Impact of Vitamin C on Biomarkers of Neurologic Injury in Survivors of Cardiac Arrest
Status:
Not yet recruiting
Trial end date:
2022-12-31
Target enrollment:
Participant gender:
Summary
Out-of-hospital cardiac arrest (OHCA) is one of the leading cause of death in the world. In
Slovenia approximately 25% of resuscitated patients survives to discharge from hospitals,
usually with poorer functional status.
One of key pathophysiological process responsible for poorer functional status is global
hypoxic-ischemic injury, which is two-stage. Primary stage occurs immediately after cardiac
arrest due to cessation of blood flow. With return of spontaneous circulation a secondary
injury occurs, of which the leading process is an imbalance between oxygen delivery and
consumption. Reperfusion exposes ischemic tissue to oxygen, resulting in the formation of
large amounts of highly reactive oxygen species (ROS) within minutes. ROS lead to oxidative
stress, which causes extensive damage to cell structures and leads to cell death.
Consequently, necrosis and apoptosis are responsible for organ dysfunction and functional
outcome of these patients.
Such injury of neural tissue causes brain damage, which is ultimately responsible for poor
neurological and thus functional outcome of OHCA survivors. The extent of brain damage can be
determined in several ways: clinically by assessing quantitative and qualitative
consciousness and the presence of involuntary movements in an unconscious patient, by
assessing activity on electroencephalographic record, by imaging of the brain with computed
tomography and magnetic resonance imaging, as well as by assessing levels of biological
markers of brain injury. Of the latter, the S-100b protein and neuron-specific enolase have
been shown to be suitable for such assessment.
Oxidative stress is counteracted by the body with endogenous antioxidants that balance excess
free radicals and stabilize cellular function. Vitamin C (ascorbic acid) is the body's main
antioxidant and is primarily consumed during oxidative stress. Large amounts of ROS rapidly
depletes the body's vitamin C stores.
Humans cannot synthesise vitamin C and enteral uptake of vitamin C is limited by transporter
saturation. On the other hand, parenteral (venous) dosing of vitamin C can achieve
concentrations of vitamin C above physiological and thus produce a stronger antioxidant
effect. The beneficial effect of parenteral dosing of vitamin C has been establish in several
preclinical and clinical studies in patients with ischemic stroke and cardiac arrest.
The investigators hypothesize that there is a similarly beneficial effect of vitamin C in
survivors of OHCA.