Search PubMed⌕ Search

Biomedical subjects

D Varon

Publications and source records attributed to D Varon.

At least 109 records · Page 6Linked to original sources
PubMed1988

Gray platelet syndrome in the elderly.

A 68-year-old male who suffered from thrombocytopenia and mild splenomegaly for 18 years was found to present agranular gray platelets on peripheral blood smear. Bone biopsy revealed a mild, diffuse, reticular fibrosis with no collagen, and electron microscopy of the platelets showed an absence of almost all the alpha-granules. Platelet thrombospondin and fibronectin analysed by SDS-polyacrylamide gel electrophoresis and Rocket immunoelectrophoresis were absent. Follow-up of 4 years showed the same parameters with no evidence of active myeloproliferative or dysmyelopoietic disorders. Hemorrhagic diathesis was limited to ecchymoses and postprostatectomy bleeding, necessitating platelet transfusion. This led us to conclude that our patient probably had a constitutional primary alpha-granule deficiency or gray platelet syndrome. This extremely rare defect has been described in less than 10 patients, all of them very young. Our observation shows that these patients may have a long, uneventful survival.

Aged↗
PubMed1988

A new group of defibrillatory drugs in the classification of antiarrhythmic agents.

Ventricular antiarrhythmic therapy is aimed traditionally at preventing arrhythmias and ventricular fibrillation. Recently, a new approach has been introduced, where drug therapy facilitates the ability of the heart for spontaneous defibrillation. The chemical features and the electrophysiologic properties are discussed below. The introduction of this new group of defibrillating antiarrhythmic drugs implies the extension of the common classification of antiarrhythmic drugs.

Animals↗
PubMed1988

Magnesium fluxes in ventricular fibrillation and defibrillation in untreated and dibenzepine HC1 pretreated cats.

Serum magnesium concentration (S-Mg) was estimated in 12 anesthetized cats before and after central thoracotomy, during an electrically induced ventricular fibrillation (VF) and after defibrillation (DEF), and again, in the same experimental animals, after the administration of 3 mg/kg of dibenzepine HC1--a tricyclic antidepressant reported to facilitate spontaneous DEF--as well as during a subsequently induced VF and after the spontaneous DEF which followed. In the first part of the experiment, the surgery and the induction of VF caused no significant change of mean serum magnesium concentration (S-Mg) or serum calcium concentration (S-Ca), whereas the DEF was accompanied by Mg efflux (a significant increase of mean S-Mg from 0.824 mmol/l, SD 0.182, n = 12 to 0.991 mmol/l, SD 0.182, n = 12; P less than 0.05). In the second part of the experiment, following the administration of dibenzepine HCl there was Mg influx (a lowering of mean S-Mg to 0.891 mmol/l, SD 0.160, n = 12; P less than 0.05). During VF in the pretreated cats, S-Mg remained unchanged, while S-Ca decreased significantly (P less than 0.05), followed by a rebound Ca++ efflux (a systematic rise of S-Ca) as the animals defibrilated spontaneously. Concomitantly, there was Mg efflux (a systematic rise of S-MG), the mean S-Mg rising from 0.879 mmol/l, SD 0.143, n = 9 to 1.083 mmol/l, SD 0.257, n = 7, ie to virtually the same value as that obtained after electrically induced DEF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Reduction of infarct size following acute coronary occlusion by augmenting collateral blood supply induced by infusion of tricyclic antidepressants.

Previously, it has been shown that following occlusion of the left anterior descending artery (LAD) in cats, i.v. administration of tricyclic antidepressants (TCAD) significantly decreases the incidence of ventricular fibrillation (VF), which terminates spontaneously upon appearance. Furthermore, this treatment significantly decreases the size of the unperfused ventricular muscle (ischemic myocardium) from 44%-84% (mean 61%) to 17%-56% (mean 34%). This latter effect was demonstrated by using color demarcation of the perfused myocardium with the injection of a dye into the left atrium after 2 h of LAD occlusion in both control and treated cats. It was assumed that reduction of the unperfused area was due to an increase of collateral blood supply to the ischemic area. Although the beneficial effect of TCAD on the collateral blood supply has been clearly demonstrated in cats randomly assigned to two groups, the present study was designed to investigate the changes in the size of the ischemic area in the same animal by using two different dyes. Both dyes were injected into the left auricle after the LAD occlusion: The first was injected before the TCAD treatment and the second after the treatment. Two days after fixation in 4% formaldehyde, the hearts were sliced into three or four transverse sections. Examination of the sections indicated that there were three types of myocardial markings: (a) totally unperfused myocardium; (b) an area perfused by both colors; (c) an area perfused only by the second dye, indicating an increased collateral blood supply, the effectiveness of which was increased by the TCAD treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

The effect of tricyclic antidepressants on ventricular fibrillation and collateral blood supply following acute coronary occlusion.

