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Biomedical subjects

R D Vann

Publications and source records attributed to R D Vann.

16 recordsLinked to original sources

Ascent rate, post-dive exercise, and decompression sickness in the rat.

The effects of ascent rate and post-dive exercise on the incidence of decompression sickness (DCS) were investigated in six groups of 20 rats exposed for 2 h at a pressure equivalent to 240 feet of sea water (fsw; 735 kPa). Ascent rates were 30, 45, and 60 fsw/min (92, 138, 184 kPa/min), and the rats either rested after the exposure or exercised by walking for 30 min on a treadmill at 1.6 m/min. Post-dive signs included respiratory distress, difficulty walking, paralysis, and death. DCS was scored as non-fatal at 30-min post-dive or fatal at any time. Analysis by ordinal logistic regression indicated more DCS with post-dive exercise (P = 0.0112) and at 45 (P = 0.0011) and 60 fsw/min (P = 0.0001) compared to 30 fsw/min. Survival analysis suggested earlier death at 60 fsw/min compared to 30 fsw/min (P = 0.0006). Similar effects have been reported for the less severe DCS that occurs in humans.

Animals

Patency and blood flow in gas denucleated arterial prostheses.

Biomaterials exposed to blood often fail due to thrombosis. Gas nuclei (air) in the material are thrombogenic and a potential cause of failure. The effects of gas nuclei on patency and blood flow were studied in 4 mm diameter arterial grafts (Gore ePTFE; Johnson and Johnson Vitagraft ePTFE; Bard ACG EXS) in the femoropopliteal position of dogs. Control and denucleated (air-free) grafts were implanted bilaterally. Grafts were denucleated by immersion in degassed saline and exposure to 4 torr vacuum and 3,000-20,000 psig pressure. Graft patency was determined at harvest in 46 dogs. Blood flow was measured with acoustic flow probes in eight dogs. Denucleated graft patency was 60% after 2 days of implant while control patency was 22% (P < .05). Measured blood flow was higher in denucleated grafts than in control grafts (P < .02) in 4 of 5 dogs which had significantly different flows. Patency and flow decreased to zero for both control and denucleated grafts over periods of up to 80 days. Air in the control grafts may have been absorbed within several days, leading to late similarity with the denucleated grafts. Thus, removing the air from 4 mm ePTFE grafts decreased acute thrombosis and increased the patency.

Animals

Flying after diving and decompression sickness.

Reports of 1,159 decompression sickness (DCS) incidents during recreational diving were analyzed by logistic regression for the effects of flying on the occurrence of Type II DCS, complete relief of symptoms after one recompression, and residual symptoms 3 months after treatment. The relevant diver populations were those who: 1) did not fly; 2) had symptoms before flying but flew anyhow; 3) and did not have symptoms before flying but developed symptoms during or after flight. Of the total DCS population, 13.9% had preflight symptoms while 5.6% developed symptoms during or after flight. Symptoms which occurred during or after flight were no more serious and their responses to recompression no less successful than symptoms in nonflying divers. There was a statistically significant association between divers who flew with pre-existing symptoms and Type II DCS, incomplete relief with one recompression, and residual symptoms after 3 months.

Adult

Absence of intravascular bubble nucleation in dead rats.

Bubble formation in the inferior vena cavae (IVC) of dead rats was investigated after 6-15-h exposures to air at 123 atm abs (12.5 MPa) and decompression to 1 atm abs at 13.6 atm/min (1.4 MPa/min). The maximum estimated air-supersaturation attained in the IVCs after decompression was 6.1-18.3 atm (0.6-1.8 MPa). Bubbles were detected by light microscopy, buoyancy, and underwater dissection. No bubbles formed in 42 blood-filled IVCs that were isolated from the circulation by ligatures, but bubbles were always observed in unisolated IVCs (P < 0.000005). Other isolated IVCs were filled with tap water, water and bubbles, or water and iron filings. Bubbles formed in 13% of the IVCs filled with tap water, in 16% of the IVCs containing water with preexisting bubbles, and in 80% of the IVCs containing water with iron filings. Results indicate that at the air supersaturations attained in the isolated IVCs a) blood is resistant to de novo bubble formation; b) preexisting bubbles are dissolved by compression; c) bubbles in water originate from preexisting gas nuclei; and d) iron filings harbor gas nuclei that are able to survive 122 atm (12.4 MPa) overpressures and form bubbles on subsequent decompression.

Air

Quantification of gas denucleation and thrombogenicity of vascular grafts.

