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Biomedical subjects

A Girolami

Publications and source records attributed to A Girolami.

At least 523 records · Page 29Linked to original sources
PubMed1979

The effect of certain antiplatelet drugs on in vitro malonylaldehyde (MDA) production.

Several antiaggregating agents were tested with regard to their effect on platelet malonylaldehyde (MDA) production which seems to be a good marker of prostaglandin metabolism. Non-steroidal antiinflammatory compounds, namely acetylsalicylic acid (ASA), ditazole and sulfinpyrazone, showed a sure, statistically significant, inhibitory effect on MDA production while theophylline, adenosine and alpha-blocking agent nycergoline did not. Dipyridamole on the contrary, was demonstrated to have a mild but still statistically significant effect on the inhibition of platelet MDA production.

Blood Platelets↗
PubMed1979

Electroimmunoassay of factor IX in patients with liver damage and vitamin K unresponsive coagulation disorder.

Factor IX antigen and activity were assayed in a group of patients with liver disease and in a group of patients in coumarin therapy. In patients with liver disease there was a similar decrease in activity and antigen. On the other hand factor IX activity is decreased in coumarin treatment with factor IX antigen remaining normal. Factor IX electrophoretic mobility in liver disease is normal.

Blood Coagulation Disorders↗
PubMed1979

Short heparin thrombin clotting time, increased fibrinogen and platelet aggregates count in coronary disease: a probable hypercoagulable state.

Several indices of plasmatic and platelet coagulability (H.T.C.T., AT III, fibrinogen and Wu-Hoak test) were studied in 82 patients with acute and chronic coronary artery disease. The results were compared with those obtained in a control group. The most interesting result is the consistent shortening of H.T.C.T. as compared to the control group, particularly in patients with acute myocardial infarction. H.T.C.T. was always inversely correlated with the fibrinogen level. Those data suggest an important influence of fibrinogen levels on H.T.C.T., but this observation does not rule out the possibility that the heparin neutralizing activity (PF 4) will also influence the test. No positive correlation between H.T.C.T. and AT III could be observed. The elevated levels of AT III in acute myocardial infarction did not confirm the existence of a consumption of AT III due to chronic intravascular coagulation in these patients. The Wu-Hoak test increased only in patients with acute coronary disease, never in the other groups. In conclusion, H.T.C.T. may be assumed to be a valid test for indicating the existence of a possible hypercoagulability state.

Adult↗
PubMed1979

Platelet fibrinogen: subcellular localization by means of immunofluorescent studies in normals and in congenital afibrinogenemia.

We have studied the site of fibrinogen localization in normal platelets and in the platelets of a patient with congenital afibrinogenemia (CA). The methods employed were: direct immunofluorescence technique (DIT) and indirect immunofluorescence technique (IIT). By means of the DIT normal platelets were shown to have a clear peripheral staining. Such staining disappeared after treatment with proteolytic enzymes and after specific blocking experiments. Such peripheral staining of platelets was absent in congenital afibrinogenemia even after fibrinogen infusion. By means of the IIT platelets were shown to have a considerable amount of fibrinogen. Such protein was demonstrated to represent an important part of platelet surface, since intact platelets were able to absorb completely a specific antifibrinogen antiserum.

Afibrinogenemia↗
PubMed1978

Rigidity of red cells in essential hypertension.

Both viscosity of blood and the rigidity of red cells are of consequence in the mechanism of hypertension. While the details of this mechanism are still elusive, the evidence presented might open the way for a wider inquiry into the role of blood rheology in hypertension.

Blood Pressure↗
PubMed1978

[Rheologic, coagulative parameters and study of fibrinolysis in patients with coronary heart disease before and after aorto-coronary by-pass (author's transl)].

A study has been made of 31 patients with coronary heart disease where diagnosis had been clearly ascertained both from a clinical and strumental point of view. All patients had undergone aorto-coronary by-pass surgery. The controls of the parameters under observation (whole-blood and plasmatic viscosity, hematocrit, fibrinogen, euglobulin lysis, T protothrombin, T of partial thromboplastin, thromboelastogram antithrombin III, plasminogen, alfa2-macroglobulin and fractions C'3c, C'3c, C'4 of the complement) were carried out as follows: basic sample taken, I control (8th-10th day), II control (15th-20th day), III control (45th-50th day), IV control (85th-90th day) after surgical operation. A global examination of our results showed significant changes in the rheologic coagulative and fibrinolytic parameters after an aorto-coronary surgical operation. The slight tendency toward hypercoagulability met with in the basic blood sample (slight increase of whole-blood viscosity, hyperfibrinogenemy, inhibition of fibrinolytic activity) does not change significantly after surgical operation. This seems to indicate that the coronary by-pass does not in any way alter the evolution of arteriosclerosis.

Adult↗
PubMed1978

Coumarin-induced abnormal factor IX: an immunological study in humans.

An excess of factor IX antigen or protein with respect to factor IX activity is present in coumarin treated patients. The average factor IX antigen value found in a group of 16 patients was 96.2 (S.D. = 24.46) whereas the average clotting activity was 19 (S.D. = 4.54) (p less than 0.001). In the electroimmunoassay system a normal peak or precipitate were seen in every instance. In haemophilia B--no peak or precipitate were seen. The coumarin induced abnormal factor IX shows a more anodic migration in the bidimensional immunoelectrophoresis system as compared with the normal counterpart. On the contrary, the factor IX protein present in haemophilia BM or in haemophilie B+ migrates as normal factor IX.

