Cerebral Polyamine Metabolism in Reversible Hypoglycemia of Rat: Relationship to Energy Metabolites and Calcium

Thirty minutes of insulin-induced reversible hypoglycemic coma (defined in terms of cessation of EEG activity) was produced in anesthetized rats. At the end of the hypoglycemic coma or after recovery for 3, 24, or 72 h induced by glucose infusion, the animals were reanesthetized and their brains frozen in situ. Two control groups were used: untreated controls without prior manipulations, and insulin controls, which received injections of insulin followed by glucose infusion to maintain blood glucose within the physiological range. The brains of these latter animals were frozen 3, 24, or 72 h after glucose infusion. Tissue samples from the cortex, striatum, hippocampus, and thalamus were taken to measure ornithine decarboxylase (ODC) activity, and putrescine and spermidine levels, as well as phosphocreatine (PCr), ATP, glucose, and lactate content. In addition, 20-microns thick coronal sections taken from the striatum and dorsal hippocampus were used for histological evaluation of cell damage and also stained for calcium. Insulin in the absence of hypoglycemia produced a significant increase in ODC activity and putrescine level but had no effect on the profiles of energy metabolites or spermidine. During hypoglycemic coma, brain PCr, ATP, glucose, and lactate levels were sharply reduced, as expected. Energy metabolites normalized after 3 h of recovery. In the striatum, significant secondary decreases in PCr and ATP contents and rises in glucose and lactate levels were observed after 24 h of recovery. ODC activity, and putrescine and spermidine levels were unchanged during hypoglycemic coma. After 3 h of recovery, ODC activity increased markedly throughout the brain, except in the striatum. After 24 h of recovery, ODC activity decreased and approached control values 2 days later. Putrescine levels increased significantly throughout the brain after reversible hypoglycemic coma, the highest values observed after 24 h of recovery (p less than or equal to 0.001, compared with controls). After 72 h of recovery, putrescine levels decreased, but still significantly exceeded control values. Reversible hypoglycemic coma did not produce significant changes in regional spermidine levels except in the striatum, where an approximately 30% increase was observed after 3 and 72 h of recovery (p less than or equal to 0.01 and p less than or equal to 0.05, respectively). Twenty-four hours after hypoglycemic coma, intense calcium staining was apparent in layer III of the cerebral cortex, the lateral striatum, and the crest of the dentate gyrus. After 72 h of recovery, the intense calcium staining included also cortical layer II, the septal nuclei, the subiculum, and the hippocampal CA1-subfield.(ABSTRACT TRUNCATED AT 400 WORDS)     

Accidental deep hypothermia with cardiac arrest. Prompt complete recovery after rewarming by extracorporeal circulation. Case report

BACKGROUND: Deep accidental hypothermia (core temperature <28 degrees C) is an uncommon medical emergency requiring rapid active core rewarming. Extracorporeal circulation has become the treatment of choice for deep hypothermic patients with cardiac arrest. CASE REPORT: We report on a 30-year-old patient who suffered from deep accidental hypothermia (core temperature 24.8 degrees C) and cardiac arrest by prolonged exposure to a cold urban environment as a consequence of severe ethylalcohol intoxication. The rewarming with the aid of extracorporeal circulation was initiated shortly after his arrival at the hospital. External cardiac massage was maintained until full ECC fl ow was established. The patient was weaned from extracorporeal circulation after 157 min, awaked 4 hours later and consequently extubated within 16 hours after rewarming with no neurological impairment. At 3-week follow-up, the patient was fully re-integrated in his work and personal life. CONCLUSION: This case demonstrates the excellent prognosis of a young victim in the case of deep accidental hypothermia with cardiac arrest, provided that deep hypothermia precedes the cardiac arrest and rewarming by extracorporeal circulation is immediately applied. Simultaneous ethyl alcohol intoxication can be considered a protective factor improving the patient's outcome. Complete recovery was achieved within 24 hours after the accident.     

