Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The in vivo generation of .OH free radicals in specific brain regions can be measured by intracerebral microdialysis perfusion of salicylate, avoiding many of the pitfalls inherent in systemic administration of salicylate. Direct infusion of salicylate into the brain can minimize the hepatic hydroxylation of salicylate and its contribution to brain levels of 2,5-DHBA. Levels of 2,5-DHBA detected in the brain dialysate may reflect the .OH adduct plus some enzymatic hydroxylation of salicylate in the brain. After minimizing the contribution of enzyme and/or blood-borne 2,5-DHBA, the present data demonstrate the validity of the use of 2,3-DHBA and apparently 2,5-DHBA as indices of .OH formation in the brain. Therefore, intracranial microdialysis of salicylic acid and measurement of 2,3-DHBA appears to be a useful .OH trapping procedure for monitoring the time course of .OH generation in the extracellular fluid of the brain. These results indicate that nonenzymatic and/or enzymatic oxidation of the dopamine released by MPTP analogues in the extracellular fluid may play a key role in the generation of .OH free radicals in the iron-rich basal ganglia. Moreover, a site-specific generation of cytotoxic .OH free radicals and quinone/semiquinone radicals in the striatum may cause the observed lipid peroxidation, calcium overload, and retrograde degeneration of nigrostriatal neurons. This free-radical-induced nigral injury can be suppressed by antioxidants (i.e., U-78517F, DMSO, and deprenyl) and possibly hypothermia as well. In the future, this in vivo detection of .OH generation may be useful in answering some of the fundamental questions concerning the relevance of oxidants and antioxidants in neurodegenerative disorders during aging. It could also pave the way for the research and development of novel neuroprotective antioxidants and strategies for the early or preventive treatment of neurodegenerative disorders, such as Parkinson's disease (Wu et al., this issue), amyotrophic lateral sclerosis, head trauma, and possibly Alzheimer's cognitive dysfunction as well. In conclusion, this in vivo free-radical trapping procedure provides evidence to support a current working hypothesis that a site-specific formation of cytotoxic .OH free radicals in the basal ganglia may be one of the neurotoxic mechanisms underlying nigrostriatal degeneration and Parkinsonism caused by the dopaminergic neurotoxin MPTP. Addendum added in proof: The controversy concerning possible neurotoxic and/or neuroprotective roles of NO. in cell cultures was discussed and debated at the symposium (Wink et al., this issue; Dawson et al., this issue; Lipton et al., this issue).(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:In vivo generation of hydroxyl radicals and MPTP-induced dopaminergic toxicity in the basal ganglia. 783 34

An evoked potential differs from the EEG mainly in two ways: 1. The EEG is a random, continuous signal, which arises from the ongoing activity of the outer layers of the cortex. An evoked potential is the brain's response to a repetitive stimulus along a specific nerve pathway. 2.EEG signals range from 10-200 milliVolt (mV). Evoked potentials are smaller in amplitude (1-5-20 microVolt requiring precise electrode positioning and special techniques (signal averaging) to extract the specific response from the underlying EEG "noise". The technique of signal averaging, as originally described by Dawson in 1954 [69J, has been further developed in computer processing. The technique is now used by applying a stimulus repeatedly--preferably at randomized intervals--and to record the evoked response over the corresponding area of the brain, averaging out mathematically the change over the number of stimuli. Rationale for the use of EPs in the OR and the ICU. Evoked potentials (EPs) serve the following major purposes: 1. Monitoring of the functional integrity of neural structures that may be at risk during, for instance, ECC (extracorporeal circulation) or endarterectomy indicating cerebral hypoxia. 2. Monitoring of the effects of anesthetic agents and other centrally active drugs, which, besides the cortex, affect deeper neuronal structures. 3. Orthopedic cases where the spinal cord is at risk such as Harrington rod insertion and removal. 4. Clamping of the abdominal aortic artery during aneurysmectomy resulting in a potential damage of the lower parts of the spinal cord. 5. Clipping of an intracerebral aneurysm, which may be impeding blood flow to vital cerebral textures. 6. An indicator of cerebral hypoxia when the blood pressure is deliberately lowered. 7. Operation on peripheral nerves and nerve roots to identify early trauma. 8. Monitoring the cerebral function during controlled hypothermia when the EEG becomes flat. 9. Monitoring of the pathophysiological conditions after severe head trauma and the effects of therapy. 10. An intraoperative warning device of unsuspected awareness during light anesthesia when movement is abolished by muscle relaxants and cardiovascular responses are modified by vasoactive drugs. In case of the latter the stimulus is a small electrical potential applied to the skin of the hand. Thereafter, the stimulus travels along the specific nervous pathways inducing (= generating) potential activation at various sites. The generation of potential changes at various sites along the pathway is an index for the integrity of the nerve. Thus, the evoked potential can be considered a neurophysiological response (usually of the cortex) to impulses originating from some externally stimulated sensory nerve. They provide a physiological measure of the functional integrity of the sensory nerve pathway, which can be used as a clinical diagnostic tool as well as for intraoperative monitoring. The evoked potential usually is recorded from the specific cortical area corresponding to the stimulus input. The classification of evoked potentials. Stimulating a sensory nervous pathway induces evoked potentials. If the auditory nerve is stimulated by "clicks" from headphones, it is called the auditory evoked potential (AEP). The early part of the AEP waveform (less than 10 msec) is called the Brainstem Auditory Evoked Potential (BAEP) since it reflects the passing of the impulse through the brainstem. If a nerve on the arm or the leg is stimulated by a small electrical current applied to the overlying skin, it is called the Somatosensory Evoked Potential (SSEP). If, however, the retina is stimulated by means of flicker light or a sudden change in a checkerboard pattern, the evoked potential thus recorded over the corresponding cortical area is called the Visual Evoked Potential (VEP). Evoked potentials are used both as a diagnostic tool and as a monitoring technique. As diagnostic tests, evoked potentials are useful to evaluate neurologic disorders such as: a) multiple sclerosis, b) acoustic nerve tumors, and c) optic neuritis. As a monitoring modality, evoked potentials are used during all surgical procedures, which might compromise part of the brain or the spinal cord.
 ...
PMID:Cerebral monitoring in the operating room and the intensive care unit - an introductory for the clinician and a guide for the novice wanting to open a window to the brain. Part II: Sensory-evoked potentials (SSEP, AEP, VEP). 1616 23