Susan R. Kayar

Pharmacological Interventions to Decompression Sickness in Rats : Comparison of Five Agents

INTRODUCTION This research investigated whether decompression sickness (DCS) risk or severity could be reduced using drug interventions that are easier to implement and equal to or more efficacious than recompression therapy. METHODS Using a rat model of DCS, anti-inflammatory or anticoagulant drugs, including lidocaine, aspirin (ASA), methylprednisolone (MP), alpha-phenyl-N-butylnitrone (PBN), and transsodium crocetinate (TSC) were tested to determine their effect on incidence of DCS, death, and time of symptom onset. Each treatment group consisted of approximately 40 animals that received the drug and approximately 40 controls. Animals were exposed to one of five compression and decompression profiles with pressure ranging from 6.3 ATA (175 fsw) to 8.0 ATA (231 fsw); bottom time was either 60 or 90 min; and decompression rate was either 1.8 or 15 ATA x min(-1). Following decompression, the rats were observed for 30 min while walking on a wheel. DCS was defined as an ambulatory deficit or abnormal breathing. RESULTS None of the drugs reached statistical significance for all DCS manifestations. Lidocaine post-dive and MP were the only treatments with marginally (P < 0.15) significant differences in DCS outcomes compared to controls. Lidocaine post-dive significantly decreased the incidence of neurological DCS from 73-51%. MP significantly extended the time of onset of death from DCS from 5.4 min to 7.1 min. DISCUSSION Of the treatments investigated, lidocaine given post-dive has the best chance of success in adjuvant therapy of DCS. Future studies might investigate adjuvant drugs given in combination or during recompression.

METABOLISM AND THERMOREGULATION IN GUINEA PIGS IN HYPERBARIC HYDROGEN : EFFECTS OF PRESSURE

Abstract 1. 1. To analyze the effects of pressure and gas composition on thermoregulation, guinea pigs were exposed to 10–60 atm breathing O2 and H2 (hydrox), O2 and He (heliox), or O2, N2 and He (N2-trimix), at 26–36°C. 2. 2. There were significant differences (P 3. 3. There was a significant correlation (P

Probabilistic Modelling for Estimating Gas Kinetics and Decompression Sickness Risk in Pigs During H2 Biochemical Decompression

We modelled the kinetics of H2 flux during gas uptake and elimination in conscious pigs exposed to hyperbaric H2. The model used a physiological description of gas flux fitted to the observed decompression sickness (DCS) incidence in two groups of pigs: untreated controls, and animals that had received intestinal injections of H2-metabolizing microbes that biochemically eliminated some of the H2 stored in the pigs’ tissues. To analyse H2 flux during gas uptake, animals were compressed in a dry chamber to 24 atm (ca 88% H2, 9% He, 2% O2, 1% N2) for 30–1440 min and decompressed at 0.9 atm min−1 (n = 70). To analyse H2 flux during gas elimination, animals were compressed to 24 atm for 3 h and decompressed at 0.45–1.8 atm min1(n = 58). Animals were closely monitored for 1 h post-decompression for signs of DCS. Probabilistic modelling was used to estimate that the exponential time constant during H2 uptake (τin) and H2 elimination (τout) were 79 ± 25 min and 0.76 ± 0.14 min, respectively. Thus, the gas kinetics affecting DCS risk appeared to be substantially faster for elimination than uptake, which is contrary to customary assumptions of gas uptake and elimination kinetic symmetry. We discuss the possible reasons for this asymmetry, and why absolute values of H2 kinetics cannot be obtained with this approach.

On beginning a second century of decompression sickness research: where are we and what comes next?

It is just 100 years since the publication of J. S. Haldanes groundbreaking work on the prevention of decompression sickness (DCS). While we still do not know the exact mechanisms that underlie DCS, probabilistic modeling now allows good estimation of risk for a given set of conditions, although reduction of risk to zero remains impractical. Unfortunately, individual monitoring for intravascular bubbles has not proven a good predictor of symptomatic DCS. Current research aims to identify underlying biological factors that, once understood, may allow development of preventive measures and treatment that go beyond recompression. With one or more drugs to combat DCS, we should be able to eliminate the residual risk, extend dive profiles beyond current limits, and rescue people who have exceeded the limits and taken a hit.