Abstract
The aim of the literature review was to present modern views on the possible mechanisms of the disturbances of capillary blood flow in severe brain injury (TBI). The critical analysis of the concept of secondary brain damage and possible mechanisms of the disturbances of cerebral microcirculation in TBI are presented. We also discuss modern methodologies for assessing capillary blood flow in patients with brain damage. The attention is focused on the causes of the disturbances of cerebral microcirculation in TBI, as well as in various forms of fat embolism in severe combined TBI. Possibilities of prevention and early correction of damaged capillary blood flow in brain injury, as well as the supposed reasons for the failure of some clinical trials, including the widely known CRASH, are analyzed. It is noted that an integrative approach to the assessment of cerebral microcirculation in conjunction with brain metabolism reflects not just the variability of cerebral blood flow and functional disorders of perfusion and metabolism coupling in traumatic brain injury. It is emphasized that ischemia is not the only cause of post-traumatic disorders of pial circulation. We highlight directions for future research of posttraumatic disturbances of cerebral microcirculation as a leading factor of secondary brain insults. The possibility of pharmacological and non-pharmacological correction of microcirculatory disorders in TBI is outlined.
Highlights
Произведено сопоставление концепции вторичных повреждений головного мозга и возможных механизмов развития нарушений церебральной микроциркуляции при черепно-мозговой травме (ЧМТ)
Hypoxia-inducible factor-1alpha signaling in aquaporin upregulation after traumatic brain injury // Neurosci
Classification and regression transit time heterogeneity and flow-metabolism coupling tree for prediction of outcome after severe head injury using after traumatic brain injury // J. of Cerebral Blood Flow & simple clinical and laboratory variables // J
Summary
Произведено сопоставление концепции вторичных повреждений головного мозга и возможных механизмов развития нарушений церебральной микроциркуляции при ЧМТ. В эксперименте было показано, что при- Нарушение нейроваскулярного сопряжения менение антагонистов к эндотелину-1А приводило Под нейроваскулярным сопряжением в настояк восстановлению перфузии капиллярного русла в щее время подразумевается изменение локального течение 1-х суток и умеренной гиперперфузии в по- церебрального кровотока и оксигенации мозга в следующие 2-е суток [53]. Cerebral hyperglycolysis following severe traumatic brain injury in humans.
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