RESUMO
1. Four structural systems are involved in the process of platelet activation that leads to aggregation: 1) the membrane system, i.e., the cytoplasmic membrane, the dense tubular structure and the open canalicular structure; 2) alpha and dense granules; 3) the peripheral microtubular coils; 4) the microfibrillar meshwork of actin-myosin bundles. 2. We added four compounds which modify cell ultrastructure to normal platelet-rich plasma to analyze the behavior of the structural systems of platelet activation: vinblastine (100 micrograms/ml) and cimetidine (100 micrograms/ml) that act on the membrane system, ticlopidine (200 micrograms/ml) and colchicine (100 micrograms/ml) that affect primarily the microtubular structure, cytochalasin B (30 micrograms/ml) and phorbol myristate acetate (100 ng/ml) that act upon the granular system, and cytochalasin D (30 micrograms/ml) and concanavalin A (50 micrograms/ml) that influence the microfibrillar structure. Platelet aggregation was stimulated by epinephrine or thrombin. 3. Cimetidine and ticlopidine prevented aggregation. However, neither substance affected the microtubular structure. Colchicine and cytochalasin B only partially impaired aggregation, because pieces of microtubules remained in the presence of these substances. The other substances did not present anti-aggregant activity and did not preserve the microtubules. 4. We infer that the disappearance of the microtubules is necessary to produce aggregation. When they remain intact no aggregation is produced, even though the other structural systems are activated.
Assuntos
Microtúbulos/fisiologia , Agregação Plaquetária/fisiologia , Plaquetas/efeitos dos fármacos , Plaquetas/fisiologia , Plaquetas/ultraestrutura , Cimetidina/farmacologia , Colchicina/farmacologia , Concanavalina A/farmacologia , Citocalasina B/farmacologia , Citocalasina D/farmacologia , Humanos , Agregação Plaquetária/efeitos dos fármacos , Acetato de Tetradecanoilforbol/farmacologia , Ticlopidina/farmacologia , Vimblastina/farmacologiaRESUMO
1. Four structural systems are involved in the process of platelet activation that leads to aggregation: 1) the membrane system, i.e., the cytoplasmic membrane, the dense tubular structure and the open canalicular structure; 2) alpha and dense granules; 3) the peripheral microtubular coils; 4) the microfibrillar meshwork of actin-myosin bundles. 2. We added four compounds which modify cell ultrastructure to normal platelet-rich plasma to analyze the behavior of the structural systems of platelet activation: vinblastine (100 micrograms/ml) and cimetidine (100 micrograms/ml) that act on the membrane system, ticlopidine (200 micrograms/ml) and colchicine (100 micrograms/ml) that affect primarily the microtubular structure, cytochalasin B (30 micrograms/ml) and phorbol myristate acetate (100 ng/ml) that act upon the granular system, and cytochalasin D (30 micrograms/ml) and concanavalin A (50 micrograms/ml) that influence the microfibrillar structure. Platelet aggregation was stimulated by epinephrine or thrombin. 3. Cimetidine and ticlopidine prevented aggregation. However, neither substance affected the microtubular structure. Colchicine and cytochalasin B only partially impaired aggregation, because pieces of microtubules remained in the presence of these substances. The other substances did not present anti-aggregant activity and did not preserve the microtubules. 4. We infer that the disappearance of the microtubules is necessary to produce aggregation. When they remain intact no aggregation is produced, even though the other structural systems are activated.
Assuntos
Humanos , Agregação Plaquetária/fisiologia , Microtúbulos/fisiologia , Agregação Plaquetária/efeitos dos fármacos , Plaquetas , Cimetidina , Colchicina , Concanavalina A , Citocalasina B , Citocalasina D , Acetato de Tetradecanoilforbol , Ticlopidina , VimblastinaRESUMO
A new type of primary thrombocytopathy is described. Three main alterations were found: (1) a defect of the aggregation reaction with ADP, epinephrine and collagen and a normal response to ristocetin and arachidonic acid; (2) a moderate deficiency of platelet procoagulant activity, and (3) a combined hypertrophy of the two membrane systems of the platelet--the open canalicular and the dense tubular. The latter defect is shown as an abnormal membrane complex situated on one of the platelet poles. This thrombocytopathy is discussed as a new variety of primary platelet disorder.
