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Updated: May 2, 2026
Standardized Hemorrhagic Shock Induction Guided by Cerebral Oximetry and Extended Hemodynamic Monitoring in Pigs
Published on: May 21, 2019
Monitoring hemodynamic and metabolic alterations during severe hemorrhagic shock in rat brains
Nannan Sun1, Weihua Luo2, Lin Z Li3
1Britton Chance Center for Biomedical Photonics, Wuhan National Laboratory for Optoelectronics, Huazhong University of Science and Technology, Wuhan, Hubei, PR China; Department of Biomedical Engineering, Key Laboratory of Biomedical Photonics of Ministry of Education, Huazhong University of Science and Technology, 1037 Luoyu Road, Wuhan, Hubei 430074, PR China; Department of Radiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA; Department of Biochemistry and Biophysics, Britton Chance Laboratory of Redox Imaging, Johnson Research Foundation, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Rationale And Objectives:
Our long-term goals are to identify imaging biomarkers for hemorrhagic shock and to understand how the preservation of cerebral microcirculation works. We also seek to understand how the damage occurs to the cerebral hemodynamics and the mitochondrial metabolism during severe hemorrhagic shock.
Materials And Methods:
We used a multimodal cerebral cortex optical imaging system to obtain 4-hour observations of cerebral hemodynamic and metabolic alterations in exposed rat cortexes during severe hemorrhagic shock. We monitored the mean arterial pressure, heart rate, cerebral blood flow (CBF), functional vascular density (FVD), vascular perfusion and diameter, blood oxygenation, and mitochondrial reduced nicotinamide adenine dinucleotide (NADH) signals.
Results:
During the rapid bleeding and compensatory stage, cerebral parenchymal circulation was protected by inhibiting the perfusion of dural vessels. During the compensatory stage, although the brain parenchymal CBF and FVD decreased rapidly, the NADH signal did not show a significant increase. During the decompensatory stage, FVD and CBF maintained the same low level and the NADH signal remained unchanged. However, the NADH signal showed a significant increase after the rapid blood infusion. FVD and CBF rebounded to the baseline after the resuscitation and then declined again.
Conclusions:
We present for the first time simultaneous imaging of cerebral hemodynamics and NADH signals in vivo during the process of hemorrhagic shock. This novel multimodal method demonstrated clearly that severe hemorrhagic shock imparts irreversible tissue damage that is not compensated by the autoregulatory mechanism. Hemodynamic and metabolic signatures including CBF, FVD, and NADH may be further developed to provide sensitive biomarkers for stage transitions in hemorrhagic shock.
