The life-saving effect of hyperbaric oxygenation during early-phase severe blunt chest injuries.

The effect of hyperbaric oxygenation (HBO2) on survival during the early phase of severe blunt chest injury (BChI) has not been elucidated. Our aim was to investigate this effect on human victims of BChI. We monitored cardiac index (CI), stroke volume index (SVI), PaO2 and PaO2/FiO2 in 18 victims treated conventionally, and 8 victims treated under combined conventional and HBO2 treatment. Out of the 18 victims, 4 survived (Group A) and 14 died (Group B). Another 8 victims, in Group C, received HBO, and all survived. Human victims showed marked reductions in all cardiorespiratory values during the first 24 h. Group B persistently tended towards a decrease in SVI, PaO2/FiO2 and PaO2, eventually reaching fatal levels. The survivors developed a cardiorespiratory function characterized by a tendency towards recovery of all monitored parameters, more notable in Group C, which showed an earlier and more significant normalization vs. Group A (P<0.01). Our clinical data suggest that the earliest possible HBO2 treatment after severe blunt trauma can significantly enhance victims' survival.

Relationship between intracranial pressure and cortical spreading depression following fluid percussion brain injury in rats.

Traumatic brain injury (TBI) is known to be accompanied by an increase in intracranial pressure (ICP) and in some cases, by spontaneous generation of cortical spreading depression (CSD) cycles. However, the role of CSD in the pathophysiology of cerebral contusion is still unknown. A multiparametric monitoring assembly was placed on the right hemisphere of the rat brain to evaluate ICP, DC potential, extracellular K(+), cerebral blood flow (CBF), and electrocorticogram in 27 rats during 5 h. Fluid percussion brain injury (FPBI) with the magnitude of the impact 2.9, 3.3, 4.1, and 5.0 atmospheres was induced to the left parietal cortex in animal groups A, B, C, and D, respectively. A slow increase in ICP was evident, and was pronounced in group C and especially in group D, where four of nine animals died during the monitoring. At the end of the 5 h experiment, the mean ICP levels were 6.75 +/- 2.87, 8.40 +/- 2.70, 12.75 +/- 4.03, 29.56 +/- 9.25, and the mean total number of CSD cycles was 2.00 +/- 1.41, 4.29 +/- 4.23, 11.71 +/- 13.29, and 20.11 +/- 19.26 in groups A, B, C, and D, respectively. The maximal level of intensity of CSD cycle generation after FPBI was obtained in group D, where almost constant activity was maintained until the end of the experiment. A significant coefficient of correlation between ICP level and total number of CSD cycles was found for all ICP measurements (r = 0.47-0.63, p < 0.05, n = 27), however more significant (p < 0.001) was the coefficient during the period of monitoring between 2 and 4 h after FPBI. Our results suggest that numerous repeating CSD cycles are typical phenomena in moderate and especially severe forms of FPBI. The rising number of CSD cycles under condition of an ICP level >/=20 mm Hg may demonstrate, with high probability, the unfavorable development of TBI, caused by growing secondary hypoxic insult.

Hyperbaric oxygenation affects rat brain function after carbon monoxide exposure.

The application of hyperbaric oxygenation (HBO2) has been recommended for correction of neurological injury in severely CO-poisoned patients. However, the mechanisms of HBO2 action on brain mitochondrial function under the circumstances is not yet understood completely. In the present study, the effect of HBO2 on the rat brain after CO exposure was evaluated by measuring the intramitochondrial NADH and its responses to anoxic test or repetitive induction spreading depression (SD) leading to brain activation. A unique monitoring system for bilateral monitoring of brain NADH redox state was used. Rats were exposed to 3000 ppm CO for 30 (group A) or 60 min (C). In groups B and D, after CO exposure, the rats were exposed to HBO2 (3 atm abs for 30 min). Following CO exposure in groups A and C, a definite decrease in the amplitude of the NADH response and significant increase in the number of waves of NADH was noted during induced cortical SD. Anoxic test in these two groups led to a significant decrease of maximum levels of NADH (reduction) at the end of observation. The amplitude, and the number of SD waves and magnitude of NADH deviation during anoxic test in group B after application of HBO2, was not significantly different from the values measured under the initial conditions. However, in group D, tendency of maintenance of the parameter's initial level was weaker or absent. The results obtained indicated that suppression of brain energy metabolism is a characteristic manifestation of CO poisoning in rats. Restoration of cerebral energy metabolism by adequate dosage of HBO2 may become an important factor for recovery of brain activities after CO poisoning.

