Affiliations: Department of Lis Maternity Hospital, Hematology Institute, Tel Aviv University, Tel Aviv, Israel | Department of Biochemistry, Hebrew University‐Hadassah Medical School, Jerusalem, Israel | Tel Aviv Sourasky Medical Center, Tel Aviv, Israel | Sackler Faculty of Medicine, Internal Medicine “D”, Tel Aviv University, Tel Aviv, Israel
Note: [] Unfortunately deceased in a tragic accident.
Abstract: In order to differentiate between the contributions of cellular and plasmatic factors to the elevated aggregation in pregnancy‐induced hypertension (PIH), we determined RBC aggregation in autologous plasma and in plasma‐free medium. The aggregation was determined as a function of shear stress, to evaluate the strength of the intercellular interaction. These procedures were applied to RBC from PIH women (n=20), normotensive pregnant (NTP) women (n=15), and non‐pregnant (control) women (n=15). The average aggregate size (AAS) in plasma for PIH, NTP and control RBC was 38.7±3.2, 28.4±3.0, and 11.5±2.2 (P<0.05, between the three groups), respectively. For the same groups, the aggregation in plasma‐free standard medium was 17.3±2.0, 12.0±1.2 and 10.0±1.6 (P<0.05 between PIH and the other two groups), respectively. The contribution of plasma to the elevated aggregation was 75% and 88% for PIH and NTP respectively. τS50, the shear stress required to singly disperse 50% of the RBC population, in plasma and in standard medium, was about the same for PIH and NTP, and both were markedly higher than that for control RBC. These findings suggest that the increased aggregation of RBC from women with PIH, over those at of NTP women, may be due largely to changes in cellular factors and the increased aggregability has the potential to affect blood flow mainly in low‐flow states such as in the placental intervillous space.