In previous studies, we showed that dibenzepin HCl (D) and other tricyclic antidepressants (TCAD), given either before or during occlusion of the left anterior descending artery (LAD), decreased the incidence of ventricular fibrillation (VF) following occlusion and reperfusion. Moreover, once VF develops in treated animals, it changes into a transient type, reverting spontaneously to a sinus rhythm. In the treated cats, retrograde perfusion of the occluded coronary artery was observed, most likely as a result of increased collateral blood flow. This latter effect is the subject of the present study. The LAD was occluded at its origin in 43 cats, 28 of which were treated either with D or with 5-iminodibenzyl HCl; the remaining 15 were untreated controls. Two hours after the occlusion, methylene blue was injected into the left atrium to determine color demarcation between the perfused and unperfused myocardium, and the cat was then killed. After fixing for 2 or 3 days in 4% formaldehyde, the hearts were sectioned transversely. The results showed that in the 15 control cats, the blood-supplied (blue) area ranged between 16% and 56% of the left ventricular muscle (mean 39%), while in the 28 treated cats the blue area was between 44% and 83% (mean 66%). These results clearly indicate the beneficial effect of TCAD on the blood supply of the occluded area and can explain, in part, the ability of these drugs to prevent VF even if infused after the coronary occlusion, and their protective effect against VF following reperfusion. No other antiarrhythmic drugs have been shown to possess this latter action.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Hypereosinophilic syndrome associated with polycythemia vera.

A 60-year-old woman presented with relapse of polycythemia vera associated with hypereosinophilic syndrome (HES) with abnormal immunologic measures, including increased serum IgE and IgG levels, high levels of circulating immune complexes, rheumatoid factor, and antinuclear antibodies. Treatment with hydroxyurea was followed by a dramatic response of both the polycythemia vera and the HES, with return to normal of the abnormal immunologic measures. This case report documents that evidence of immunologic and myeloproliferative causes of HES may coexist in the same patient.

Eosinophilia↗
PubMed1983

The combining ability of glycoproteins IIb, IIIa and Ca2+ in EDTA-treated nonaggregable platelets.

Platelets deprived of calcium and incubated at 37 degrees C for 10 min lose their ability to bind fibrinogen or aggregate with ADP when adequate concentrations of calcium are restored. Since the calcium complex of glycoproteins (GP) IIb and IIIa is the presumed receptor for fibrinogen, it seemed appropriate to examine the behavior of these glycoproteins in incubated nonaggregable platelets. No differences were noted in the electrophoretic pattern of nonaggregable EDTA-treated and aggregable control CaEDTA-treated platelets when SDS gels of Triton X-114 fractions were stained with silver. GP IIb and IIIa were extracted from either nonaggregable EDTA-treated platelets or aggregable control platelets with calcium-Tris-Triton buffer and subjected to sucrose density gradient centrifugation or crossed immunoelectrophoresis. With both types of platelets, these glycoproteins formed a complex in the presence of calcium. If the glycoproteins were extracted with EDTA-Tris-Triton buffer, or if Triton-solubilized platelet membranes were incubated with EGTA at 37 degrees C for 30 min, GP IIb and IIIa were unable to form a complex in the presence of calcium. We conclude that inability of extracted GP IIb and IIIa to combine in the presence of calcium is not responsible for the irreversible loss of aggregability that occurs when whole platelets are incubated with EDTA at 37 degrees C.

Blood Platelets↗
PubMed1983

A monoclonal anti-platelet antibody with decreased reactivity for autoimmune thrombocytopenic platelets.

Two monoclonal anti-platelet antibodies, 3B2 and 8G11, have been raised that are specific for normal human platelets. 3B2 is unique in that it has decreased reactivity for platelets from 16 patients with autoimmune thrombocytopenic purpura [mean platelet count, 65,000 +/- 6,000 (SEM)]. With 8G11 in an enzyme-linked immunosorbent assay, the mean of the ratios of patient platelet OD to control platelet OD was 0.95 +/- 0.07, whereas with 3B2, the mean of the ratios of patient platelet OD to control OD was 0.24 +/- 0.04, P less than 0.001. With 3B2 the mean of the OD ratios of five patients with autoimmune thrombocytopenic purpura in remission (greater than 150,000 platelets per mm3) compared to controls was 0.80 +/- 0.14. 3B2 did not react with platelets from a patient with Glanzmann's thrombasthenia, in which membranes lack glycoproteins IIb and IIIa (GPIIb and GPIIIa). Platelet membranes were run on crossed immunoelectrophoresis against a rabbit polyclonal anti-human platelet membrane antibody with 125I-labeled purified 3B2 in an intermediate spacer gel. 3B2 reacted with the GPIIb-GPIIIa-Ca2+ complex in the presence of excess Ca2+ and with GPIIb alone in the presence of excess EGTA. When Triton X-100-solubilized platelet membranes were immunoprecipitated with 3B2 plus rabbit anti-mouse IgG, reduced, and run on NaDodSO4/polyacrylamide gel electrophoresis, a single protein band was obtained with a molecular weight of 120,000 (the molecular weight of GPIIb). Thus, the reactivity of monoclonal antibody 3B2 with GPIIb or the GPIIb-GPIIIa-Ca2+ complex appears to be inhibited by the presence of autoantibody on platelets.

Animals↗