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ACTIVATION OF COAGULATION AND FIBRINOGEN LOSS AFTER USING AN EXTRACORPOREAL CIRCULATION.

Alterations of the coagulation potential of heparinized blood after using an extracorporeal circulation have been studied by means of a toluidine blue-calcium chloride reagent. This technique was originally used to detect the effect of activation by contact on the coagulation mechanism in heparinized blood. It has been shown that it also detects, in the presence of heparin, the clotpotentiating effect of blood cell contents liberated in vitro by mechanical trauma to blood. Variable destruction of platelets, red cells, and white cells occurred in heparinized sheep blood recirculated in a heart-lung machine in vitro. This was accompanied by increased clotting potential. Complete coagulation was prevented by heparin and fibrinogen levels remained unaltered. Similar enhancement of the coagulation potential and destruction of blood cells were detected in the blood of heparinized patients and sheep after perfusion for open-heart surgery. The coagulation changes were usually transient, and impaired coagulation associated with significant fibrinogen loss was detected in most samples taken after the neutralization of heparin. It is suggested that the coagulation changes are due to activation by contact of the coagulation mechanism during perfusion and to the clot-accelerating effect of blood cell contents. The results support the hypothesis that coagulation defects and fibrinogen loss after using an extracorporeal circulation are due, at least in part, to intravascular coagulation. This is thought to occur, especially during neutralization of heparin, while the coagulation mechanism is hyperactive.

Aminocaproates↗

THE THALASSAEMIA TRAIT IN AN ENGLISH FAMILY.

Nine cases of the thalassaemia trait are described in an English family. The problem of distinguishing these cases from those of the common hypochromic anaemias by simple laboratory tests is discussed.Iron-resistant hypochromic anaemia in people of British ancestry may be caused by the thalassaemia trait. Such cases have been reported by Bywaters (1938), Israëls, Suderman, and Hoogstraten (1955), Israëls and Turner (1955), and Havard, Lehmann, and Bodley Scott (1958). Dacie (1960) mentions similar cases and Callender, Mallet, and Lehmann (1961) recently described the finding of 25 cases in three English families.

Anemia, Sideroblastic↗

THALASSAEMIA IN SCOTS.

Five cases of thalassaemia minor and 11 symptomless trait carriers have been detected in four Scottish families, only one of which is known to have foreign ancestry. It is suggested that the condition is commoner than was once thought, and that the diagnosis should be considered in any patient with refractory hypochromic anaemia in which the red cells show increased osmotic resistance.

Anemia, Sideroblastic↗

METHOD USING ORTHO-TOLIDINE FOR THE QUANTITATIVE DETERMINATION OF HAEMOGLOBIN IN SERUM AND URINE.

Following a study of the spectrophotometric properties of ortho-tolidine and its oxidation products, with particular attention to variation brought about by change in the hydrogen ion concentration, a method for the quantitative estimation of haemoglobin in serum and urine in which ortho-tolidine is substituted for benzidine in a peroxidase system is described. The method is designed to measure haemoglobin value within the range 0-125 mg. per 100 ml. Evidence is presented showing that it gives results equal in accuracy and reproducibility to a benzidine method in common use and for reasons stated is a more satisfactory technique for estimating the haemoglobin content of urine.

Amines↗