Effect of nitric oxide on spinal evoked potentials and survival rate in rats with decompression sickness.

Nitric oxide (NO) releasing agents have, in experimental settings, been shown to decrease intravascular nitrogen bubble formation and to increase the survival rate during decompression sickness (DCS) from diving. The effect has been ascribed to a possible removal of preexisting micronuclei or an increased nitrogen washout on decompression through augmented blood flow rate. The present experiments were conducted to investigate whether a short- or long-acting NO donor [glycerol trinitrate (GTN) or isosorbide-5-mononitrate (ISMN), respectively] would offer the same protection against spinal cord DCS evaluated by means of spinal evoked potentials (SEPs). Anesthetized rats were decompressed from a 1-h hyperbaric air dive at 506.6 kPa (40 m of seawater) for 3 min and 17 s, and spinal cord conduction was studied by measurements of SEPs. Histological samples of the spinal cord were analyzed for lesions of DCS. In total, 58 rats were divided into 6 different treatment groups. The first three received either saline (group 1), 300 mg/kg iv ISMN (group 2), or 10 mg/kg ip GTN (group 3) before compression. The last three received either 300 mg/kg iv ISMN (group 4), 1 mg/kg iv GTN (group 5), or 75 µg/kg iv GTN (group 6) during the dive, before decompression. In all groups, decompression caused considerable intravascular bubble formation. The ISMN groups showed no difference compared with the control group, whereas the GTN groups showed a tendency toward faster SEP disappearance and shorter survival times. In conclusion, neither a short- nor long-acting NO donor had any protective effect against fatal DCS by intravenous bubble formation. This effect is most likely due to a fast ascent rate overriding the protective effects of NO, rather than the total inert tissue gas load.

Effect of oxygen breathing and perfluorocarbon emulsion treatment on air bubbles in adipose tissue during decompression sickness.

Decompression sickness (DCS) after air diving has been treated with success by means of combined normobaric oxygen breathing and intravascular perfluorocarbon (PFC) emulsions causing increased survival rate and faster bubble clearance from the intravascular compartment. The beneficial PFC effect has been explained by the increased transport capacity of oxygen and inert gases in blood. However, previous reports have shown that extravascular bubbles in lipid tissue of rats suffering from DCS will initially grow during oxygen breathing at normobaric conditions. We hypothesize that the combined effect of normobaric oxygen breathing and intravascular PFC infusion could lead to either enhanced extravascular bubble growth on decompression due to the increased oxygen supply, or that PFC infusion could lead to faster bubble elimination due to the increased solubility and transport capacity in blood for nitrogen causing faster nitrogen tissue desaturation. In anesthetized rats decompressed from a 60-min hyperbaric exposure breathing air at 385 kPa, we visually followed the resolution of micro-air bubbles injected into abdominal adipose tissue while the rats breathed either air, oxygen, or oxygen breathing combined with PFC infusion. All bubble observations were done at 101.3 kPa pressure. During oxygen breathing with or without combined PFC infusion, bubbles disappeared faster compared with air breathing. Combined oxygen breathing and PFC infusion caused faster bubble disappearance compared with oxygen breathing. The combined effect of oxygen breathing and PFC infusion neither prevented nor increased transient bubble growth time, rate, or growth ratio compared with oxygen breathing alone. We conclude that oxygen breathing in combination with PFC infusion causes faster bubble disappearance and does not exacerbate transient bubble growth. PFC infusion may be a valuable adjunct therapy during the first-aid treatment of DCS at normobaric conditions.

Effect of oxygen and heliox breathing on air bubbles in adipose tissue during 25-kPa altitude exposures.

At altitude, bubbles are known to form and grow in blood and tissues causing altitude decompression sickness. Previous reports indicate that treatment of decompression sickness by means of oxygen breathing at altitude may cause unwanted bubble growth. In this report we visually followed the in vivo changes of micro air bubbles injected into adipose tissue of anesthetized rats at 101.3 kPa (sea level) after which they were decompressed from 101.3 kPa to and held at 25 kPa (10,350 m), during breathing of oxygen or a heliox(34:66) mixture (34% helium and 66% oxygen). Furthermore, bubbles were studied during oxygen breathing preceded by a 3-h period of preoxygenation to eliminate tissue nitrogen before decompression. During oxygen breathing, bubbles grew from 11 to 198 min (mean: 121 min, +/-SD 53.4) after which they remained stable or began to shrink slowly. During heliox breathing bubbles grew from 30 to 130 min (mean: 67 min, +/-SD 31.0) from which point they stabilized or shrank slowly. No bubbles disappeared during either oxygen or heliox breathing. Preoxygenation followed by continuous oxygen breathing at altitude caused most bubbles to grow from 19 to 179 min (mean: 51 min, +/-SD 47.7) after which they started shrinking or remained stable throughout the observation period. Bubble growth time was significantly longer during oxygen breathing compared with heliox breathing and preoxygenated animals. Significantly more bubbles disappeared in preoxygenated animals compared with oxygen and heliox breathing. Preoxygenation enhanced bubble disappearance compared with oxygen and heliox breathing but did not prevent bubble growth. The results indicate that oxygen breathing at 25 kPa promotes air bubble growth in adipose tissue regardless of the tissue nitrogen pressure.