Electroencephalographic Prediction of Fatal Anoxic Brain Damage after Resuscitation from Cardiac Arrest

Ninety-three electroencephalograms (E.E.G.s) were recorded within a week of cardiac resuscitation from 41 patients in whom the subsequent outcome was known to be either recovery of cerebral function or death with associated pathological evidence of gross anoxic brain damage. A statistical analysis of observations on these E.E.G.s yielded a discriminant function for predicting death or survival. Predictions based on each of the 93 individual E.E.G.s would have been correct in 92 and at a confidence level better than 99%. The same discriminant function was found to be applicable to a further 19 patients who died but did not undergo neuropathological studies and to 33 others in whom the clinical picture was complicated by such factors as uraemia or head injury. Thus it seems that the presence or absence of fatal brain damage after cardiac arrest can be reliably predicted from E.E.G.s taken within a week of resuscitation. An estimate of the probability of survival is now routinely included in the clinical report on each E.E.G. taken after cardiac arrest.     

Phase Synchronization in Electroencephalographic Recordings Prognosticates Outcome in Paediatric Coma

Brain injury from trauma, cardiac arrest or stroke is the most important cause of death and acquired disability in the paediatric population. Due to the lifetime impact of brain injury, there is a need for methods to stratify patient risk and ultimately predict outcome. Early prognosis is fundamental to the implementation of interventions to improve recovery, but no clinical model as yet exists. Healthy physiology is associated with a relative high variability of physiologic signals in organ systems. This was first evaluated in heart rate variability research. Brain variability can be quantified through electroencephalographic (EEG) phase synchrony. We hypothesised that variability in brain signals from EEG recordings would correlate with patient outcome after brain injury. Lower variability in EEG phase synchronization, would be associated with poor patient prognosis. A retrospective study, spanning 10 years (2000–2010) analysed the scalp EEGs of children aged 1 month to 17 years in coma (Glasgow Coma Scale, GCS, <8) admitted to the paediatric critical care unit (PCCU) following brain injury from TBI, cardiac arrest or stroke. Phase synchrony of the EEGs was evaluated using the Hilbert transform and the variability of the phase synchrony calculated. Outcome was evaluated using the 6 point Paediatric Performance Category Score (PCPC) based on chart review at the time of hospital discharge. Outcome was dichotomized to good outcome (PCPC score 1 to 3) and poor outcome (PCPC score 4 to 6). Children who had a poor outcome following brain injury secondary to cardiac arrest, TBI or stroke, had a higher magnitude of synchrony (R index), a lower spatial complexity of the synchrony patterns and a lower temporal variability of the synchrony index values at 15 Hz when compared to those patients with a good outcome.     

Effects of self poisoning with maprotiline.

Self poisoning with maprotiline was studied in 41 patients (43 episodes) consecutively admitted to an intensive care unit. Thirty five patients had taken more than one drug or alcohol. Fifteen patients were in coma grade III or IV; 17 patients were still not conscious after 24 hours in the intensive care unit. Among six patients given ventilation the mean duration of ventilation in the five who recovered was 36 hours. Three patients had a cardiorespiratory arrest, and one patient died. Twenty eight patients had a QRS interval of 100 ms or more, and 15 patients had seizures. In six patients seizures were precipitated by physostigmine. Cardiotoxicity after overdosage of maprotiline is equal to if not greater than that found after overdosage of conventional tricyclic antidepressants. Overdosage of maprotiline is more often associated with seizures than overdosage with tricyclic antidepressants. Physostigmine further increases the risk of seizures and should not be used in cases of overdosage of maprotiline.     

Survey of 3765 cardiopulmonary resuscitations in British hospitals (the BRESUS Study): methods and overall results.

