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Biomedical subjects

G Cella

Publications and source records attributed to G Cella.

At least 73 records · Page 4Linked to original sources
PubMed1986

Platelet factor 4 (PF4) and heparin released platelet factor 4 (HR-PF4) in diabetes mellitus. Effect of the duration of the disease.

Several investigators have reported an altered platelet function in diabetes mellitus as measured by elevated levels of platelet specific proteins platelet factor 4 (PF4) and B-thromboglobulin (BTG). We studied 20 insulin dependent (IDD), 20 non insulin dependent (NIDD) diabetic males without overt clinical symptoms of cardiovascular disorders and 30 normal controls. We evaluated PF4, BTG and heparin released platelet factor 4 (HR-PF4) as measured 2.5 minutes after a bolus injection of 5,000 I.U. of a commercial mucous heparin. The patients showed normal levels of both PF4 and BTG. Furthermore HR-PF4 failed to show statistically significant variation between patients and controls. However when the diabetics were divided on the basis of the duration of the disease, the IDD had an increased HR-PF4 mean level and the trend became statistically significant when diabetes existed more than 17 years (patients HR-PF4 149.1 ng/ml, range 17.3-194; controls HR-PF4 110.9 ng/ml range 50-160, less than p less than 0.05). NIDD failed to reveal the same pattern. Although the significance of HR-PF4 is unknown, insulin dependent diabetes mellitus after many years could cause a potentially dangerous, silent vascular damage with enhanced platelet vessel wall interaction as measured by an elevated HR-PF4.

Adolescent↗
PubMed1986

Effects on platelets and on the clotting system of four glycosaminoglycans extracted from hog mucosa and one extracted from aortic intima of the calf.

A commercial heparin preparation, a heparin fraction with a molecular weight of 12,000 Daltons, heparan sulfate, dermatan sulfate obtained from hog mucosa, and mesoglycan, an heparinoid obtained from calf aortic intima were investigated. Commercial mucous heparin had a stimulatory effect on platelet aggregation induced by ADP, while the others failed to do so. Dermatan sulfate had a dose dependent inhibition and commercial mucosal heparin, a dose dependent stimulation, on serotonin release induced by ADP. Both the commercial mucosal heparin and dermatan sulfate showed an inhibition and the other glycosaminoglycans (GAGs) a negligible effect on collagen induced platelet aggregation. The collagen induced serotonin release was clearly reduced by all GAGs; heparan sulfate had this activity only at the highest doses used. Commercial mucosal heparin produced the highest activity on clotting systems as measured by activated partial thromboplastin time, while mesoglycan had the strongest anti-factor Xa specific activity as measured by a clotting assay. Dermatan sulfate was the weakest on both assays. When we injected intravenously an equivalent amount (about 60 mg) of heparin fraction, heparan sulfate, dermatan sulfate and mesoglycan in three different volunteers with an interval of 20 days after each injection, we had an immediate platelet factor 4 (PF4) release only with heparin fraction, heparan sulfate and mesoglycan. Heparin fraction and mesoglycan, in spite of having a wide discrepancy in anticoagulant effect, caused almost the same PF4 release. GAGs which can neutralize PF4 and which can also have specific anti-factor Xa activity could represent a great advantage in thrombosis prophylaxis.

Animals↗
PubMed1985

Disappearance of human platelet factor 4 (PF4) in rabbits: does an immediate component exist?

Twelve male New Zealand rabbits were injected with 21 micrograms/kg of human platelet factor 4 antigen (PF4). The decay of the protein followed a monoexponential curve for the first 5 mins, with a half-life (t 1/2) of 1.94 mins and a calculated concentration at 0 time (CO) of 79.4 ng/ml. Five rabbits were pre-treated with heparin (2.500 I.U. i.v.) and 3 mins later were injected with the same amount of PF4. PF4 decay followed a monoexponential curve with a t 1/2 of 25.3 mins, and with CO of 380.8 ng/ml. This value is not greatly different from the one calculated assuming an immediate and uniform distribution in plasma (482.7 ng/ml for a plasma volume of 43.5 ml/kg). The 12 rabbits injected with PF4 were divided in 3 groups, in which heparin was given at 10', 30' or 60' after PF4, respectively. After heparin the peak levels of PF4 were 139.9 ng/ml, 65.3 ng/ml and 52.7 ng/ml, respectively. The following monoexponential PF4 decay had t 1/2 of 20.7, 25.6 and 26.0 mins, respectively. In a separate group of 4 animals, we studied heparin decay after an intravenous bolus of 2.500 I.U. Heparin decay could not be described by a monoexponential equation and was different from the decay of PF4 injected after heparin. On the basis of the present data we suggest the presence of an immediate component of PF4 decay, most likely due to uptake by the tissues. Heparin pretreatment may avoid this uptake process.

