Effect of β-adrenergic blockers on the sickling phenomenon

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Abstract
Dichloroisoproterenol (DCI) and propranolol inhibited sickling in vitro when added to red-cell suspensions [from human sickle-cell anemia subjects] prior to deoxygenation. The effectiveness was maximal between PO2 [partial pressure of O2] of 30-40 mmHg (1 mmHg = 133.322 Pa [Pascals]. When cells were sickled at a low O2 tension (PO2 = 32 mmHg) and DCI added, the drug decreased the degree of sickling while the suspension was maintained at the same O2 tension. The antisickling effect of these drugs was not antagonized by isoproterenol, a .beta.-adrenergic stimulator, by the addition of cAMP or increase of the intracellular C concentration. Other .beta.-blockers, such as MJ1999 (sotalol) and timolol, did not show antisickling activity. DCI, propranolol and timolol had some effect on the delay time of gelation of sickle-cell Hb (Hb S), as well as on the O2 affinity of sickle cells.