OBJECTIVE--To determine the circumstances, incidence, and outcome of cardiopulmonary resuscitation in British hospitals. DESIGN--Hospitals registered all cardiopulmonary resuscitation attempts for 12 months or longer and followed survival to one year. SETTING--12 metropolitan, provincial, teaching, and non-teaching hospitals across Britain. SUBJECTS--3765 patients in whom a resuscitation attempt was performed, including 927 in whom the onset of arrest was outside the hospital. MAIN OUTCOME MEASURE--Survival after initial resuscitation, at 24 hours, at discharge from hospital, and at one year, calculated by the life table method. RESULTS--There were 417 known survivors at one year, with 214 lost to follow up. By life table analysis for every eight attempted resuscitations there were three immediate survivors, two at 24 hours, 1.5 leaving hospital alive, and one alive at one year. Survival at one year was 12.5% including out of hospital cases and 15.0% not including these cases. Each hospital year averaged 30 survivors at one year: three who had an arrest outside hospital, seven who had one in the accident and emergency department, seven in the cardiac care unit, 10 in the general wards, and three in other, non-ward areas. Within the hospitals survival rates were best in those who had an arrest in the accident and emergency department, the cardiac care unit, or other specialised units. Outcome varied 12-fold in subgroups defined by age, type of arrest, and place of arrest. CONCLUSION--71% of the mortality at one year in patients undergoing attempted resuscitation occurred during the initial arrest. Hospital resuscitation is life saving and cost effective and warrants appropriate attention, training, coordination, and equipment.     

Examination of Physiological Function and Biochemical Disorders in a Rat Model of Prolonged Asphyxia-Induced Cardiac Arrest followed by Cardio Pulmonary Bypass Resuscitation

Background

Cardiac arrest induces whole body ischemia, which causes damage to multiple organs particularly the heart and the brain. There is clinical and preclinical evidence that neurological injury is responsible for high mortality and morbidity of patients even after successful cardiopulmonary resuscitation. A better understanding of the metabolic alterations in the brain during ischemia will enable the development of better targeted resuscitation protocols that repair the ischemic damage and minimize the additional damage caused by reperfusion.

Method

A validated whole body model of rodent arrest followed by resuscitation was utilized; animals were randomized into three groups: control, 30 minute asphyxial arrest, or 30 minutes asphyxial arrest followed by 60 min cardiopulmonary bypass (CPB) resuscitation. Blood gases and hemodynamics were monitored during the procedures. An untargeted metabolic survey of heart and brain tissues following cardiac arrest and after CPB resuscitation was conducted to better define the alterations associated with each condition.

Results

After 30 min cardiac arrest and 60 min CPB, the rats exhibited no observable brain function and weakened heart function in a physiological assessment. Heart and brain tissues harvested following 30 min ischemia had significant changes in the concentration of metabolites in lipid and carbohydrate metabolism. In addition, the brain had increased lysophospholipid content. CPB resuscitation significantly normalized metabolite concentrations in the heart tissue, but not in the brain tissue.

Conclusion

The observation that metabolic alterations are seen primarily during cardiac arrest suggests that the events of ischemia are the major cause of neurological damage in our rat model of asphyxia-CPB resuscitation. Impaired glycolysis and increased lysophospholipids observed only in the brain suggest that altered energy metabolism and phospholipid degradation may be a central mechanism in unresuscitatable brain damage.     

Brain nuclear DNA survives cardiac arrest and reperfusion.

Iron-mediated peroxidation of brain lipids is known to occur during reperfusion following cardiac arrest. Since in vitro damage to DNA is caused by similar iron-dependent peroxidation, we tested whether free radical damage to genomic DNA also develops during reperfusion following cardiac arrest and resuscitation. Genomic DNA was isolated from the cerebral cortex in (i) normal dogs, (ii) dogs subjected to a 20-min cardiac arrest, and (iii) dogs resuscitated from a 20-min cardiac arrest and then allowed to reperfuse for 2 or 8 h. DNA strand nicks were evaluated by in vitro labeling of newly created 3' and 5' termini. DNA base damage was evaluated utilizing reaction with piperidine prior to labeling of 5' termini. The 3' DNA termini were labeled before and after digestion with exonuclease III, and the 5' DNA termini were labeled before and after treatment with piperidine. In vitro experiments with genomic DNA damaged by oxygen radicals verified that these labeling methods identified radical damage. In the experimental animal groups, terminal incorporation and electrophoretic mobility of brain nuclear DNA are not significantly changed either by 20 min of complete brain ischemia or during the first 8 h of reperfusion. We conclude that genomic DNA is not extensively damaged during cardiac arrest and early reperfusion, and therefore such DNA damage does not appear to be an important early aspect of the neurologic injury that accompanies cardiac arrest and resuscitation.     

