PubMed Health⌕ Search

Biomedical subjects

M Colucci

Publications and source records attributed to M Colucci.

At least 91 records · Page 5Linked to original sources
PubMed1981

Platelet aggregation and stimulation of leucocyte procoagulant activity by rickettsial lipopolysaccharides in rabbits and in man.

The effects in vitro of 4 purified lipopolysaccharide (LPS) preparations from Rickettsiae on platelets and leucocytes were studied in rabbits and in man. All LPS induced aggregation in rabbit platelet-rich plasma but to differing degrees. This activity was abolished by inactivation of complement. None of the preparations induced aggregation of human platelets. Both rabbit and human leucocytes, when incubated with each of the rickettsial LPS preparations, generated a potent procoagulant activity (tissue factor). These findings add further support to the concept that rickettsial LPS behave as typical LPS from gram-negative bacteria and may be relevant to the understanding of the mechanism(s) responsible for triggering intravascular coagulation in rickettsial diseases.

Animals↗
PubMed1981

Leucocyte-dependent platelet activation: an alternative pathway for initiation of blood clotting in inflammation.

Fibrin deposition is a prominent feature of several inflammatory diseases but the extract mechanism(s) leading to fibrinogen-fibrin conversion has not been completely clarified. We describe here a new cellular pathway for initiation of blood clotting resulting from a leucocyte-platelet interaction. Human washed platelet suspensions, free of leucocytes, isolated from whole blood or leucocyte-enriched platelet-rich plasma (PRP) after four hours' incubation with bacterial endotoxin, had strong procoagulant activity (40-100-fold that of control platelets). When platelets were challenged with endotoxin in the absence of white blood cells (i.e. in PRP) the subsequently washed platelets were devoid of procoagulant activity indicating that leucocytes are essential mediators in the development of platelet coagulant activity induced by endotoxin. This property is mostly confined to the mononuclear fraction. 'Stimulated' platelets have the peculiarity that they trigger blood coagulation by activating factor X independently of both the intrinsic and extrinsic pathways. These findings add a new function to circulating mononuclear cells and provide experimental evidence for an unrecognized cellular pathway of fibrin formation in inflammatory diseases.

Blood Coagulation↗
PubMed1981

Role of leucocyte procoagulant activity in endotoxin-induced DIC: evidence from comparative studies in rats and rabbits.

We have investigated the ability of rat and rabbit leucocytes to generate coagulant activity (PCA) in response to endotoxin in vitro and in vivo. On prolonged incubation with endotoxin (10 microgram/ml f.c.) isolated rabbit leukocytes developed strong PCA as measured by clotting and amidolytic assay. In contrast, rat leucocyte failed to produce any PCA even in the presence of huge amounts of endotoxin (200 microgram/ml f.c.) When rabbits were given two spaced endotoxin injections (25 microgram/kg b.w., 24 h apart) blood leucocytes harvested 30--60 min after the second injection consistently showed marked PCA. Again, unlike injections (up 2 mg/kg b.w.) were completely devoid of PCA. These findings support the view that leucocytes are involved in endotoxin-induced disseminated intravascular coagulation in rabbits. On the other hand the poor response of rat leucocytes to endotoxin might help explain the resistance of rats to DIC and Sanarelli-Shwartzman reaction.

Animals↗
PubMed1981

Reduced generation of procoagulant activity by endotoxin-stimulated mononuclear cells from patients with chronic myeloid leukaemia.

The capacity of blood mononuclear cells to produce procoagulant activity upon stimulation with bacterial endotoxin in vitro was studied in 21 untreated patients with chronic myeloid leukaemia (CML). Procoagulant activity developed by patients' cells after prolonged incubation with endotoxin was significantly lower than that produced by cells from a matched control group (P less than 0.001). Reduced activity was seen in all patients when each of them was compared to a matched control studied simultaneously. It was below 50% of the control in 19 patients, and in eight of these it was less than 10%. These findings suggest that qualitative abnormalities in mononuclear cell function may exist in CML and might explain why these patients are less prone to thrombotic complications than those with other myeloproliferative diseases.

Adult↗
PubMed1981

Reduced platelet factor X-activating activity: a possible contribution to bleeding complications in polycythaemia vera and essential thrombocythaemia.

A recently described platelet coagulant activity, factor X-activating activity (FXAA), was studied in 33 patients with polycythaemia vera and in 5 with essential thrombocythaemia, in order to gain information about possible mechanisms responsible for the haemostatic disorders observed in myeloproliferative diseases. Other parameters of platelet function including bleeding time, spontaneous and ADP-, epinephrine- or collagen-induced platelet aggregation, serotonin content and malondialdehyde (MDA) production in response to thrombin, were investigated simultaneously. Compared to the range obtained from 27 control subjects (60-150%), FXAA was low in all 9 patients with bleeding complications (range: 5-39%), in 1 out of 7 patients with thrombotic manifestations (range: 38-200%) and in 9 out of 22 patients without symptoms (range: 38-500%). Only the bleeding group differed significantly from each of the others. Moreover, of all patients with reduced FXAA, those with bleeding could be clearly distinguished from those without such symptoms on the basis of the degree of the defect. Increased FXAA (above 150%) was found in 2 out of 7 thrombotic patients and in 2 out of 22 asymptomatics. MDA production was significantly lower in the haemorrhagic group and enhanced in the thrombotic one as compared to control subjects or asymptomatic patients. However, a large area of overlap was observed between the four groups. None of the other platelet function parameters studied (bleeding time, platelet aggregation, platelet serotonin content) correlated with the clinical type of haemostatic complication. Our results suggest a significant association between reduced FXAA and bleeding tendency. These findings may be of relevance in understanding the pathogenesis of abnormal bleeding in patients with polycythaemia vera and essential thrombocythaemia.

