Hyperthermia associated morphological changes in white blood cells

Li, Ting Hon Stanford; Wong, Man Sin; Wong, Hung Fan; Wong, Wai Keung; Chan, Ching Bill

doi:10.1111/ijlh.13480

Cited by 3 publications

(1 citation statement)

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“…Leukocytes have reportedly demonstrated a hyper-segmented spoke-like botryoid pattern of the nucleus in humans [ 16 ], and Ward et al [ 17 ] described the botryoid neutrophils and hyper-lobulated lymphocytes in normal blood heated to 42.2 °C for 10 min. The incidence is lower, but eosinophils and basophils are also known to present botryoid nuclei [ 18 ]. Consequently, the nucleus changes of the neutrophils and other leukocytes have been previously reported in heat-related illnesses [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

Morphological Changes in Blood Cells in a Rat Model of Heatstroke: A Pilot Study

Iba

Sawada

Kondo

et al. 2022

JCM

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Despite the increasing threat of heatstroke with global warming, pathophysiologic injury continues to be defined. In addition, morphological changes of the peripheral blood cells in heatstroke have not been well characterized. We evaluated pathophysiologic changes in bone marrow and blood cells in a rat heatstroke model using a 39.5 °C climate chamber. After three hours of incubation, blood and bone marrow samples were collected for morphology, and the direct effects of heat on leukocytes in vitro were evaluated using time-lapse observation. The blood cell count and peripheral/bone marrow smear were examined either in a lethal model (core body temperature exceeded 42.5 °C) or in a sublethal model (<41.5 °C). Significant decreases in platelet and white blood counts occurred in the lethal model (>35% and >20% decreases, respectively) and changes were less in the sublethal model. Platelet clumping with the appearance of large platelets was observed. The neutrophils often demonstrated hyper-segmented nuclei, and lymphocytes showed reactive or blast-like changes. Further, the direct effect of heat on leukocytes noted apoptotic cell death at 41.5 °C, but subsequent necrosis at 43 °C. In summary, our rodent model showed that heatstroke causes platelet aggregation, leukocyte injury, and aponecrotic cell death. Such changes were milder and reversible in sublethal heatstroke. The appearance of immature cells may result from damage to the bone marrow microenvironment. These findings may provide useful information for potential diagnostic and therapeutic considerations.

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