Treatment of tyramine-induced brain edema with anion transport inhibitor L-644,711

Tyramine induces coma in phenelzine-treated dogs. Development of coma in these animals is associated with brain edema, abnormal brain scans of Tc-99m-diethylene-triamine-penta-acetic acid (Tc-99m-DTPA), and elevated levels of CSF catecholamines. We found that the intravenous administration of 6-7 mg/kg of a single dose of L-644,711 given fifteen minutes after the oral administration of tyramine to phenelzine-pretreated animals followed by an infusion of normal saline containing 6-7 mg/kg of the drug given over a period of 2 hr caused reversal of brain injury. This was accompanied by full recovery within a period of 24 hr of all the animals tested. A follow-up study revealed that 24 hr after treatment with L-644,711 CSF levels of catecholamines and brain images of Tc-99m-DTPA were indistinguishable from normal controls. Animals that received no drug died from unresolved coma within 4 to 24 hr. Animals that had recovered due to therapy with L-644,711 were given 10-14 days rest followed by a repetition of the phenelzine and tyramine treatment but denied L-644,711 therapy. These animals also died of unresolved coma within 24 hr. This preliminary study suggest that the use of L-644,711 may constitute an important advance in treatment of brain edema of a wide range of neurological disorders.     

Clinical Experiences with Assisted Circulation

Of primary importance in the clinical application of mechanical support for the failing circulation are the selection of patients and definition of criteria for assessing the therapeutic results. Experimental and clinical observations suggest that serial measurements of arteriovenous oxygen difference are a reliable rough measurement of the adequacy of the existing cardiac output to meet the oxygen requirements of the tissues. Patients with a decreasing cardiac output may profit from assisted circulation. Thirteen such patients are presented, all of whom were in intractable heart failure. Seven “medical” patients underwent common femoral vein-to-artery perfusion with an oxygenator for an average of 135 minutes. Of these, one patient who had already had two cardiac arrests died, six patients showed striking clinical and biochemical improvement for hours to days, and two patients were discharged from the hospital. Of particular interest were five in whom the indication for assisted circulation was irreversible cardiac arrest. Three patients were resuscitated, and one, who had neurological signs usually accepted as those of anoxic cerebral damage for 45 minutes, recovered completely.     

Shear Injuries of the Brain

A blow to the head will impart rotational velocity to the brain and, depending on its magnitude, will produce effects ranging from concussion to profound neurological dysfunction. Resultant shear strains distort and rupture axons, blood vessels and major fibre tracts. Thirty-seven patients with head injury that was not complicated by significant hemorrhage or superficial laceration of the brain had coma or severe dementia, spastic quadriparesis, incontinence and autonomic dysfunction. These patients survived 24 hours to 243 days. Gross pathological examination revealed little, but there was microscopic evidence of axonal and small vessel injury in all; this was localized to the basal and midsagittal areas of the diencephalon and mesencephalon, particularly in those less severely injured. Such changes represent the basic pathology of all head injury. Data from this study suggest that concussion depends upon varying degrees of damage to the axon as well as the neuron. The current definition of concussion—immediate loss of consciousness with rapid and complete recovery of cerebral function—should not exclude the fact that a small number of neurons may have been permanently disconnected or have perished.     

Contrast Water Therapy and Exercise Induced Muscle Damage: A Systematic Review and Meta-Analysis

The aim of this systematic review was to examine the effect of Contrast Water Therapy (CWT) on recovery following exercise induced muscle damage. Controlled trials were identified from computerized literature searching and citation tracking performed up to February 2013. Eighteen trials met the inclusion criteria; all had a high risk of bias. Pooled data from 13 studies showed that CWT resulted in significantly greater improvements in muscle soreness at the five follow-up time points (<6, 24, 48, 72 and 96 hours) in comparison to passive recovery. Pooled data also showed that CWT significantly reduced muscle strength loss at each follow-up time (<6, 24, 48, 72 and 96 hours) in comparison to passive recovery. Despite comparing CWT to a large number of other recovery interventions, including cold water immersion, warm water immersion, compression, active recovery and stretching, there was little evidence for a superior treatment intervention. The current evidence base shows that CWT is superior to using passive recovery or rest after exercise; the magnitudes of these effects may be most relevant to an elite sporting population. There seems to be little difference in recovery outcome between CWT and other popular recovery interventions.     

