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Biomedical subjects

E T Flynn

Publications and source records attributed to E T Flynn.

At least 19 recordsLinked to original sources
PubMed1992

Effects of an increased PO2 during recompression therapy for the treatment of experimental cerebral arterial gas embolism.

In this study we investigated the efficacy of an initial compression to 6 atm abs on a 53% nitrogen:47% oxygen mixture (PO2 = 2.8 atm abs) before breathing oxygen at 2.8 and 1.9 atm abs for the treatment of feline cerebral arterial gas embolism. Neurophysiologic function was determined by measuring the cortical somatosensory evoked potential (SEP) amplitude in anesthetized ventilated cats. Air was infused into the carotid artery until the SEP amplitude was reduced to less than 10% of baseline values. The animals were randomly separated into 3 groups. The first group (CONTROL) (n = 7) served as control and remained at the surface, breathing air. The second group (NITROX) (n = 10) was compressed to 6 atm abs breathing a 53:47% nitrox mixture for 30 min followed by breathing 100% oxygen at 2.8 and 1.9 atm abs. The third group (HBO) (n = 10) was compressed to 2.8 and 1.9 atm abs breathing 100% oxygen. Air infusion suppressed the SEP amplitude to the same level in all groups. The CONTROL group recovered 27.6 +/- 31.2% (mean +/- standard deviation) of the baseline SEP amplitude, whereas the NITROX group recovered 63.2 +/- 28.2%, and the HBO group recovered 66.0 +/- 19.3%. An analysis of variance with repeated measures revealed that both treatment profiles promote significant (P = 0.03) recovery of the SEP amplitude compared to no treatment. We find no additional benefit, however, by initiating treatment at 6 atm abs, even when additional oxygen is provided.

Analysis of Variance↗
PubMed1992

Management of herniated intervertebral disks during saturation dives: a case report.

During research saturation dives at 5.0 and 5.5 atm abs, 2 divers developed an acute herniation of the nucleus pulposus of the L5-S1 intervertebral disk. In both cases the pain was severe enough to require intravenous morphine or intramuscular meperidine. Although the symptoms presented by these divers are frequently considered to be an indication for immediate surgical consultation, we decided that emergency decompression posed an unacceptable risk that decompression sickness (DCS) would develop in the region of acute inflammation. In both cases strict bedrest and medical therapy were performed at depth. In the first case, 12 h was spent at depth before initiating a standard U.S. Navy saturation decompression schedule with the chamber partial pressure of oxygen elevated to 0.50 atm abs. In the second case, a conservative He-N2-O2 trimix decompression schedule was followed to the surface. In both cases, no initial upward excursion was performed. The required decompression time was 57 h 24 min from 5.5 atm abs and 55 h 38 min from 5.0 atm abs. During the course of decompression, the first diver's neurologic exam improved and he required decreasing amounts of intravenous narcotic; we considered both to be evidence against DCS. The second diver continued to have pain and muscle spasm throughout decompression, however he did not develop motor, reflex, or sphincter abnormalities. Both divers have responded well to nonsurgical therapy.

Adult↗
PubMed1992

Comparison of two recompression profiles in treating experimental cerebral air embolism.

The standard treatment for cerebral arterial gas embolism (CAGE) is an initial recompression to 6 atm abs on air for 30 min followed by oxygen breathing at 2.8 and 1.9 atm abs. It has been suggested that initial recompression to 2.8 atm abs on O2 may be as beneficial, thus avoiding potential treatment complications associated with the deeper depth. To test this hypothesis, we measured the recovery of the somatosensory evoked potential (SEP) following air embolism in anesthetized, ventilated cats. Air was infused into the carotid artery in increments of 0.08 ml until the SEP amplitude was reduced to less than 10% of the baseline value for 15 min. Three groups were studied. A control group (n = 10) received no further treatment after SEP suppression. The second group (6 atm abs/HBO] (n = 8) was compressed to 6 atm abs on air for 30 min followed by O2 breathing at 2.8 atm abs for 100 min. The third group (HBO) (n = 8) was compressed to 2.8 atm abs on O2 for 130 min. The control group recovered 28.8 +/- 18.2% (mean +/- SD) of the baseline amplitude, whereas the 6 atm abs/HBO group recovered 48.6 +/- 22.6%, and the HBO group recovered 62.0 +/- 20.3%. An analysis of variance revealed that only the HBO group had significantly (P less than 0.01) better recovery than the control group. There was no significant difference in SEP recovery between the 2 treatment groups. These results suggest that treating CAGE at 2.8 atm abs with O2 is a viable alternative to the current therapy.

Animals↗
PubMed1991

Cerebral air embolism treated by pressure and hyperbaric oxygen.

