RESUMO
The time has come when a traditional hematologist of a developing country needs to change his frame of mind from time consuming, error prone, not so precise manual methodologies to economical, safe and precise automated procedures. More important is his role as a guide and teacher for his juniors who are exposed to automated laboratories from the beginning of their residency. At this juncture, one needs to be thorough with the principles of instrumentation, different models available, their merits and demerits and how and where these fit with the requirements of the laboratory. The haematologists also must be aware that automation has its own problems, limitations, disadvantages and interfering elements. The article discusses the present state of art.
Assuntos
Contagem de Eritrócitos/métodos , Hematologia/economia , Hemoglobinas/análise , Contagem de Leucócitos/métodos , Contagem de Plaquetas/métodosRESUMO
Platelet aggregation with collagen, ADP and sodium arachidonate was significantly inhibited by 0.48 and 0.24 mg/ml of diltiazem but no significant effect occurred with 0.024 mg/ml of diltiazem. It is suggested that the antiplatelet property of diltiazem may be utilized in clinical setting and diltiazem may be tried synergistically with other antiplatelet drugs.
Assuntos
Diltiazem/farmacologia , Humanos , Agregação Plaquetária/efeitos dos fármacos , Inibidores da Agregação Plaquetária/farmacologiaRESUMO
Estimation of antithrombin III, alpha 2 macroglobulin and alpha 1 antitrypsin in patients with stable and unstable angina and acute myocardial infarction (15 cases each) were carried out. Twenty age, sex and weight matched healthy subjects were included as controls. Mean platelet factor 4(PF4) levels measured in 10 cases of each subgroup were significantly elevated in myocardial infarction (MI) (48.4 +/- 15.16 ng/ml) and III unstable angina patients (44.7 +/- 15.9 ng/ml) as compared to controls (25.42 +/- 12.47 ng/ml; P less than 0.01). Mean antithrombin III (AT III) levels were markedly reduced in all patients with MI (39.65 +/- 12.8% of normal pooled plasma) and unstable angina (37.9 +/- 16.6% of normal pooled plasma) and in 9 patients with stable angina. Alpha I antitrypsin and alpha 2 macroglobulin levels in these cases showed no significant difference compared to normals. Reduced AT III in coronary artery disease suggests a prethrombotic tendency in these patients. Raised PF4 levels in acute phase of the disease suggests heightened platelet activation.