Animals↗
PubMed1985

Serial studies of platelet factor 4 and beta thromboglobulin during exercise in patients with coronary artery disease.

In vivo activation of platelets can be accurately measured by radioimmunoassays of platelet factor 4 (PF4) and beta thromboglobulin (beta TG). Studies that attempt to correlate increases in PF4 and beta TG levels with exercise-induced myocardial ischemia have yielded conflicting results. To further examine the natural history of release of PF4 and beta TG we used a method of serial samplings of these proteins during and after exercise in nine normal subjects and 24 patients with coronary artery disease (CAD). Mean values for PF4 and beta TG at rest, during each stage, and immediately after treadmill exercise were the same for normal subjects and for patients with positive and negative responses to exercise-tolerance tests (ETTs). However, nonparametric analysis and regression equations disclosed differences in trends of PF4 level during exercise; PF4 levels increased in normal subjects during exercise, while patients with positive ETTs had no change in PF4 levels and patients with negative ETTs actually showed a decrease in PF4. This investigation confirmed that exercise-induced myocardial ischemia is not associated with platelet aggregation as manifested by the release of the platelet-specific proteins PF4 and beta TG. Statistical analysis suggested that prior reports of elevated levels of PF4 during exercise could have been caused by technical and methodologic difficulties that were associated with the collection and handling of the samples.

Adult↗
PubMed1985

Platelet factor 4 release induced by intravenous administration of heparin.

When heparin is injected intravenously, it can induce an immediate release of platelet factor 4 PF4), probably from the non-platelet pool of endothelial cells. We evaluated this release in a group of normal subjects and patients with cardiovascular disorders or thrombocytosis after an intravenous injection of a bolus of 5,000 I.U. of a commercial mucous heparin. The mean level in normals was 102 +/- 32 (range 50-160) ng/ml and no correlation was found before and after heparin injection between PF4 and heparin level, body weight or platelet count. Only three cardiovascular patients had an elevated level of PF4 released by heparin (HR-PF4) that could be the expression of an increased platelet turnover, whereas all the patients with thrombocytosis had an extremely elevated level of HR-PF4. These patients have much more PF4 available for the binding sites of endothelial cells since only a small percentage of potential binding sites are normally occupied "in vivo". Although no correlation could be found between platelet count and HR-PF4 in subjects with a normal platelet count or in patients with thrombocytosis there was a positive correlation, however, when all the cases were considered together. The other proteins with heparin affinity, B-thromboglobulin, antithrombin III and fibronectin were not influenced by a bolus of heparin and did not correlate in normals as well in patients with HR-PF4.

Adolescent↗
PubMed1984

Clearance and in vivo release by heparin of human platelet factor 4 (PF4) in the rabbit.

13 male New Zealand rabbits were injected with two different doses (25 micrograms/Kg and 100 micrograms/Kg) of human platelet factor 4 antigen (PF4). The disappearance of the protein was extremely fast with an half-life for the fast component of 1.07 +/- 0.16 and 1.76 +/- 0.11 min respectively. The half-life for the slow component, detectable only with the highest dosage, was 18.8 min. The administration of 2500 I.U. of heparin 30 min after PF4 administration induced a partial release of the injected protein and its clearance from plasma was slow, with half-life of 23.3 +/- 5.9 min and 30.9 +/- 2.19 min respectively.

Animals↗
PubMed1984

Effects of low-molecular-weight heparin on platelets as compared with commercial heparin.