We used pressure and hyperbaric oxygen to treat 2 patients with cerebral air embolism, occurring as the result of invasive medical procedures, and neither suffered any permanent damage detectable by clinical examination and MRI. This outcome contrasts with reports of infarct and disability among untreated victims of air embolism.

Adult↗
PubMed1990

Bubble-induced dysfunction in acute spinal cord decompression sickness.

Five anesthetized dogs undertook a chamber dive, on air, to 300 feet of seawater for 15 min. After the dive, spinal cord decompression sickness was detected by recording a reduced amplitude of the somatosensory evoked potential compared with predive base-line values. After the diagnosis of decompression sickness and rapid perfusion fixation of the animal, the spinal cord was removed and examined histologically. Numerous space-occupying lesions (SOL) that disrupted the tissue architecture were found in each cord, mainly in the white matter. The size and distribution of the SOL were determined using computerized morphometry. Although SOL occupied less than 0.5% of the white matter volume, we tested a number of algorithms to assess whether the SOL may have been directly involved in the loss of spinal cord function that followed the dive. We determined that the loss of somatosensory evoked potential amplitude may be attributed to the SOL if 30-100% of the spinal cord fibers that they displaced were rendered nonconducting. A number of possible mechanisms by which SOL may interfere with spinal nerve conduction are discussed.

Animals↗
PubMed1990

Response of antioxidant enzymes to intermittent and continuous hyperbaric oxygen.

Rats and guinea pigs were exposed to O2 at 2.8 ATA (HBO) delivered either continuously or intermittently (repeated cycles of 10 min of 100% O2 followed by 2.5 min of air). The O2 time required to produce convulsions and death was increased significantly in both species by intermittency. To determine whether changes in brain and lung superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSHPx) correlated with the observed tolerance, enzyme activities were measured after short or long HBO exposures. For each exposure duration, one group received continuous and one intermittent HBO; O2 times were matched. HBO had marked effects on these enzymes: lung SOD increased (guinea pigs 47%, rats 88%) and CAT and GSHPx activities decreased (33%) in brain and lung. No differences were seen in lung GSHPx or brain CAT in rats or brain SOD in either species. In guinea pigs, but less so in rats, the observed changes in activity were usually modulated by intermittency. Increases in hematocrit, organ protein, and lung DNA, which may also reflect ongoing oxidative damage, were also slowed with intermittency in guinea pigs. Intermittency benefited both species by postponing gross symptoms of toxicity, but its modulation of changes in enzyme activities and other biochemical variables was more pronounced in guinea pigs than in rats, suggesting that there are additional mechanisms for tolerance.

Animals↗
PubMed1990

Atmosphere contamination following repainting of a human hyperbaric chamber complex.

The Naval Medical Research Institute currently conducts hyperbaric research in a Man-Rated Chamber Complex (MRCC) originally installed in 1977. Significant engineering alterations to the MRCC and rusting of some of its interior sections necessitated repainting, which was completed in 1988. Great care was taken in selecting an appropriate paint (polyamide epoxy) and in ensuring correct application and curing procedures. Only very low levels of hydrocarbons were found in the MRCC atmosphere before initial pressurization after painting and curing. After pressurization, however, significant chemical contamination was found. The primary contaminants were aromatic hydrocarbons: xylenes (which were a major component of both the primer and topcoat paint) and ethyl benzene. The role that pressure played in stimulating off-gassing from the paint is not clear; the off-gassing rate was observed to be similar over a large range in chamber pressures from 1.6 to 31.0 atm abs. Scrubbing the chamber atmosphere with the chemical absorbent Purafil was effective in removing the contaminants. Contamination has been observed to slowly decline with chamber use and is expected to continue to improve with time. However, this contamination experience emphasizes the need for a high precision gas analysis program at any diving facility to ensure the safety of the breathing gas and chamber atmosphere.

Air Pollutants↗
PubMed1990

Treatment of experimental cerebral air embolism with lidocaine and hyperbaric oxygen.

Experiments were performed to assess the combined therapeutic effects of hyperbaric oxygen (HBO) and i.v. lidocaine on neural function after ischemia induced by cerebral air embolism in anesthetized cats. Neural function was determined by measuring the somatosensory evoked potential (SEP) amplitude. Air was infused into the carotid artery in increments of 0.08 ml to maintain the SEP amplitude at 10% or less of baseline values for 15 min. Three groups were studied. A control group (n = 9) received no further treatment after SEP suppression. An HBO group (n = 8) was treated with oxygen at 2.8 atm abs for 130 min. A third group (n = 8) received an i.v. lidocaine infusion in addition to HBO. Air infusion suppressed the SEP amplitude to the same level in all groups. The control group recovered 27.4 +/- 5.5% (mean +/- SEM) of the baseline SEP amplitude, whereas the HBO group recovered 62.0% +/- 7.2%, and the HBO plus lidocaine group recovered 75.3 +/- 5.7%. The results show that both HBO and the combination of HBO and lidocaine promote a significant recovery of the SEP amplitude compared to no treatment. However, lidocaine therapy adds no benefit to HBO therapy alone.

