelial dysfunction and inflammation play a crucial role in all stages of atherosclerosis, from the beginning, during progression, and, finally, in its highest clinical expression: acute coronary syndromes. In this process, fibrinogen, an acute phase reactant with active participation in endothelial function, thrombosis and inflammation has proved to be an independent variable to cardiovascular risk together with its participation in resistance phenomena to different antithrombotic approaches. The reasons by which fibrinogen is elevated in cardiovascular disease and atherosclerosis are, in general, only incompletely understood; but all cells involved in the atherogenetic process are able to produce cytokines, which induce an acute phase reaction that increases fibrinogen levels in plasma. The potential pathophysiological mechanisms by which elevated fibrinogen levels mediate cardiovascular risk are multiple. Fibrinogen forms the substrate for thrombin an represents the final step in the coagulation cascade, it is essential for platelet aggregation, it modulates endothelial function, it promotes smooth muscle cell proliferation and migration, it interacts with the binding of plasmin with its receptor and, finally, it represents a major acute phase protein. Epidemiological studies have established sufficient evidence to consider fibrinogen as a strong, consistent, and independent cardiovascular risk marker or factor. Based on all these implications, the target of this review is an analysis of physiopathogenic and epidemiologic evidence searching for guidelines to establish whether fibrinogen as a risk factor or marker is the lost link between cardiovascular disease and classic risk factors. CONCLUSION: Analyses of the respective studies suggest that fibrinogen is an important and independent cardiovascular risk factor, clearly associated with conventional risk factors and genetic polymorphisms. Whether or not fibrinogen is causally involved in atherothrombogenesis still remains to be determined and despite of unsolved issues that are waiting conclusive answers, fibrinogen has emerged as an important additional marker of cardiovascular risk.


Subject(s)
Adult , Aged , Female , Humans , Male , Middle Aged , Cardiovascular Diseases , Fibrinogen/physiology , Age Factors , Aspirin , Atherosclerosis/blood , Atherosclerosis , Atherosclerosis , Biomarkers , Cross-Over Studies , Cardiovascular Diseases/blood , Cardiovascular Diseases , Coronary Disease/blood , Coronary Disease , Coronary Disease , Exercise , Follow-Up Studies , Fibrinogen , Fibrinogen , Fibrinolytic Agents , Hypolipidemic Agents , Inflammation/blood , Longitudinal Studies , Polymorphism, Genetic , Platelet Aggregation Inhibitors , Risk Factors , Socioeconomic Factors , Smoking/adverse effects
4.
Medicina (B.Aires) ; 65(2): 121-125, 2005. ilus, tab
Article in Spanish | LILACS | ID: lil-426085

ABSTRACT

El objetivo de este trabajo fue investigar el perfil de viscosidad sanguínea y evaluar la influencia de factores plasmáticos ( fibrinógeno) y celulares ( agregación eritrocitaria ) en un grupo de pacientes hipertensos comparados con un grupo de paciente normotensos. Se trabajó con sangre anticoagulada de pacientes hipertensos no diabéticos (n=3) e indivíduos sanos (n=40). La viscosidad plasmática y de sangre entera se determinaron con un viscosímetro cono-plato. La agregación eritrocitaria se estudió por observación microscopia de los agregados y cuantificación a través de un parâmetro de forma denominado ASP ( Aggregation Shape Parameter), definido como la relación de área proyectada respecto al perímetro. El fibrinógeno se determino con un coagulómetro por el método de Clauss. Los valores de viscosidad de sangre entera resultaron significativamente aumentados en los pacientes hipertensos respecto de los normales para todas las velicidades estudiadas. Los valores de viscosidad plasmática solo presentaron diferencia significativas a bajas velocidades de corte (1.15 a 11.56 seg •1) . Los pacientes hipertensos presentaron agregados amorfos e irregulares, lo que se refleja en los valores alterados de ASP, significativamente mayores (p<0.001) en paciente hipertensos (0.69± 0.11) respecto de los indivíduos normales ( 0.25± 0.12). Los valores de fibrinógeno resultaron ligeramente superiores en los pacientes hipertensos respecto del grupo control (p< 0.01). Numerosos parámetros hemorreológicos juegan un papel importante en la patogénesis de la hipertensión. Entre estos factores hemorreológicos, valores parâmetros podrían estar en la hipertensión ( hematrocito, fibrinógeno plasmático, deformabilidad y agragación eritrocitaria , viscosidad sanguínea y plasmática). En este trabajo, se pudo demostrar anormalidades en la agregación eritrocitaria, detectada por los valores de ASP que podría estar involucrado en las complicaciones vasculares de la hipertensión.


Subject(s)
Adult , Middle Aged , Humans , Male , Female , Hemorheology , Hypertension/blood , Blood Viscosity/physiology , Erythrocyte Aggregation/physiology , Fibrinogen/physiology , Hypertension/physiopathology
5.
Rev. Soc. Cardiol. Estado de Säo Paulo ; 14(3): 521-529, Maio-Jun. 2004. ilus
Article in Portuguese | LILACS | ID: lil-407468

ABSTRACT

A biologia molecular evolui de forma vertiginosa e atualmente é tida como ferramenta indispensável na compreensão de doenças complexas e multifatoriais como a doença arterial coronariana. Tal abordagem gera uma nova forma de avaliação de doenças conhecidas e propicia a criação de novas técnicas, novos métodos diagnósticos e possíveis abordagens terapêuticas, interferindo diariamente no desfecho clínico final do paciente. O número de publicações em genética cardiovascular aumentou cinco vezes nos últimos 20 anos e a descoberta de novos polimorfismos e mutações bem como marcadores de inflamação, coagulação e genes relacionados ao metabolismo lipídico contribuem para se conhecer cada vez mais os aspectos intrínsecos envolvidos na aterosclerose. Este artigo irá abordar os principais avanços nessa área, identificando os polimorfismos mais comuns e sua relevância clínica segundo grandes ensaios e meta-análises,bem como fazer um breve racional acerca do desenho atual dos ensaios clínicos em biologia molecular