Physiologic and biochemical monitoring during hyperbaric oxygenation: a review.

Hyperbaric oxygenation (HBO2) is an important treatment given to various groups of patients exposed to pathologic situations (i.e., carbon monoxide exposure). Since many hyperbaric patients are critically ill and are being treated for life-threatening disorders, it is necessary to monitor various physiologic and biochemical parameters. This is a review of 193 publications covering a wide range of monitored parameters representing metabolic, hemodynamic, respiratory, electrical, and biochemical activities. The significance of monitoring the physiologic, medical, and specific oxygen toxicity effects during HBO2 exposure (MHBO2) is described and emphasized. Further development of new monitoring devices and technologies will enable the improvement of patient management during HBO2 treatment given under various medical conditions. This review also presents new ideas about possible future monitoring of brain function under HBO2 conditions in experimental animals as well as under clinical conditions.

Effects of carbon monoxide on the brain may be mediated by nitric oxide.

Carbon monoxide (CO) is known to be a toxic molecule due to the high affinity of hemoglobin for it. However, it has recently been shown that low doses of CO may play a physiological role. The aim of the present study was to examine processes occurring in the brain during exposure to 1,000 parts per million CO that result in an increase in cerebral blood flow (CBF) but are not accompanied by changes in oxidation metabolism. This study was carried out in awake rats with the multiprobe assembly developed in this laboratory for the simultaneous continuous measurement of CBF, intramitochondrial NADH redox levels, direct current potential, and extracellular concentrations of K+, Ca2+, and H+ as well as the electrocorticogram. Exposure to 1,000 parts per million CO in air resulted in an increased CBF without any concomitant changes in any of the other metabolic or ionic parameters measured. This indicates that tissue hypoxia was not the trigger for this vasodilation. Injection of N omega-nitro-L-arginine (L-NNA), a nitric oxide synthase inhibitor, before exposure to CO effectively blocked the increase in CBF that was observed when the animal was exposed to CO without prior injection of L-NNA. Furthermore, electrocorticographic depression was observed after the combined treatment of L-NNA and CO. In conclusion, exposure to relatively low doses of CO apparently does not have a deleterious effect on oxidative metabolism because the increase in CBF after this exposure is sufficient to prevent changes in oxidative metabolism, as indicated by the fact that NADH levels remained constant. This protective autoregulatory effect may be mediated by nitric oxide.

Multiparametric monitoring of the awake brain exposed to carbon monoxide.

We have applied in vivo real-time techniques to monitor the physiological changes associated with exposure to a pattern of carbon monoxide (CO) known to cause brain oxidative stress. Using a multiparametric monitoring device connected to the brain, we exposed unanesthetized rats to two levels of CO, 0.1 and 0.3% in air. Energy metabolism was evaluated by the optical monitoring of relative cerebral blood flow (CBF) and intramitochondrial redox state. Ionic homeostasis was assessed by measurements of K+,Ca2+, and H+ or Na+ levels in the extracellular space. The electrical parameters monitored were the electrocorticogram and direct current steady potential. Under 1,000 ppm of CO, the CBF was increased significantly without any measurable change in the NADH redox state, suggesting that the cause for the increased CBF was not hypoxia. Exposing the awake rat to 1,000 ppm of CO (40 min) followed by 3,000 ppm of CO (20 min) led to an increase in CBF followed by episodes of spontaneous brain depolarizations characterized by changes in ionic homeostasis and blood flow. These changes were similar to those recorded under cortical spreading depression. In most animals exposed to 3,000 ppm of CO, spontaneous oscillations in CBF and NADH redox state that were negatively correlated were recorded. The results indicate that an inspired CO level of 0.1% had effects largely restricted to blood flow, whereas at a higher CO level an additional impairment in energy supply resulted in a complex pattern of effects similar to that caused by brain ischemia.