Antigens↗
PubMed1978

Studies on factor XIII antigen in congenital factor XIII deficiency. A tentative classification of the disease in two groups.

Immunological and immunofluorescent studies carried out on plasma and platelets of three cases of congenital factor XIII deficiency are reported. Two of these patients were originally thought to have normal factor XIII subunit S and no subunit A. However, repeated assays carried out using different lots of antiserum showed that in reality the patients lacked both subunit S and subunit A. The false positive finding was due to the presence of a anti-factor VIII contaminant in the antiserum originally used. The third patient had a normal subunit S and no subunit A. No factor XIII antigen was found by the indirect immunofluorescent technique in normal, factor XIII deficiency and von Willebrand's disease platelets. On the contrary, by using the non-monospecific antiserum a fluorescent pattern similar to that observed by using an anti-factor VIII antiserum, had been noted. On the basis of the data presented in this paper a tentative classification of factor XIII deficiency in two groups is proposed: Type I is characterized by the lack of both factor XIII subunit S and A. Type II is characterized by a normal subunit S and no subunit A. The need for a re-evaluation of published case of factor XIII deficiency by means of monospecific antisera is indicated.

Antigens↗
PubMed1978

No change of whole blood of plasma viscosity in cardiac patients after subcutaneous calcium heparin.

Whole blood viscosity, plasma viscosity and haematocrit were studied in a group of cardiac patients before and during subcutaneous heparin treatment. No significant change was noted in any of the parameters investigated. Relative viscosity (whole blood viscosity/plasma viscosity ratio) was also unaffected. These data indicate that heparin has no effect on the rheology of blood in vitro.

Adult↗
PubMed1978

Evidence against the presence of "inhibitors" in coumarin treated patients.

Coumarin drugs or vitamin K absence cause a decrease of factor II, VII, IX and X activities and the appearance of pre-factors into the circulation. Such pre-factors have been postulated to inhibit thrombin conversion. The current of research on the alleged activity of such "inhibitors" is taken into consideration. Thrombotest discrepancy, mixing experiments etc.) speak against the inhibitor theory. So far the only sure demonstration of the presence of coumarin induced pre-factors has been obtained by immunological means. However, this does not say anything about their biological activity. These pre-factors could well be "inert" as far as clotting is concerned. Until new, unequivocal data on the subject will be available, any method or technique claiming to be able to detect or monitor the "inhibitory" effect should be accepted with extreme caution. Too many unjustified views have been put forward in recent years.

Coumarins↗
PubMed1978

Immunofluorescent evaluation of platelet alpha-1-antitrypsin and alpha-2-macroglobulin.

Rabbit raised anti-alpha-1-antitrypsin or anti alpha-2-macroglobulin antisera at dilution of less than 1:80 yielded non-specific staining on human platelets by indirect immunofluorescent technique. A similar pattern was in fact obtained by using normal rabbit sera at the same dilution and was due to the presence of smooth muscle autoantibodies. This indicates that human platelets do not contain significant quantities of these antigens. In agreement with the above, only microamounts of alpha-1-antitrypsin and alpha-2-macroglobulin were found to be present in human platelets by means of the electroimmunoassay.

Blood Platelets↗
PubMed1978

Decreased thrombotic mortality and morbidity after valvular cardiac surgery as a consequence of adequate coumarin anticoagulation. A retrospective study in 516 patients.

Two almost identical groups of 258 patients each who underwent surgery for the substitution of one or more than one cardiac valve were taken into consideration. After surgery all patients, with the exception of those who received a porcine allograph, were given coumarin drugs for 1 year for thrombosis prophylaxis. In the first group of patients operated in 1972 and 1973 the laboratory follow-up and the therapeutic range were neither constant nor uniform. In the case of the second group, which included patients operated in 1974 and 1975, adequate laboratory follow-up and constantly adequate therapeutic ranges were always kept. This retrospective study has shown a statistically significant decrease in mortality due to thromboembolism and to unknown causes in the second group of patients (x2 = 8,313, "p" less than 0,0025). A decrease of the non-lethal embolic complications was also noted in the second group of patients (x2 = 6,813, "p" less than 0,0025). On the other hand, bleeding complications were greater in the second group of patients (x2 = 3,485, "p" less than 0,05) and this was interpreted as secondary to the higher anticoagulation administered to the latter patients. The results indicate that an adequate coumarin anticoagulation seems able to decrease the incidence of lethal or non-lethal thromboembolic complications after cardiac valve replacement significantly.

Adolescent↗
PubMed1977

Apparent "inhibition" as tested by means of the dilution curve system in patients with clotting defect due to liver damage.

At equivalent Thrombotest basal values on undiluted non-contacted plasma, there is no difference between coumarin plasma and liver damage plasma in the dilution curve system. A hemophilia BM plasma with longer basal clotting times yielded a much flatter curve and a very large "inhibitory" effect (greater than 6 Units). A coumarin plasma with the same basal Thrombotest clotting times as Hemophilia BM plasma, namely 100 seconds, yielded a much steeper curve and a very low inhibition (0.7 Units). These findings are against the presence of inhibitors in coumarin or liver damage plasmas.

Blood Coagulation Disorders↗