cardiovascular-agents and Hemolysis

Glucose-6-phosphate dehydrogenase (G6PD) deficiency can present a diagnostic dilemma owing to the varying degrees of disease severity and the wide range of precipitating factors. Here, we report a case of a 56-year-old man who presented with signs and symptoms of heart failure and, during the course of treatment, developed intravascular hemolysis. On investigation, he was found to be G6PD deficient. Following discontinuation of the fixed-dose combination of isosorbide dinitrate and hydralazine, the clinical condition of the patient improved, and there were no further episodes of hemolysis. The case highlights the need for a high degree of suspicion of G6PD deficiency in patients with unexplained signs and symptoms of intravascular hemolysis.

Topics: Cardiovascular Agents; Drug Combinations; Glucosephosphate Dehydrogenase Deficiency; Hemolysis; Humans; Hydralazine; Isosorbide Dinitrate; Male; Middle Aged

Carbon monoxide (CO) intoxication severely interferes with the oxygen-transporting function of haemoglobin. Beyond that, CO participates in the regulation of apoptosis. CO could be generated from CO-releasing molecules (CORM), such as the tricarbonyl-dichlororuthenium (II) dimer (CORM-2), which is presently considered for the treatment of vascular dysfunction, inflammation, tissue ischaemia and organ rejection. CORM-2 is at least partially effective by modifying gene expression and mitochondrial potential. Erythrocytes lack nuclei and mitochondria but may undergo suicidal cell death or eryptosis, characterized by cell shrinkage and phospholipid scrambling of the cell membrane. Eryptosis is triggered by the increase in cytosolic Ca²⁺ activity ([Ca²⁺](i)). The present study explored whether CORM-2 influences eryptosis. To this end, [Ca²⁺](i) was estimated from Fluo-3-fluorescence, cell volume from forward scatter, phospholipid scrambling from annexin-V-binding and haemolysis from haemoglobin release. CO-binding haemoglobin (COHb) was estimated utilizing a blood gas analyser. As a result, exposure of erythrocytes for 24 hr to CORM-2 (≥5 μM) significantly increased COHb, [Ca²⁺](i) , forward scatter, annexin-V-binding and haemolysis. Annexin-V-binding was significantly blunted by 100% oxygen and was virtually abolished in the nominal absence of Ca²⁺. In conclusion, CORM-2 stimulates cell membrane scrambling of erythrocytes, an effect largely due to Ca²⁺ entry and partially reversed by O₂.

Topics: Adult; Air Pollutants; Apoptosis; Blood Banks; Calcium Signaling; Carbon Monoxide; Carboxyhemoglobin; Cardiovascular Agents; Cell Size; Erythrocyte Membrane; Erythrocytes; Hemolysis; Humans; Microscopy, Confocal; Organometallic Compounds; Oxygen; Phosphatidylserines; Surface Properties

Staphylococcus beta-haemolysin exhibits the same broad spectrum of antagonistic activity against smooth muscle stimulants as described recently for Colisan. The antispasmodic effect develops slowly and can be removed only by repeated washing. The pattern of haemolytic activities of Colisan is characteristically different from that of beta-haemolysin, but resembles closely alpha-toxin. Both staphylococcus toxins can destroy paramecium and entamoeba, but the ratio of the titres at which they kill paramecium and entamoeba respectively (P:A value) is different. The P:A value of beta-haemolysin is similar to that of Colisan.

Topics: Antitoxins; Cardiovascular Agents; Cell Death; Entamoeba; Exotoxins; Hemolysin Proteins; Hemolysis; Muscle Relaxants, Central; Muscle, Smooth; Staphylococcus; Toxins, Biological; Type C Phospholipases

Topics: Cardiovascular Agents; Ether; Ethers; Glycerol; Glyceryl Ethers; Guaiacol; Hemolysis; Humans; In Vitro Techniques; Mephenesin; Methocarbamol; Muscle Relaxants, Central