Quinidine leukopenia and thrombocytopenia with a drug-dependent leukoagglutinin.
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Biomedical subjects
Publications and source records attributed to O Castro.
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The effects of in vivo hyperoxia and hypoxia on the intravascular survival of 51Cr-labeled human sickle erythrocytes (SS RBS's) were studied after transfusion into rats and guinea pigs. The function of these animals' reticuloendothelial and complement systems had been previously inhibited by ethyl palmitate and cobra venom factor, thus allowing extension of the survival of the heterologous human RBC's. In the blood of rats breathing ambient air the 51Cr half-life survival of RBC's from 11 patients with sickle-cell anemia (mean, 7.1 hours; range, 2.0 to 16.5 hours) was significantly shorter (p less than 0.001) than that of five control subjects (mean, 17.5 hours; range, 12.0 to 26.5 hours). When rats transfused with sickle RBC's were exposed to 100 per cent O2, a mean increment of 16.5 per cent blood 51Cr activity was observed within the first 15 to 60 minutes of hyperoxia. Subsequent oxygen deprivation (7 to 8 per cent O2) resulted in an equally rapid decrease (mean, 35.6 per cent) in blood 51Cr activity. Continuation of hypoxia for up to 17 hours did not cause further acceleration of 51Cr activity. Continuation of hypoxia for up to 17 hours did not cause further acceleration of 51 Cr RBC clearance. Under these conditions the slope of the sickle RBC survival curve was similar to that in animals kept in ambient air. After hypoxic rats were allowed to breate room air again, mean 51Cr blood activity increased by 41.7 per cent. Sickle RBC's transfused to guinea pigs exhibited similar oxygen-dependent survival characteristics. The survival of 51Cr RBC's from four adult control subjects and of unlabeled fetal RBC's from three human cord blood samples was unaffected by oxygen changes. When rats that had been transfused with sickle reticulocytes labeled in vitro with 59Fe were made hypoxic, a decrease in blood 59Fe activity was observed. The extent of this decrease was comparable to that in rats transfused with 51Cr labeled RBC's from the same patients. There was increased liver and spleen 51Cr activity in animals transfused with 51Cr SS RBC's and killed during hypoxia when compared to that of hyperoxic animals. These studies suggest that a minor population of sickle cells is removed from circulation during hypoxia and circulates again upon reoxygenation of the animals. Erythrocyte aging does not appear to be responsible for this phenomenon. The oxygen-depdendent circulation of a population of SS RBC's in this animal system is probably due to reversible sickling and trapping of sickled cells in the microcirculation.
Use of racemic epinephrine hydrochloride (Vaponefrin), delivered by intermittent positive-pressure breathing, in the treatment of laryngotracheobronchitis (croup) produced acute beneficial results in a controlled study. However, symptoms often recurred within two hours, suggesting that this form of treatment should not be used in the emergency room and the patient then sent home. This treatment had no effect on arterial oxygen gas pressure. The changes in clinical status 24 to 36 hours after admission into the study were similar for the patients in the treatment and control groups, suggesting that the natural history of the disease was not drastically altered by this form of treatment.
A man with sideroblastic anemia had a splenectomy because of a salmonella abscess of the spleen that had ruptured into the colon. Two months later he developed recurrent thrombophiebitis and fatal thromboembolism associated with thrombocytosis. A review of the literature showed multiple additional cases of sideroblastic anemia with thrombocytosis and thromboembolism after splenectomy. In many of these cases the patient died. Splenectomy for treatment of a sideroblastic anemia probable is contraindicated. If splenectomy is done, long-term therapy to avoid thromboembolic complications probably should be maintained for many months or even years.
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Survival characteristics, after transfusion, of erythrocytes from patients with homozygous sickle-cell disease were studied in rats. The study was made possible by previous injection of the animals with ethyl plamitate, which depressed reticuloendothelial system function, and with a factor in cobra venom that inactivated complement. This treatment prevented the rapid phagocytosis and intravascular hemolysis of donor erythrocytes that usually follow a heterologous transfusion. Both immediate after transfusion recovery and survival of (51)Cr-labeled sickle erythrocytes were decreased in comparison to the values obtained for control erythrocytes from individuals without sickle-cell anemia. Survival of sickle erythrocytes was improved during exposure of the animals to 100% O(2). Hypoxia (7-10% O(2)) resulted in the abrupt removal of 35-60% of sickle erythrocytes from the rats' circulation. Variations in oxygen tension did not affect survival of control erythrocytes. The usefulness of this convenient animal model for the study of sickle-cell anemia is suggested by the similarities between our results and the behavior of sickle erythrocytes in humans. The system may also be suitable for studying a wide variety of other human erythrocyte disorders.
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