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Morphologic changes of red blood cells during hemorrhagic shock replicate changes of aging
T L Berezina1, S B Zaets, V L Kozhura
1Department of Surgery, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark 07103-2714, USA.
Abstract:
Blood loss leads to the reduction in vitality of red blood cells (RBCs). However, the changes in morphology at different stages of hemorrhagic shock have not been studied. Thus, the aim of this study was to identify and quantitate the sequence of morphological changes in RBCs during hemorrhage. This study was performed on 15 adult inbred dogs. Blood samples were taken before hemorrhage, when the mean arterial pressure reached 40 mm Hg (initial stage of shock), and at a mean arterial pressure level of 20 mm Hg (decompensated stage of shock). The volume of blood removed averaged 33.6+/-8.9 and 55.1+/-6.9 mL/kg, respectively. Evaluation of RBC morphology was performed by computerized light microscopic morphometry and scanning electron microscopy. At the early stage of hemorrhage the number of "young-appearing" RBCs with large visible surface areas (41-50 microm2) increased from 17.7%+/-3.1% to 26.6%+/-3.5% (P < 0.05). Concomitantly, the number of "old-appearing" RBCs with small visible surface area (20-30 microm2) significantly decreased from 5.3%+/-2.7% to 2.7%+/-2.3% (P < 0.01). At the stage of decompensated blood loss, the opposite phenomenon was observed. The number of "old-appearing" RBCs increased to 8.2%+/-1.1% (P < 0.01), whereas the number of "young-appearing" RBCs decreased to 12.3%+/-4.2% (P< 0.01). The changes in visible surface area of RBCs was accompanied by significant alterations in their shape. The percentage of abnormal shaped RBCs increased from 8.9%+/-1.1% before the hemorrhage to 36.4%+/-5.8% at the stage of decompensated hemorragic shock (P < 0.01). Thus, during the late decompensated stage of hemorrhagic shock, RBCs assume shape and surface area changes that are similar to those seen in aging. These changes in RBC size and shape may be due to the effects of shock-induced oxidative stress.