In humans, the location of brain regions responsible for mediating the ventilatory response to CO2 remains unknown. Most of the available knowledge has been derived from animal studies or from pathophysiological correlations in patients presenting altered control of breathing. Magnetic resonance imaging at a specific pulse sequence designed to assess changes in brain tissue microcirculation was performed in 11 healthy volunteers, during steady-state conditions, while breathing 100% O2 or 5% CO2-95% O2. In one subject, 10% CO2-90% O2 was employed to examine a dose-response effect. Significant changes in image signal intensity consistently occurred in ventral and dorsal regions of medullary structures as well as in the midline pons and ventral cerebellum. These responses appeared to be dose dependent and reproducible. Magnetic resonance imaging revealed patterns of activation in brain stem and cerebellar regions during hypercapnic ventilatory challenge. These areas may underlie mechanisms for mediating the response to chemoreceptor activation.
Many studies suggest that hyperbaric oxygen therapy (HBOT) can provide some clinically curative effects on blast-induced traumatic brain injury (bTBI). The specific mechanism by which this occurs still remains unknown, and no standardized time or course of hyperbaric oxygen treatment is currently used. In this study, bTBI was produced by paper detonators equivalent to 600 mg of TNT exploding at 6.5 cm vertical to the rabbit's head. HBO (100% O2 at 2.0 absolute atmospheres) was used once, 12 h after injury. Magnetic resonance spectroscopy was performed to investigate the impact of HBOT on the metabolism of local injured nerves in brain tissue. We also examined blood-brain barrier (BBB) integrity, brain water content, apoptotic factors, and some inflammatory mediators. Our results demonstrate that hyperbaric oxygen could confer neuroprotection and improve prognosis after explosive injury by promoting the metabolism of local neurons, inhibiting brain edema, protecting BBB integrity, decreasing cell apoptosis, and inhibiting the inflammatory response. Furthermore, timely intervention within 1 week after injury might be more conducive to improving the prognosis of patients with bTBI.
Hypoxic-ischaemic encephalopathy (HIE) is a result of perinatal hypoxia-ischaemia (HI), and it greatly contributes to child mortality and morbidity worldwide. 1-3 Perinatal HI brain injury is often caused by disruption of placental blood flow and leads to impaired gas exchange, resulting in low oxygen and low metabolic substrates levels in the central nervous system. Cerebral palsy, epilepsy and learning disabilities are a potential long-term neurological consequences of these detrimental events in the developing brain. 4 It has been established that brain damage following HI is a complex disease with multiple contributing mechanisms and pathways.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.