Analysis of Variance↗
PubMed1989

Effect of lidocaine after experimental cerebral ischemia induced by air embolism.

To investigate possible approaches to the treatment of neural damage induced by air embolism and other forms of acute cerebral ischemia, somatosensory evoked potentials (SEP's) were measured after cerebral air embolism in the anesthetized cat. Air was introduced into the carotid artery in increments of 0.08 ml until the SEP amplitude was reduced to approximately 10% or less of baseline values. Either a saline or lidocaine infusion was begun 5 minutes after inducing cerebral ischemia. In the saline-treated group, SEP amplitude was reduced to 6.7% +/- 1.6% (mean +/- standard error of the mean) of baseline, with a return to 32.6% +/- 4.7% of baseline over a 2-hour period. In the lidocaine-treated group, SEP amplitude was reduced to 5.9% +/- 1.5%, with a return to 77.3% +/- 6.2% over a 2-hour period. The results suggest that lidocaine administration facilitates the return of neural function after acute cerebral ischemia induced by air embolism.

Animals↗
PubMed1988

Is there a role for the autochthonous bubble in the pathogenesis of spinal cord decompression sickness?

Histological examination by light and electron microscopy of the spinal cords of four dogs rapidly perfusion-fixed after the onset of decompression sickness revealed the presence of numerous non-staining, space-occupying lesions that were absent in similarly prepared sections of control or ischemic spinal cords. We propose the hypothesis that these lesions are caused by the liberation of a gas phase. The possible significance of these lesions in the evolution of spinal cord dysfunction is discussed with reference to the principal theories of the pathogenesis of spinal cord decompression sickness.

Animals↗
PubMed1988

Central nervous system decompression sickness: latency of 1070 human cases.

Many aspects of central nervous system (CNS) decompression sickness (DCS) are poorly understood, including the temporal pattern of its presentation and the pathogenic mechanisms involved in the development of the disease. Using case histories and clinical series published in the literature and retrieved from treatment center records, this study is an attempt to define the interval between surfacing from a hyperbaric exposure and the onset of symptoms of CNS DCS. The results of 1070 cases of human CNS DCS were included in the study. The results show that the disease generally occurs rapidly: over 50% became symptomatic within 10 min of returning to 1 ATA, and in only 15% of cases was the onset of symptoms delayed for more than 1 h. Cerebral DCS had a more rapid onset than spinal cord disease: 50% of cerebral cases became apparent within about 3 min and a similar proportion of spinal cord cases within about 9 min from surfacing. The influence of these results on the diagnosis and treatment of dysbaric illness, on the safety of certain diving practices, and on possible pathogenic mechanisms is discussed.

Central Nervous System Diseases↗
PubMed1988

Experimental determination of latency, severity, and outcome in CNS decompression sickness.

Twenty-eight dogs underwent a 300 fsw chamber dive designed to generate spinal cord decompression sickness (DCS), which was detected by observing a reduction in the amplitude of the spinal somatosensory evoked potential (SEP). After an interval of 15 min on the surface following diagnosis, the animals received a therapeutic recompression. The latency was defined as the time between surfacing from the dive and the diagnosis of DCS, the severity as the minimum SEP amplitude, and the outcome as the amplitude of the SEP after 2 h of treatment. Significant correlations between latency and severity (P less than 0.05), latency and outcome (P less than 0.01), and severity and outcome (P less than 0.05) were found. Canine spinal cord latency is shown to be very similar to that found in man up to a surface interval of 30 min. The association between latency, severity, and outcome of spinal cord DCS is discussed with reference to the possible mechanisms involved in this disease.

Adrenal Cortex Hormones↗
PubMed1987

Tracheal pressure and impedance as determinants of gas exchange during high frequency ventilation.

This work explores the use of catheter pressure transducers to measure time averaged, mean squared pressure (MSP) in the trachea of anesthetized animals during high frequency ventilation using a prototype Emerson oscillator with a 25 ml stroke volume at 15 and 34 Hz. Tidal volume and MSP were varied by shunting a portion of the ventilator output for the study of the effect of driving pressure on ventilation. A given level of ventilation was accomplished at a lower driving pressure at the lower frequency. Both ventilation as assessed by a modified nitrogen washout procedure and gas exchange were related to MSP and oscillatory frequency by the substitution of MSP/Z2 for alveolar ventilation in the equations of Jaeger et al. (1984). The technique and equations describing it were validated by the prediction of impedance changes resulting from shifts in oscillatory frequency. The calculated impedances matched experimentally measured values found in dogs by other investigators. Catheter pressure transducers are thus shown to be a useful tool for quantifying high frequency ventilation when coupled with a knowledge of respiratory impedance. The technique offers advantages over existing techniques, the most notable being ease of use due to the catheters' exceptional frequency response.