Appraisal of pediatric cardiopulmonary resuscitation.

Sixty-six patients more than 30 days and less thant 16 years of age suffering an unexpected cardiac arrest in an 18-month period were included in a study of resuscitative measures in children. Six children survived to be discharged from hospital. Respiratory disease accounted for most (29%) of the cardiac arrests, but it also had the most favourable prognosis, 21% of the 19 patients surviving. None of the patients survived whose cardiac arrest was secondary to sepsis or trauma, even when the resuscitative efforts were initially successful. Only 1 of the 41 patients who had a cardiac arrest outside of hospital survived, and only 1 of the 34 patients who presented with asystole survived, and then with considerable damage to the central nervous system. The interval between cardiac arrest and application of basic life support was substantially shorter among the survivors. Also, most of the survivors did not present with asystole. The results of this study suggest that survival among resuscitated children is no better than that among adults but can be improved with early recognition and monitoring of children at risk. earlier application of basic and advanced life support, improved education of medical and lay personnel, and further research into pediatric resuscitative techniques.     

Non-heart-beating organ donors as a source of kidneys for transplantation: a chart review

BACKGROUND: Organ transplantation is the treatment of choice for patients with end-stage organ failure, but the supply of organs has not increased to meet demand. This study was undertaken to determine the potential for kidney donation from patients with irremediable brain injuries who do not meet the criteria for brain death and who experience cardiopulmonary arrest after withdrawal of ventilatory support (controlled non-heart-beating organ donors). METHODS: The charts of 209 patients who died during 1995 in the Emergency Department and the intensive care unit at the Foothills Hospital in Calgary were reviewed. The records of patients who met the criteria for controlled non-heart-beating organ donation were studied in detail. The main outcome measure was the time from discontinuation of ventilation until cardiopulmonary arrest. RESULTS: Seventeen potential controlled non-heart-beating organ donors were identified. Their mean age was 62 (standard deviation 19) years. Twelve of the patients (71%) had had a cerebrovascular accident, and more than half (10 [59%]) did not meet the criteria for brain death because one or more brain stem reflexes were present. At the time of withdrawal of ventilatory support, the mean serum creatinine level was 71 (29) mumol/L, mean urine output was 214 (178) mL/h, and 9 (53%) patients were receiving inotropic agents. The mean time from withdrawal of ventilatory support to cardiac arrest was 2.3 (5.0) hours; 13 of the 17 patients died within 1 hour, and all but one died within 6 hours. For the year for which charts were reviewed, 33 potential conventional donors (people whose hearts were beating) were identified, of whom 21 (64%) became donors. On the assumption that 40% of the potential controlled non-heart-beating donors would not in fact have been donors (25% because of family refusal and 15% because of nonviability of the organs), there might have been 10 additional donors, which would have increased the supply of cadaveric kidneys for transplantation by 48%. INTERPRETATION: A significant number of viable kidneys could be retrieved and transplanted if eligibility for kidney donation was extended to include controlled non-heart-beating organ donors.     

Pyruvate stabilizes electrocardiographic and hemodynamic function in pigs recovering from cardiac arrest

Cardiac electromechanical dysfunction may compromise recovery of patients who are initially resuscitated from cardiac arrest, and effective treatments remain elusive. Pyruvate, a natural intermediary metabolite, energy substrate, and antioxidant, has been found to protect the heart from ischemia-reperfusion injury. This study tested the hypothesis that pyruvate-enriched resuscitation restores hemodynamic, metabolic, and electrolyte homeostasis following cardiac arrest. Forty-two Yorkshire swine underwent pacing-induced ventricular fibrillation and, after 6 min pre-intervention arrest, 4 min precordial compressions followed by transthoracic countershocks. After defibrillation and recovery of spontaneous circulation, the pigs were monitored for another 4 h. Sodium pyruvate or NaCl were infused i.v. (0.1 mmol·kg⁻¹·min⁻¹) throughout precordial compressions and the first 60 min recovery. In 8 of the 24 NaCl-infused swine, the first countershock converted ventricular fibrillation to pulseless electrical activity unresponsive to subsequent countershocks, but only 1 of 18 pyruvate-treated swine developed pulseless electrical activity (relative risk 0.17; 95% confidence interval 0.13–0.22). Pyruvate treatment also lowered the dosage of vasoconstrictor phenylephrine required to maintain systemic arterial pressure at 15–60 min recovery, hastened clearance of excess glucose, elevated arterial bicarbonate, and raised arterial pH; these statistically significant effects persisted up to 3 h after sodium pyruvate infusion, while infusion-induced hypernatremia subsided. These results demonstrate that pyruvate-enriched resuscitation achieves electrocardiographic and hemodynamic stability in swine during the initial recovery from cardiac arrest. Such metabolically based treatment may offer an effective strategy to support cardiac electromechanical recovery immediately after cardiac arrest.     