Subject(s)
Humans , Arteriosclerosis/physiopathology , Arteriosclerosis/genetics , Molecular Biology/methods , Molecular Biology/trends , Coronary Disease/physiopathology , Coronary Disease/genetics , Genetics/trends , Polymorphism, Genetic/physiology , Polymorphism, Genetic/genetics , Fibrinogen/physiology , Fibrinogen/genetics , P-Selectin/physiology , P-Selectin/genetics
9.
Arq. neuropsiquiatr ; 55(4): 737-40, dez. 1997. graf
Article in Portuguese | LILACS | ID: lil-209371

ABSTRACT

No protocolo de avaliaçäo clínico-laboratorial de pacientes com acidente vascular cerebral (AVC) aterotrombótico dosamos e analisamos níveis de fibrinogênio plasmático (técnica de Clauss automatizada), para determinar seu possível papel como fator de risco trombogênico em 29 pacientes (20 homens e 9 mulheres) com idades entre 25 a 79 anos (mediana=55); todos tinham tido AVC aterotrombótico. Eles foram classificados em 2 grupos segundo alteraçöes de fluxo nas carótidas: g1 - sem alteraçäo de fluxo (n=19) e g2 - com alteraçöes de fluxo (n=10). Resultados- A média das dosagens de fibrinogênio no g1 foi de 269 e no g2 de 353 mg/dl. Quarenta e sete por cento dos pacientes do g1 e 80 por cento do g2, apresentaram medidas >300 mg/dl. As diferenças obtidas entre os grupos neste estudo foram significante. Conclusäo- Considerando o nível de risco epidemiológico de 300 mg/dl, nossos resultados sugerem que o fibrinogênio é um fator de risco independente para AVC aterotrombótico, especialmente naqueles com alteraçäo de fluxo carotídeo.


Subject(s)
Female , Humans , Aged , Middle Aged , Adult , Cerebrovascular Disorders , Fibrinogen/analysis , Risk Factors , Brain Ischemia/blood , Cerebrovascular Disorders/blood , Fibrinogen/physiology , Intracranial Embolism and Thrombosis/blood , Statistics, Nonparametric
10.
Arch. neurociencias ; 1(4): 273-8, oct.-dic. 1996. tab, ilus
Article in Spanish | LILACS | ID: lil-210823

ABSTRACT

Estudios previos en humanos confirman la relación traumatismo craneoencéfalico (TCE) -edema agudo pulmonar neurogénico (EAPN) con hemorragia cerebral. El propósito del trabajo fue inducir EAPN mediante la producción de TEC por el método de sangre autóloga masiva (MSAM) en ratón; así como determinar si el fibrinógeno crioprecipitado (CP), produce los mismos efectos que sangre autóloga (SA). Se inyectó 25 y 50 mcl de SA, CP o agua destilada (AD) a ratones taconic vía ICV a 20 animales por grupo. La administración de AD no indujo EAPN, todos los ratones que recibieron SA o CP mostraron EAPN; más intenso cuando se inyectó CP (15/20) respecto a SA (5/10); algunas lesiones observadas con CP fueron; en encéfalo: hemorragia focal (HF) y laminar (HL); en aracnoides y vasos subaracnoideos: edema (Ed) y congestión (C); en neuropilo: C, Ed, HF y multifocal; en vasos cerebrales: C, en sistema ventricular: C, Edi, HF y HL, en pulmón fueron: patrón alveolar conservado y atelectasia; en bronquiolos: C, Ed y HF; en alvéolos: C, Ed y HF; en tabiques interalveolares: C, Ed y HF; en pleuras: C y HF. Al inyectar murieron inmediatamante (MI) 9 ratones que recibieron 25 MCL de CP y 12 con 50 mcl, 6 ratones MI con 25 ó 50 mcl de SA y ninguno con 25 ó 50 mcl de AD (controles). Lo anterior indica que el CP produce lesiones similares que SA, pero induce la MI en mayor proporción, además, el edema encefálico y pulmonar fue mayor con CP


Subject(s)
Mice , Animals , Craniocerebral Trauma/chemically induced , Fibrinogen/physiology , Mice/surgery , Neurologic Manifestations , Pulmonary Edema/chemically induced , Histological Techniques , Blood Transfusion, Autologous/methods
12.
Rev. ciênc. farm ; 14: 59-65, 1992. ilus
Article in Portuguese | LILACS | ID: lil-167907

ABSTRACT

Vários estudos mostram que o sangue humano lisa espontaneamente enquanto o sangue de outras espécies animais necessitam de altas concentraçöes de ativadores. Nossos resultados mostram que o plasma de rato näo tratado é capaz de lisar a fibrina murina, mas näo a fibrina humana ou bovina. Porém, quando tratamos estes animais com adrenalina, um conhecido ativador do sistema fibrinolítico, o plasma destes animais é capaz de digerir a fibrina humana e bovina. Estes resultados mostram que o uso da fibrina adequada para cada espécie de animal estudado pode evitar resultados discrepantes nos diferentes laboratórios que estudam atividade fibrinolítica


Subject(s)
Humans , Animals , Male , Rats , Plasminogen Activators/physiology , Cattle , Epinephrine/physiology , Fibrinogen/physiology , Fibrinolysis/physiology , Fibrin/physiology , Plasminogen/physiology , Rats, Inbred Strains
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