Animals↗
PubMed1987

An analysis of decrements in vital capacity as an index of pulmonary oxygen toxicity.

Decrements in vital capacity (% delta VC) were proposed by the Pennsylvania group in the early 1970s as an index of O2-induced lung damage. These workers used the combined effects of PO2 and time of exposure to develop recommendations to limit expected % delta VC. Adopting this general approach, we fitted human pulmonary O2 toxicity data to the hyperbolic equation % delta VC = Bs.(PO2 - B1).(time)B3 using a nonlinear least squares analysis. In addition to the data considered in 1970, our analysis included new data available from the literature. The best fit was obtained when 1) an individual slope parameter, Bs, was estimated for each subject instead of an average slope; 2) PO2 asymptote B1 = 0.38 ATA; and 3) exponent B3 = 1.0. Wide individual variation imposed large uncertainty on any % delta VC prediction. A 12-h exposure to a PO2 of 1 ATA would be expected to yield a median VC decrement of 4%. The 80% confidence limits, however, included changes from +1.0 and -12% delta VC. Until an improved index of pulmonary O2 toxicity is developed, a simplified expression % delta VC = -0.011.(PO2 - 0.5).time (PO2 in ATA and time in min) can be used to predict a median response with little loss in predictability. The limitations of changes in VC as an index are discussed.

Humans↗
PubMed1987

Role of oxygen in the production of human decompression sickness.

In the calculation of decompression schedules, it is commonly assumed that only the inert gas needs to be considered; all inspired O2 is ignored. Animal experiments have shown that high O2 can increase risk of serious decompression sickness (DCS). A trial was performed to assess the relative risks of O2 and N2 in human no-decompression dives. Controlled dives (477) of 30- to 240-min duration were performed with subjects breathing mixtures with low (0.21-0.38 ATA) or high (1.0-1.5 ATA) Po2. Depths were chosen by a sequential dose-response format. Only 11 cases of DCS and 18 cases of marginal symptoms were recorded despite exceeding the presently accepted no-decompression limits by greater than 20%. Analysis by maximum likelihood showed a shallow dose-response curve for increasing depth. O2 was estimated to have zero influence on DCS risk, although data variability still allows a slight chance that O2 could be 40% as effective as N2 in producing a risk of DCS. Consideration of only inert gases is thus justified in calculating human decompression tables.

Decompression Sickness↗
PubMed1987

Hormonal changes during decompression sickness.

Changes in plasma hormone levels were studied in anesthetized dogs during decompression sickness. Hormone levels were measured in 4 groups: control (no dive, n = 9); air group (air dive, ventilated with air postdive, n = 6); helium-oxygen (He-O2) group (air dive, ventilation changed to He-O2 at 30 min postdive, n = 9); nonsurvivor group (air dive, died within 30 min postdive, n = 9). Dived animals were subjected to repetitive dives until pulmonary artery pressure doubled. Plasma epinephrine (Epi) and norepinephrine (NE) concentrations rapidly increased postdive in all animals. Serum angiotensin-converting enzyme (ACE) activity increased postdive in the He-O2 group only, and these increases were small. Diving did not alter serum concentrations of cortisol, thyroxine (T4), or triiodothyronine (T3); however, T4 and T3 fell in all animals, probably as a consequence of anesthesia. He-O2 breathing did not affect concentrations of Epi, NE, cortisol, T4, T3, or serum ACE activity.

Animals↗
PubMed1987

Effects of He-O2 breathing during experimental decompression sickness following air dives.

The effects of ventilation with He-O2 during decompression sickness (DCS) and venous air embolism were studied. Fifteen anesthetized dogs were mechanically ventilated and subjected to repeated air dives until pulmonary artery pressure at least doubled within 10 min postdive. At 30 min postdive, ventilation was either continued with air (controls, n = 7) or changed to He-O2 (n = 8) for an additional 90 min. All animals developed pulmonary hypertension, systemic hypotension, hemoconcentration, hypoxemia, hypercarbia, and pulmonary edema. Breathing air or He-O2 postdive did not alter these responses, but He-O2 breathing produced an 11% increase in pulmonary vascular resistance (PVR). In 3 other anesthetized dogs that were not subjected to dives, ventilation was changed to He-O2 at various times during an intravenous infusion of air; He-O2 breathing caused a 22% increase in PVR. We conclude that breathing He-O2 during DCS resulting from air dive can intensify pulmonary vascular obstruction.

Animals↗