Introduction
Hypoxic-ischemic encephalopathy is a major cause of infant mortality and morbidity with long-term neurological sequelae. Hypoxic brain injury is an evolving process that results from an initial insult and extends during the reperfusion phase of injury.1,2 It is characterized by symptoms such as seizure, difficulty in starting and maintaining respiration, circulatory impairment, abnormal muscular tonus, and a decrease in reflexes.3 Transient ischemia of the cerebral vasculature followed by reperfusion leads to a secondary cascade of pathophysiological events, characterized by a complex inflammatory response.4 In particular, it activates immune cells in hypoxia-ischemia-induced cell damage or cell death, microglia, and astrocytes. These activated cells lead to the synthesis and production of pro-inflammatory cytokines such as interleukin 1b, interleukin 6, and tumor necrosis factor-a. Pro-inflammatory cytokines increase the expression of mediators that induce vascular permeability, the migration of leukocytes, and promote local inflammatory reactions.5-7 The production of leukocytes and the number of circulating neutrophils increase. Cell damage occurs due to the production of reactive and toxic metabolites such as hydrogen peroxide, superoxide anion, and hypochlorous acid from neutrophils.8 Thrombocytes play a fundamental role in hemostasis. However, recent studies have revealed that thrombocytes also play an essential role in infection and inflammation.9,10 Mean platelet volume (MPV) is a value that indicates thrombocyte activation and can be used as a biomarker in inflammation. Changes in the MPV have been studied in many diseases.11-13 Therapeutic hypothermia constitutes one of the most important therapies providing neuroprotection, and has been reported to reduce brain damage by reducing the production of inflammatory cells and inflammatory cytokines.14
The aim of this study was to investigate the inflammatory cell response in NE before and during TH.