Prophylaxis of encephalopathies and risk factors of atherogenesis development in the postresuscitation period in rats by means of succinic acid.

The effect of oral administration of succinic acid was studied in 66 rats exposed to 10 min cardiac arrest with further resuscitation. A total of 30 mg/kg of the drug were administered daily for 5 days starting with day 3 up to day 7 after resuscitation. The experiments have revealed that treatment with succinic acid caused normalization of the orienting behavior in an 'open field' test, decrease of the intensity of response to electric shock, normalization of free radical formation in the brain and serum and reduced cerebral morphological changes.

Postresuscitation changes in brain free radical-mediated processes and nitric oxide synthase activity in rats: effects of individual behavior in "emotional resonance" test.

Effects of 7-min cardiac arrest and individual behavior on free radical-mediated processes and nitric oxide synthase (NOS) activity was evaluated in brains of male Wistar rats one hour and one week after resuscitation. "Emotional resonance" test was used for the behavioral selection of rats. The test includes factors of significance for rats: the choice between large and lighted or small and dark space as well as signals of pain of another rat.

Cardiac arrest induces decrease of nitric oxide synthase activity and increase of free radical generation in rat brain regions.

Rats were subjected to 15 min cardiac arrest and sacrificed 1 h or 15-20 days after resuscitation. Homogenates of brain regions were assayed for nitric oxide synthase (NOS) activity (by measuring the mononitrosyl iron complex of NO with diethyl dithiocarbamate and endogenous brain Fe2+ using electron spin resonance spectroscopy) and generation of free radicals (FRG; by measuring H2O2-induced, luminol-dependent chemiluminescence). Cardiac arrest induced marked decrease of NOS activity and the increase of FRG, most prominent in cerebellum and less marked in cerebral cortex.

Cerebral resuscitation from cardiac arrest: pathophysiologic mechanisms.

Both the period of total circulatory arrest to the brain and postischemic-anoxic encephalopathy (cerebral postresuscitation syndrome or disease), after normothermic cardiac arrests of between 5 and 20 mins (no-flow), contribute to complex physiologic and chemical derangements. The best documented derangements include the delayed protracted inhomogeneous cerebral hypoperfusion (despite controlled normotension), excitotoxicity as an explanation for selectively vulnerable brain regions and neurons, and free radical-triggered chemical cascades to lipid peroxidation of membranes. Protracted hypoxemia without cardiac arrest (e.

Post-resuscitation disease--a new nosological entity. Its reality and significance.

Experimental and clinical investigations of patients resuscitated after cardiac arrest or terminal states, testify to the fact that in the post-resuscitation period alongside processes of recovery and compensation, a number of new pathological phenomena develop. The latter differ substantially from those caused by ischemia and hypoxia. These post-resuscitation processes involve not only the CNS, but also the entire body and may lead to severe disability and even death of the seemingly successfully revived body.