Cardiovascular parameters in a mixed-sex swine study of severe decompression sickness treated with the emulsified perfluorocarbon Oxycyte.

Intravenous perfluorocarbons (PFC) have reduced the effects of decompression sickness (DCS) and improved mortality rates in animal models. However, concerns for the physiological effects of DCS combined with PFC therapy have not been examined in a balanced mixed-sex population. Thirty-two (16 male, 16 female) instrumented and sedated juvenile Yorkshire swine were exposed to 200 feet of seawater (fsw) for 31 min of hyperbaric air. Pulmonary artery pressure (PAP), cardiac output (CO), and systemic arterial pressure (SAP) were monitored before (control) and after exposure. Animals were randomized to treatment with Oxycyte (5 ml/kg; Oxygen Biotherapeutics, Inc., Morrisville, NC) vs. saline (control) with 100% oxygen administered upon DCS onset; animals were observed for 90 min. Parameters recorded and analyzed included PAP, CO, and SAP. In all animals PAP began to rise prior to cutis marmorata (CM) onset, the first sign of clinical DCS, generally peaking after CM onset. Female swine, compared with castrated males, had a more rapid onset of CM (7.30 vs. 11.46 min postsurfacing) and earlier onset to maximal PAP (6.41 vs. 9.69 min post-CM onset). Oxycyte therapy was associated with a sustained PAP elevation above controls in both sexes (33.41 vs. 25.78 mmHg). Significant pattern differences in PAP, CO, and SAP were noted between sexes and between therapeutic groups. There were no statistically significant differences in survival or paralysis between the PFC and control groups during the 48-h observation period. In conclusion, Oxycyte therapy for DCS is associated with a prolonged PAP increase in swine. These species and sex differences warrant further exploration.

The emulsified perfluorocarbon Oxycyte improves spinal cord injury in a swine model of decompression sickness.

STUDY DESIGN: A prospective, animal model for pharmacological intervention of decompression sickness (DCS), including spinal cord (SC) injury. BACKGROUND: Signs and symptoms of DCS can include joint pain, skin discoloration, cardiopulmonary congestion and SC injury; severity ranges from trivial to fatal. Non-recompressive therapy for DCS may improve time-to-treatment and therefore impact mortality and morbidity. OBJECTIVES: Oxycyte at 5 cc kg(-1) provides both SC protection and statistically significant survival benefit in a swine model of DCS. The purpose of this study was to test whether a reduced dose of Oxycyte (3 cc kg(-1)) would provide similar benefit. SETTING: Silver Spring, MD, USA METHODS: Male Yorkshire swine (N=50) underwent a non-linear compression profile to 200 fsw (feet of sea water), which was identical to previous work using the 5 cc kg(-1) dose of Oxycyte. After 31 min of bottom time, decompression was initiated at 30 fsw per minute until surface pressure was reached. Following decompression and the onset of DCS, intravenous Oxycyte or saline was administered with concurrent 100% O(2) for 1 h. The primary end point was DCS-induced mortality, with Tarlov score and SC histopathology as secondary end points. RESULTS: Oxycyte administration of 3 cc kg(-1) following surfacing produced no significant detectable survival benefit. Animals that received Oxycyte, however, had reduced SC lesion area. CONCLUSION: Further studies to determine the lowest fully efficacious dose of Oxycyte for the adjunct treatment of DCS are warranted.

Short oxygen prebreathe periods reduce or prevent severe decompression sickness in a 70-kg swine saturation model.

Disabled submarine (DISSUB) survivors are expected to achieve saturation with inert gas. However, rescue procedures may not accommodate staged decompression, raising the potential for severe decompression sickness (DCS). Alternatives to standard recompression therapy are needed. It has been demonstrated in humans that isobaric oxygen "prebreathing" (OPB) can accelerate decompression in a DISSUB scenario. In-70 kg swine saturated at 2.82 atm absolute (ATA), 1 h of OPB eliminated death and reduced severe DCS. We hypothesized that even shorter periods (<1 h) of OPB before no-stop decompression from saturation at 2.82 ATA could reduce the incidence of DCS in a large animal model. Catheterized Yorkshire swine (68.8 +/- 1.7 kg) in individual Plexiglas boxes within a large animal hyperbaric chamber were compressed to 2.82 ATA for 22 h. Following saturation and while still at depth, breathing gas was switched to >95% O(2) for 45 min (OPB(45)), 15 min (OPB(15)), or 5 min (OPB(05)) of OPB, or no OPB (control). The chamber was then decompressed without stops (0.91 ATA/min). Observers then entered the chamber and recorded signs of DCS for 2 h. All OPB periods significantly reduced the risk of developing type II DCS. OPB(45) eliminated severe DCS. Controls had a 2.5 times greater risk of developing type II DCS than OPB(05) (P = 0.016). OPB(45) and OPB(15) significantly reduced type I DCS compared with controls. These results support the potential of OPB as an alternative to staged decompression and that OPB could be expected to improve outcome in a DISSUB rescue scenario.