Adolescent↗
PubMed1981

Rat blood leucocytes, unlike rabbit leucocytes, do not generate procoagulant activity on exposure to endotoxin.

We have investigated the ability of rat and rabbit leucocytes to generate procoagulant activity (PCA) in response to endotoxin in vitro and in vivo. On prolonged incubation with endotoxin (10 micrograms/ml f.c.) isolated rabbit leucocytes developed strong PCA as measured by clotting and amidolytic assay. In contrast, rat leucocytes failed to produce any PCA even in the presence of huge amounts of endotoxin (200 micrograms/mol f.c.). When rabbits were given two spaced endotoxin injections (25 micrograms/kg consistently showed marked PCA. Again, unlike in the rabbit, rat leucocytes obtained after 2 endotoxin injections (up to 2 mg/kg body wt) showed absolutely no PCA. These findings support the view that leucocytes are involved in endotoxin-induced disseminated intravascular coagulation (DIC) in rabbits. On the other hand the poor response of rat leucocytes to endotoxin might help explain the resistance of rats to DIC and Sanarelli-Shwartzman reaction.

Animals↗
PubMed1981

Procoagulant activity of sarcoma sublines with different metastatic potential.

It has been suggested that cancer cell procoagulant activity influences metastasis formation by promoting fibrin deposition around tumors. We have investigated the procoagulant activity of various tumor cell sublines with different metastatic capacity derived from metastatic nodules of a murine fibrosarcoma. All the cells tested possessed a marked thromboplastin-like activity; they were, however, heterogeneous as regards the degree of procoagulant activity; the two cell lines with virtually no metastatic capacity showed 6--8 times higher procoagulant activity than the cells from the parent line; in contrast, the procoagulant activity of the two sublines with higher metastatic capacity did not differ significantly from that of the parent line. These findings support the hypothesis that fibrin is part of a defence reaction against cancer cell invasiveness.

Animals↗
PubMed1979

Early increase of a new platelet coagulant activity in rats fed a thrombogenic diet.

A recently described platelet coagulant activity (factor X activating activity), whose pathophysiological significance is as yet unknown, was studied in rats fed a fat-rich (thrombogenic) diet for 1, 2 and 7 weeks and compared to rats fed normal laboratory chow. Whatever the duration of the special feeding period, a highly significant shortening of the clotting time, used for measuring this activity, was observed. When the platelet coagulant activity of individual "fat-fed"rats was quantitated by reference to that of individual control animals, we found a mean increase of 350% (n = 9) after one week and 267% (n = 3) after two weeks of dietary treatment. Partial thromboplastin time, thrombin time and soluble fibrin monomer complexes did not differ in control and treated animals. It seems that platelet coagulant activity, as measured in our test system, is one of the first laboratory parameters to be modified by fat-rich diets. These findings may be relevant to an understanding of the role of platelet coagulant activities other than platelet factor 3 in thrombotic phenomena.

Animals↗
PubMed1979

Evidence that cells from experimental tumours can activate coagulation factor X.

The procoagulant activity of cells from some experimental tumours isolated in culture or in single-cell suspensions from ascitic fluid was investigated. Cells from Lewis lung carcinoma (primary and metastasis), Ehrlich carcinoma ascites and JW sarcoma ascites were able to shorten markedly the recalcification time of normal, Factor VIII- and Factor VII-deficient but not of Factor X-deficient human plasma. The same cells generated thrombin when mixed with a source of prothrombin and Factor X, absorbed bovine serum (as a source of Factor V), phospholipid and calcium chloride. Thrombin formation was not influenced by the presence of Factor VII. Cells from Sarcoma 180 ascites were completely inactive in both test systems. It is concluded that cells from some experimental tumours have the capacity to activate Coagulation Factor X directly. These findings suggest the existence of an alternative "cellular" pathway in the initiation of blood clotting distinct from both the intrinsic and extrinsic mechanisms.

Animals↗
PubMed1975

[Behavior of lipoprotein X (LP-X) in viral hepatitis].

The AA. have studied the behaviour of LP-X in fifty cases of viral hepatitis printing out a positivity in 32% of the examined cases, with a positivity of the Au-antigen in the 34% of cases. They have observed a more remarkable inclination to the cholostasis in children (40% of the cases of positivity of LP-X), concluding for a scarce specificity of such a "marker" of cholostasis.

Apoproteins↗