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Biomedical subjects

S Karpatkin

Publications and source records attributed to S Karpatkin.

At least 145 records · Page 8Linked to original sources
PubMed1975

Heterogeneity of rabbit platelets. IV. Thrombocytosis with absolute megathrombocytosis in phenylhydrazine-induced hemolytic anemia in rabbits.

Intravenous injection of phenylhydrazine into intact rabbits resulted in a thrombocytosis of 1.85 fold and megathrombocytosis (large platelets) of 2.30 fold. Splenectomy markedly impaired this response. The intravenous injection of red blood cell hemolysates gave a response similar to that of phenylhydrazine in both intact and splenectomized animals. Basal data obtained from intact and splenectomized animals; as well as kinetic data obtained following apparent splenic blockade secondary to phenylhydrazine hemolysis revealed the presence of a splenic platelet pool with preferential splenic sequestration of megathrombocytes. It is suggested that the thrombocytosis and absolute megathrombocytosis of hemolysis is due to splenic blockade by red blood cell hemolysate.

Anemia, Hemolytic↗
PubMed1975

Heterogeneity of rabbit platelets. V. Preferential splenic sequestration of megathrombocytes.

Rabbits were either splenectomized or subjected to splenic blockade with phenylhydrazine in order to determine the splenic platelet and megathrombocyte (large-platelet) pools. The average splenic platelet pool calculated from both methods was 35% of total platelets. The average splenic megathrombocyte pool was 54% of total megathrombocytes. Adrenaline injection into rabbits or dogs revealed a rapid increase in both platelet count and megathrombocyte number which peaked at 2-6 min and returned toward normal in 5-10 min. The platelet volume distribution curve was shifted to the right, indicating the release of large platelets (megathrombocytes) into the circulation. The peak rise in megathrombocyte number was significantly greater than the peak rise in platelet count. Rabbits subjected to splenic massage shifted their platelet volume distribution curve to the right in the absence of a rise in platelet count. It is concluded that the spleen preferentially sequesters megathrombocytes.

Aging↗
PubMed1975

Microthrombocytosis and platelet fragmentation associated with idiopathic/autoimmune thrombocytopenic purpura.

Platelet volume distribution curves were obtained in 20 control subjects and in 21 patients with idiopathic/autoimmune thrombocytopenic purpura. A striking increase in microthrombocytes as well as megathrombocytes was noted in 86% of patients on one or more occasions, particularly in the prsence of severe thrombocytopenia. The entire spectrum of platelet volume distribution curves noted in patients could be reproduced experimentally in rabbits following intravenous injection of anti-platelet antibody. Differential centrifugation studies with control subjects revealed that microthrombocytes were light platelets and megathrombocytes were heavy platelets. Electron microscopy in patients with thrombocytopenia revealed that microthrombocytes were composed of intact small platelets as well as platelet fragments. It is concluded that severe peripheral destruction of platelets is associated with an increase in microthrombocytes as well as megathrombocytes.

Adolescent↗
PubMed1975

On the "easy bruising" syndrome with normal platelet count. A study of 75 patients.

Seventy-five consecutive patients with normal platelet counts were investigated for "easy bruising." All had a normal coagulation profile, and all except four were women. None were on aspirin or other antiplatelet agents. Two specific groups could be delineated. In type I (44 patients, mean age, 35), platelet function was normal to supranormal. Megathrombocyte number was elevated in 60% of patients and correlated with the presence of antiplatelet antibody in 30% of patients. In type II (31 patients, mean age, 34), platelet function was abnormal: impaired epinephrine aggregation (primary and secondary wave) in 97%, impaired connective tissue aggregation in 77%, and impaired ADP aggregation in 42%. Megathrombocyte number was elevated in 71%, and antiplatelet antibody was present in 38% of patients. The "easy bruising" syndrome can be differentiated into two categories: type I, in which a platelet abnormality is unlikely, and type II, in which a platelet abnormality exists. Elevated incidence of antiplatelet antibody in both groups suggests a possible autoimmune cause.

Adenosine Diphosphate↗
PubMed1975

Elevated platelet count and megathrombocyte number in sickle cell anemia.

Eight adult patients with sickle cell anemia were followed over a 6-mo period. During this time all patients had elevated plateletcounts, 1.7-fold (mean, 438,398 +/- 86,223), and megathrombocyte numbers, 2.3-fold (mean, 79,535 +/- 38,907), during asymptomatic periods. These data are interpreted as suggesting that the elevated platelets and megathrombocytes in asymptomatic sickle cell patients result from lack of splenic sequestration. During three crises in two patients, both megathrombocyte number and platelet count fell significantly. It is speculated that platelets may be associated with the pathology in this disease. Platelet function studies performed during crises, therefore, must take into account the number of megathrombocytes.

Adult↗
PubMed1975

Effect of plasma, steroids, or steroid products on the adhesion of human opsonized thrombocytes to human leukocytes.

An in vitro system was designed in which human thrombocytes were opsonized with rabbit antihuman platelet antibody and incubated with human leukocytes in EDTA-plasma in order to measure opsonized platelet-leukocyte adhesion. Antiplatelet antibody opsonization enhanced platelet-leukocyte adhesion 2.6-fold over control nonopsonized platelets in 50 out of 56 experiments. A plasma factor was found necessary for the support of opsonized platelet-leukocyte adhesion. This factor was EDTA-stable, heat labile, and labile to freezing and thawing. Hydrocortisone at 10-2 M was extremely effective in preventing opsonized platelet-leukocyte adhesion in 11 out of 14 experiments (2 S.D. below test-control value). Plasmas from 23 different patients ingesting 20 to 120 mg. of prednisone per day, were also tested. Seventeen out of 23 (74 per cent) did not support opsonized platelet-leukocyte adhesion at in vivo steroid concentrations of 10-6 M. Dilutions of 6 of these plasma samples with pooled normal plasma from 8- to 16-fold were still incapable of supporting opsonized platelet-leukocyte adhesion, whereas higher dilutions were capable. "Nonsteroid" plasma from 9 out of 17 (53 per cent) hospitalized "sick" patients were also incapable of supporting opsonized platelet-leukocyte adhesion. "Steroid plasma" from 5 out of 6 patients with severe thrombocytopenic purpura refractory to steroid treatment, did support leukocyte adhesion of opsonized platelets. It is concluded that a plasma factor is required for opsonized platelet-leukocyte adhesion. A steroid metabolite or byproduct factor is capable of inhibiting the adhesion of antibody-coated human platelets to leukocytes at an in vivo "steroid" concentration of 10-7 M. This factor does not appear to be present in most patients refractory to steroid treatment for autoimmune thrombocytopenic purpura.

Adult↗