Assuntos
Transtornos Plaquetários/etiologia , Plaquetas/ultraestrutura , Adulto , Transtornos Plaquetários/sangue , Transtornos Plaquetários/diagnóstico , Membrana Celular/ultraestrutura , Diagnóstico Diferencial , Feminino , Humanos , Microscopia Eletrônica , Adesividade Plaquetária , Agregação Plaquetária/efeitos dos fármacos , Contagem de Plaquetas , Propriedades de SuperfícieRESUMO
In this paper we presetn our findings in relation to the ultrastructural changes that are produced in the platelets during the hemostatic activation process. When the platelets are in the resting stage they have a discoid form with are a peripheral microtubular structure that encloses numerous granules, showing an open canalicular system spreading throughout the cytoplasm. Once they are activated, sequential morphological changes take place. First of all, the microtubular structure desintegrates and is replaced by a membranous pseudotubular membranous complex which fuses itself to the granules enhancing the open canalicular system which grows until it takes a sacular-canalicular appearance. Degranulation takes place at the same time. The from of the platelets becomes spherical and irregular. Later on, a microfilament organization appears, specially in the peripheral zozne projecting into the pseudopodical prolongations which are formed in the surface, giving the platelets a very irregular filopoidal form. Finally they loose all their structure becoming hyaline and vacuolated. We believe that the pseudopodical stage is the last step of the activation, prvious to the final vacuolization and destruction
Assuntos
Humanos , Plaquetas/ultraestrutura , Membrana Celular/ultraestrutura , Citoesqueleto/ultraestrutura , Agregação PlaquetáriaRESUMO
In this paper we presetn our findings in relation to the ultrastructural changes that are produced in the platelets during the hemostatic activation process. When the platelets are in the resting stage they have a discoid form with are a peripheral microtubular structure that encloses numerous granules, showing an open canalicular system spreading throughout the cytoplasm. Once they are activated, sequential morphological changes take place. First of all, the microtubular structure desintegrates and is replaced by a membranous pseudotubular membranous complex which fuses itself to the granules enhancing the open canalicular system which grows until it takes a sacular-canalicular appearance. Degranulation takes place at the same time. The from of the platelets becomes spherical and irregular. Later on, a microfilament organization appears, specially in the peripheral zozne projecting into the pseudopodical prolongations which are formed in the surface, giving the platelets a very irregular filopoidal form. Finally they loose all their structure becoming hyaline and vacuolated. We believe that the pseudopodical stage is the last step of the activation, prvious to the final vacuolization and destruction (AU)
Assuntos
Humanos , Agregação Plaquetária , Plaquetas/ultraestrutura , Citoesqueleto/ultraestrutura , Membrana Celular/ultraestruturaRESUMO
1. We present the results of a study of the prevalence of anemia and its causes in the population of Ecuador. The following parameters were used: blood cytology, reticulocyte count, serum iron, iron binding capacity, ferritin, folic acid and vitamin B 12 concentration. 2. The study was carried out on 4 groups: 426 individuals of both sexes and all ages from the rural population of the lowlands, with a warm and humid climate; 226 individuals from the highlands, with a cold and dry climate; 1000 individuals of the urban working group from the lowlands; and 1000 individuals of the urban working group from the highlands. All subjects were chosen randomly. 3. The prevalence of anemia was 31.4% in the rural group from the lowlands, 27.9% in the rural group from the highlands, 5.5% in the urban group from the lowlands, and 2.7% in the urban group from the highlands, with an overall estimated prevalence of 20.6% for the population of Ecuador as a whole. Iron deficiency was the most frequent cause of anemia (91.3%; 18.7% of the total population), followed by bone marrow failure (6%; 1.2% of the total population), hemolysis (2.2%; 0.5% of the total population), and finally megaloblastic anemia (0.5%; 0.1% of the total population). 4. Since iron deficiency with and without anemia is very frequent, we believe it is justified to establish mechanisms for food iron enrichment for liable groups such as children and pregnant women from marginal areas.
Assuntos
Anemia/epidemiologia , Adolescente , Adulto , Idoso , Altitude , Criança , Pré-Escolar , Estudos Transversais , Equador , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Gravidez , Distribuição Aleatória , População Rural , População UrbanaRESUMO
1. We present the results of a study of the prevalence of anemia and its causes in the population of Ecuador. The following parameters were used: blood cytology, reticulocyte count, serum iron, iron biding capacity, ferritin, folic acid and vitamin B 12 concentration. 2. The study was carriede out on 4 groups: 426 individuals of both sexes and all ages from the rural population of the lowlands, with a warm and humild climate; 226 individuals from the highlands, with a cold and dry climate; 1000 individuals of the urban working group from the lowlands; and 1000 individuals of the urban working group from the highlands. All subjects were chosen randomly. 3. The prevalence of anemia was 31.4% in the rural group from the lowlands, 27.9% in the rural group from the highlands, 5.5% in the urban group from the lowlands, and 2.7% in the urban group from the highlands, with an overall estimated prevalence of 20.6% for the population of Ecuador as a whole. Iron deficiency was the most frequent cause of anemia (91.3%); 18.7% of the total population), followed by bone marrow failure (6%; 1.2% of the total population), hemolysis (2.2%); 0.5% of the total population), and finally megaloblastic anemia (0.5%; 1.1% of the population). 4. Since iron deficiency with and without anemia is very frequent, we believe it is justified to establish mechanisms for food iron enrichment for liable groups such as children and pregnant women from marginal areas