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Biomedical subjects

Edward D Thalmann

Publications and source records attributed to Edward D Thalmann.

3 recordsLinked to original sources

Cerebral blood flow and brain oxygenation in rats breathing oxygen under pressure.

Hyperbaric oxygen (HBO(2)) increases oxygen tension (PO(2)) in blood but reduces blood flow by means of O(2)-induced vasoconstriction. Here we report the first quantitative evaluation of these opposing effects on tissue PO(2) in brain, using anesthetized rats exposed to HBO(2) at 2 to 6 atmospheres absolute (ATA). We assessed the contribution of regional cerebral blood flow (rCBF) to brain PO(2) as inspired PO(2) (PiO(2)) exceeds 1 ATA. We measured rCBF and local PO(2) simultaneously in striatum using collocated platinum electrodes. Cerebral blood flow was computed from H(2) clearance curves in vivo and PO(2) from electrodes calibrated in vitro, before and after insertion. Arterial PCO(2) was controlled, and body temperature, blood pressure, and EEG were monitored. Scatter plots of rCBF versus PO(2) were nonlinear (R(2)=0.75) for rats breathing room air but nearly linear (R(2)=0.88-0.91) for O(2) at 2 to 6 ATA. The contribution of rCBF to brain PO(2) was estimated at constant inspired PO(2), by increasing rCBF with acetazolamide (AZA) or decreasing it with N-nitro-L-arginine methyl ester (L-NAME). At basal rCBF (78 mL/100 g min), local PO(2) increased 7- to 33-fold at 2 to 6 ATA, compared with room air. A doubling of rCBF increased striatal PO(2) not quite two-fold in rats breathing room air but 13- to 64-fold in those breathing HBO(2) at 2 to 6 ATA. These findings support our hypothesis that HBO(2) increases PO(2) in brain in direct proportion to rCBF.

Animals↗

Pathology: whales, sonar and decompression sickness.

We do not yet know why whales occasionally strand after sonar has been deployed nearby, but such information is important for both naval undersea activities and the protection of marine mammals. Jepson et al. suggest that a peculiar gas-forming disease afflicting some stranded cetaceans could be a type of decompression sickness (DCS) resulting from exposure to mid-range sonar. However, neither decompression theory nor observation support the existence of a naturally occurring DCS in whales that is characterized by encapsulated, gas-filled cavities in the liver. Although gas-bubble formation may be aggravated by acoustic energy, more rigorous investigation is needed before sonar can be firmly linked to bubble formation in whales.

Acoustic Stimulation↗

Risk of decompression sickness during exposure to high cabin altitude after diving.

BACKGROUND: Postdive altitude exposure increases the risk of decompression sickness (DCS). Certain training and operational situations may require U.S. Special Operations Forces (SOF) personnel to conduct high altitude parachute operations after diving. Problematically, the minimum safe preflight surface intervals (PFSI) between diving and high altitude flying are not known. METHODS: There were 102 healthy, male volunteers (34 +/- 10 [mean +/- SD] yr of age, 84.5 +/- 13.8 kg weight, 26.2 +/- 4.2 kg x m(-2) BMI) who completed simulated 60 fsw (feet of seawater)/60 min air dives preceding simulated 3-h flights at 25,000 ft to study DCS risk as a function of PFSI. Subjects were dry and at rest throughout. Oxygen was breathed for 30 min before and during flight in accordance with SOF protocols. Subjects were monitored for clinical signs of DCS and for venous gas emboli (VGE) using precordial Doppler ultrasound. DCS incidence was compared with Chi-squared; VGE onset time and time to maximum grade with one-way ANOVA (significance at p < 0.05). RESULTS: Three cases of DCS occurred in 155 subject-exposures: 1/35 and 0/24 in 2 and 3 h flight-only controls, respectively; 0/23, 1/37, and 1/36 for 24, 18, and 12 h dive-PFSI-flight profiles, respectively. DCS risk did not differ between profiles (chi2 [4] = 1.33; crit = 9.49). VGE were observed in 19% of flights. Neither VGE onset time nor time to max grade differed between profiles (82 +/- 38 min [p = 0.88] and 100 +/- 40 min [p = 0.68], respectively). CONCLUSION: Increased DCS risk was not detected as a result of dry, resting 60 fsw/60 min air dives conducted 24-12 h before a resting, 3-h oxygen-breathing 25,000 ft flight (following 30 min oxygen prebreathe). The current SOF-prescribed minimum PFSI of 24 h may be unnecessarily conservative.

Adult↗