Efficacy of lower limb compression and combined treatment of manual massage and lower limb compression on symptoms of exercise-induced muscle damage in women

Strategies to manage the symptoms of exercise-induced muscle damage (EIMD) are widespread, though are often based on anecdotal evidence. The aim of this study was to determine the efficacy of a combination of manual massage and compressive clothing and compressive clothing individually as recovery strategies after muscle damage. Thirty-two female volunteers completed 100 plyometric drop jumps and were randomly assigned to a passive recovery (n = 17), combined treatment (n = 7), or compression treatment group (n = 8). Indices of muscle damage (perceived soreness, creatine kinase activity, isokinetic muscle strength, squat jump, and countermovement jump performance) were assessed immediately before and after 1, 24, 48, 72, and 96 hours of plyometric exercise. The compression treatment group wore compressive tights for 12 hours after damage and the combined treatment group received a 30-minute massage immediately after damaging exercise and wore compression stockings for the following 11.5 hours. Plyometric exercise had a significant effect on all indices of muscle damage (p < 0.05). The treatments significantly reduced decrements in isokinetic muscle strength, squat jump performance, and countermovement jump performance and reduced the level of perceived soreness in comparison with the passive recovery group (p < 0.05). The addition of sports massage to compression after muscle damage did not improve performance recovery, with recovery trends being similar in both treatment groups. The treatment combination of massage and compression significantly moderated perceived soreness at 48 and 72 hours after plyometric exercise (p < 0.05) in comparison with the passive recovery or compression alone treatment. The results indicate that the use of lower limb compression and a combined treatment of manual massage with lower limb compression are effective recovery strategies following EIMD. Minimal performance differences between treatments were observed, although the combination treatment may be beneficial in controlling perceived soreness.     

Is Neuronal Injury Caused by Hypoglycemic Coma of the Necrotic or Apoptotic Type?

In this study, we explored if a 30 minute period of hypoglycemic coma yields damage which shows some features associated with apoptosis. To that end, we induced insulin-hypoglycemic coma of 30 min duration, and studied brain tissues after the coma period, and after recovery period of 30 min, 3 h, and 6 h. Histopathological data confirmed neuronal damage in all of the vulnerable neuronal populations. Release of cytochrome c (cyt c), assessed by Western Blot, was observed in the neocortex and caudoputamen after 3 and 6 h of recovery. In these regions, the caspase-like activity increased above control after 6 h of recovery. By laser-scanning confocal microscopy, a clear expression of Bax was observed after 30 min of coma in the superficial layers of the neocortex, reaching a peak after 30 min of recovery. Punctuate immunolabeling surrounding nuclei in soma and dendrites in cortical pyramidal neurons likely represents mitochondria, which suggests that Bax protein assembled at the surface of mitochondria in vulnerable neocortical neurons. It is concluded that although previous morphological data have suggested that cells die by necrosis, neuronal damage after hypoglycemic coma shows some features of apoptosis.     

