Cerebral blood volume increment after resuscitation measured by near-infrared time-resolved spectroscopy can estimate degree of hypoxic\u2013ischemic insult in newborn piglets

Tsutomu Mitsuie,Aya Morimoto,Kosuke Koyano,Yasuhiro Nakao,Shinji Nakamura,Yasuhiro Kuroda,Yinmon Htun,Takashi Kusaka,Takayuki Wakabayashi,Makoto Arioka

doi:10.1038/s41598-021-92586-1

Tsutomu Mitsuie, Aya Morimoto + Show 8 more

Open Access

https://doi.org/10.1038/s41598-021-92586-1

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Journal: Scientific Reports	Publication Date: Jun 23, 2021
Citations: 3	License type: open-access

Affiliation: Kagawa University Hospital, Kagawa University

Abstract

Neonatal hypoxic–ischemic encephalopathy is a notable cause of neonatal death and developmental disabilities. To achieve better outcomes, it is important in treatment strategy selection to categorize the degree of hypoxia ischemia and evaluate dose response. In an asphyxia piglet model with histopathological brain injuries that we previously developed, animals survived 5 days after insult and showed changes in cerebral blood volume (CBV) that reflected the severity of injuries. However, little is known about the relationship between changes in CBV during and after insult. In this study, an HI event was induced by varying the amount and timing of inspired oxygen in 20 anesthetized piglets. CBV was measured using near-infrared time-resolved spectroscopy before, during, and 6 h after insult. Change in CBV was calculated as the difference between the peak CBV value during insult and the value at the end of insult. The decrease in CBV during insult was found to correlate with the increase in CBV within 6 h after insult. Heart rate exhibited a similar tendency to CBV, but blood pressure did not. Because the decrement in CBV was larger in severe HI, the CBV increment immediately after insult is considered useful for assessing degree of HI insult.

Highlights

Neonatal hypoxic–ischemic encephalopathy is a notable cause of neonatal death and developmental disabilities
Blood glucose increased at the start of resuscitation and returned to baseline 360 min after insult, whereas lactate had not returned to baseline by 360 min
Compared with the control group, a significant difference was seen in pH, p O2, BE, blood glucose, lactate, and rectal temperature immediately before resuscitation in HI piglets and pH, BE, and lactate continued in the same manner until 60 min after insult

Summary

Introduction

Neonatal hypoxic–ischemic encephalopathy is a notable cause of neonatal death and developmental disabilities. In an asphyxia piglet model with histopathological brain injuries that we previously developed, animals survived 5 days after insult and showed changes in cerebral blood volume (CBV) that reflected the severity of injuries. It is important to recognize the changes in cerebral hemodynamics in neonates with HIE as early as possible after HI insult. Understanding changes in cerebral hemodynamics and cerebral oxygenation status in neonatal HIE is beneficial for the prognosis of HIE, the monitoring of ongoing therapy, and the evaluation of novel therapies. The use of near-infrared spectroscopy (NIRS) for monitoring oxygenation of the brain has provided useful insights for the management of newborns who require respiratory support, cardiovascular support, or transfusion, have HIE, or have undergone s urgery[6,7]. In neonatal HIE, HI insult affects cerebral hemodynamics and oxygenation status due to impairment in cerebral autoregulation. Oxygen saturation ( SaO2) may not always reflect the extent of brain injury[10,11], for a complete clinical picture, assessment of neonatal cerebral oxygenation and perfusion should be performed

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