Five subjects were injected with 5,000 IU of commercial heparin and low-molecular-weight heparin at an interval of 20 days after each injection. Both heparins produced the same platelet factor 4 release immediately after administration (commercial heparin 114.6 +/- 21.6 ng/ml, low-molecular-weight heparin 113.1 +/- 22.1 ng/ml). However, commercial heparin induced a more evident potentiating effect on ADP-induced platelet aggregation and was still present 60 min after injection. Low-molecular-weight heparin had a higher anti-Xa-specific activity than that determined by activated partial thromboplastin time. The opposite was true for the commercial preparation.

Adenosine Diphosphate↗
PubMed1983

Platelet factor 4 (PF4) and heparin-released platelet factor 4 (HR-PF4) in patients with cardiovascular disorders.

The recent introduction of the determinations of platelet factor 4 (PF4) and beta-thromboglobulin (beta TG) by radioimmunoassay provided a new tool to obtain knowledge of in vivo platelet activation. We evaluated the plasma level of PF4 and beta TG in 14 normal subjects (mean PF4 7.7 ng/ml; beta TG 28.8 ng/ml), in 29 patients with chronic stable cardiovascular disorders (mean PF4 9.8 ng/ml; beta TG 32.6 ng/ml) and in 15 diabetics with vascular disease (mean PF4 14.5 ng/ml; beta TG 41.8 ng/ml). The great majority had normal values and no statistical differences were noted among the three groups (p greater than 0.05). Fifteen days of treatment with 150 mg daily of dipyridamole produced a significant reduction in the levels of both proteins (p less than 0.01), in contrast of the daily administration of 650 mg of aspirin, which failed to produce any significant change (p greater than 0.5). The patients and the normal subjects were also administered 3,000 USP units intravenously of porcine heparin. The values of the heparin released-platelet factor 4 (HR-PF4), evaluated 5 minutes after the injection, showed a good correlation between platelet concentration and HR-PF4 levels (z = 2.37, p less than 0.02) in the patients. The determination of standard residual following linear regression analysis of HR-PF4 indicated the presence of two distinct patient populations. One group, including the vast majority of patients, did not differ from the control (patients mean HR-PF4 111.1 ng/ml; controls: mean HF-PF4 136 ng/ml). The other group, with severe cardiovascular disease, but with normal levels of PF4 and beta TG in almost all patients and similar platelet concentrations, showed a significantly higher HR-PF4 (219 ng/ml). Neither aspirin nor dipyridamole had any effect on the level of HR-PF4. This HR-PF4 could represent a possible marker of the interaction of platelets with a seriously damaged atherosclerotic vessel wall.

Adult↗
PubMed1982

Thrombolytic therapy.

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Arterial Occlusive Diseases↗
PubMed1982

Plasminogen activators in rat neural tissues during development and in Wallerian degeneration.

The fibrinolytic activity of blood is caused by plasminogen activators (PA) converting plasminogen to plasmin, the active fibrinolytic protease. PA activity in rat neural tissues was studied by Todd's fibrin slide technique. Cryostat sections overlayed with a film of plasminogen and fibrin were incubated for 60-90 min. PA activity was related to the size of the zone of fibrinolysis surrounding the sections. No lysis occurred with fibrin alone. In rats perfused with saline prior to decapitation the size of the zone of lysis was approximately the same as in non-perfused animals. PA activity was compared in the following tissues: adult (2-3 month) cerebellum and 6-14-day postnatal cerebellum; normal sciatic nerve and transected sciatic nerve 1-9 weeks after operation (in these experiments the sciatic nerve was crushed on the left side, on the right side it was transected and the stumps were tightly ligated to prevent regeneration); normal optic nerves and optic nerves undergoing Wallerian degeneration 1-2 weeks after enucleation of the eye. As compared to normal cerebellum PA activity was increased in 6-14-day cerebellum. PA activity was also markedly increased in both crushed and ligated sciatic nerves 1-4 weeks after operation while no differences were observed between normal sciatic nerves and sciatic nerves 9 weeks after ligation. The zone of fibrinolysis surrounding normal optic nerves and the optic nerves of blinded rats was approximately the same. It is proposed that the fibrinolytic system may be relevant to the problem of CNS regeneration.

Animals↗