Parasympathetic nervous activity mirrors recovery status in weightlifting performance after training

Heart rate variability (HRV) and parasympathetic power are closely related to the well-being and health status in humans. The main goal of the study was to determine whether these measures can reflect recovery status after weight training. After a 10-day detraining period, 7 weightlifters were challenged with a 2-hour weight training which elicited approximately fourfold increases in circulating muscle creatine kinase level and protracted pain feeling (p < 0.05). Weightlifting performance was then evaluated 3, 24, 48, and 72 hours after training to determine the degree of recovery from fatigue. Heart rate variability, circulating dehydroepiandrostendione sulfate (DHEA-S), and muscle damage markers were measured before each performance test. An electrocardiogram was recorded for 5 minutes continuously at rest in seated positions. After training, weightlifting performance of the subjects decreased below baseline in paralleled with suppressed parasympathetic power (high-frequency [HF] HRV), whereas sympathetic power (normalized low-frequency HRV) was slightly elevated at 3 hours of recovery (p < 0.05). Both weightlifting performances and parasympathetic power returned to baseline values in 24 hours and further increased above baseline during 48-72 hours of recovery in a similar fashion (p < 0.05). Circulating DHEA-S level dropped at 24 hours (p < 0.05) and returned to normal values by 48 hours. Muscle pain increased at 3 hours after training and remained higher than baseline values for the 72-hour recovery period (p < 0.05). Our data suggest that parasympathetic power, indicated by HF HRV, is able to reflect the recovery status of weightlifters after training.     

Prevention of post-ischemic brain lipid conjugated diene production and neurological injury by hydroxyethyl starch-conjugated deferoxamine.

Hydroxyethyl starch conjugated deferoxamine (DFO) was administered to rats following resuscitation from 6.5 min cardiac arrest (CA) in an attempt to prevent the iron-catalyzed production of oxygen free radicals which may lead to neurologic injury and ultimately death following restoration of spontaneous circulation (ROSC). Brain conjugated dienes were analyzed spectrophotometrically 4 and 24 hr following ROSC, and were found to be significantly elevated when compared to non-ischemic controls. Hydroxyethyl starch-DFO treated rats demonstrated no increased conjugated diene production at either period. Neurologic injury was significantly less in drug treated rats surviving 24 or 72 hours when compared to controls. While mortality was similar in drug treated or control rats for the first 24 hours following ROSC, delayed mortality (days 1-10) was significantly less in drug treated animals, presumably as a result of neurologic protection afforded by post-ischemic drug administration. Administration of DFO conjugated to hydroxyethyl starch appears to modulate the neurologic injury which occurs during brain ischemia and reperfusion.     

Recover of peripheral nerve function after prolong hypothermic cardiac arrest in a porcine model with extra corporeal life support

ObjectivesSurviving long lasting cardiac arrest following accidental hypothermia has been reported after treatment with extra corporeal life support (ECLS), but there is a risk of neurologic injury. Most surviving hypothermia patients have a prolonged stay in the intensive care unit, where most patients experience polyneuropathy. Theoretically, accidental hypothermic cardiac arrest may in itself contribute to polyneuropathy. This study was designed to examine the impact of three hours of cardiac arrest at a core temperature of 20 °C followed by reanimation of peripheral nerve function.MethodsSeven pigs were cannulated for ECLS and cooled to a core temperature of 20 °C followed by three hours of circulatory arrest where the extremities were packed with ice. After three hours, ECLS was started and rewarming was performed. During the process, neural testing of the ulnar nerve (a somatic nerve) and of the vagus nerve (an autonomic nerve) were performed and blood was drawn for analysis of p-potassium, serum-neuron-specific enolase, and S100b protein.ResultsThe ulnar nerve was cooled from 34.9±1.6 °C to 12.8±3.8 °C and the vagus nerve from 36.2±1.2 °C to 15.4±1.4 °C. Physiologic function of both somatic and autonomic nerves were strongly affected by cooling, but recovered to almost normal levels during rewarming, even after three hours of hypothermic cardiac arrest. P-potassium rose from 3.9 (3.6–4.6) mmol/l to 8.1 (7.2–9.1) mmol/l after three hours of cardiac arrest, but normalized after recirculation. There was no rise in serum-neuron-specific enolase, but a slight rise in S100b protein during three hours of hypothermic cardiac arrest was observed. All pigs obtained return of spontaneous circulation (ROSC).ConclusionsReanimation after three hours of hypothermic cardiac arrest using ECLS was possible with no or, if present, minor damage to the two nerves tested.