In vitro methods were developed to measure the air content of vascular graft walls and the thrombogenicity of this air. Gas content (volume %) of expanded polytetrafluoroethylene (ePTFE) grafts from different sources ranged from 75.5 +/- 0.4% to 61.8 +/- 0.3%. Exposure of Vitagraft ePTFE to a vacuum prior to saline immersion replaced 87.5% of the gas nuclei with saline (denucleation). Acetone and ethanol immersion produced 98.9% and 94.3% denucleation, respectively. Denucleation was essentially complete when vacuum exposure was followed by hydrostatic pressure treatment at 500 psig or greater. The influence of gas content on thrombogenicity was determined by immersing graft samples in whole canine blood and weighing the adherent thrombus. Denucleation significantly reduced adherent thrombus weight compared with control grafts (p less than 0.001). Air in Vitagraft walls was responsible for 84% of the adherent thrombus weight at four minutes. The described methods could be employed to assess the hemocompatibility of various biomaterials.

Adhesiveness

Venous gas emboli and complement activation after deep repetitive air diving.

Complement activity has been linked to decompression sickness (DCS), but the effects of intravascular bubbles on complement activation are poorly understood. We have investigated intravascular complement activation by measuring red blood cell (RBC)-bound C3d after repetitive air diving in man. Subjects were exposed to a single, 20 min, 170 fsw (feet of sea water) dive, or to 2 such dives with a 6-h surface interval. Doppler monitoring for venous gas emboli was performed postdive. Predive blood samples were studied to determine sensitivity of complement to activation by air bubbles. Other predive and postdive venous samples were evaluated for intravascular complement activation. No cases of DCS occurred in 39 dives. Baseline complement sensitivity appeared normally distributed, thus "sensitive" and "insensitive" subjects were not clearly distinguishable. RBC-bound C3d did not increase after 1 dive but did increase after the repetitive dive (P less than 0.05). Furthermore, maximum bubble grade was independent of complement activation.

Adult

Hydrostatic pressure reduces thrombogenicity of polytetrafluoroethylene vascular grafts.

A prime factor in the thrombogenicity of synthetic materials in contact with blood is the blood-gas interface. Small pockets of gas, known as gas nuclei, are trapped within surface interstices. The resulting blood-gas interface denatures plasma proteins and activates clotting factors and platelets. Expanded polytetrafluoroethylene (ePTFE) vascular prostheses 1 mm in internal diameter were placed in saline under 6,000 psig hydrostatic pressure for 2 h in an attempt to dissolve all gas nuclei (i.e., to denucleate). Carotid-carotid bypasses were performed in rats using 280-mm lengths of ePTFE. All 10 control grafts lost patency in 5 min, whereas the 14 denucleated grafts had a median patency duration of 300 min (P less than 0.01). In 15-mm-long rat femoral artery interpositional ePTFE grafts, 90% of controls thrombosed within 10 min, whereas only 7% of denucleated grafts thrombosed over the duration of the 7-day observation period (P less than 0.001). Denucleation also resulted in a significant reduction (P less than 0.02) in 111In-labeled platelet adhesion to 36% of control. Scanning electron microscopy confirmed the reduced accumulation of platelets on denucleated grafts. These data suggest that the removal of trapped air with hydrostatic pressure significantly reduces the thrombogenicity of ePTFE microvascular prostheses and may have application to other clinical (catheters, valves, tubing, etc.) or experimental (micropipettes, electrodes, etc.) materials that interface with blood.

Animals

Mammary implants, diving, and altitude exposure.

Mammary implants were exposed to various simulated dive profiles followed by altitude exposures to stimulate aircraft travel and then were observed for bubble formation and volume changes. Minimal volume changes occurred after each dive. Numerous bubbles formed, however, reaching their maximum size in 3 hours. By comparison, when implants were exposed to high altitude following a dive exposure, significant volume changes occurred. This in vitro study showed that bubble formation and volume expansion occur after exposing implants to diving and altitude, but the circumstances required to produce these changes in vivo are extremely unlikely to occur normally.

Altitude

Effects of microgravity on tissue perfusion and the efficacy of astronaut denitrogenation for EVA.

The prevention of astronaut decompression sickness (DCS) during extravehicular activity (EVA) from the Shuttle Orbiter entails basic questions about how the efficacies of pre-EVA denitrogenations are affected by physiological responses and adaptations to microgravity. Many of these questions may be answered, without requiring inflight decompression experiments, when suitable inflight measurements of N2 elimination from spacecrew breathing 100% O2 can be analyzed using an N2 elimination/DCS risk correlation which has been calibrated in ground-based studies. In order to pursue this approach in our laboratory, a potentially flight-applicable, breath-by-breath method for measuring N2 elimination from human subjects breathing 100% O2 for 2-3-h periods has been developed. The present report describes this development with particular emphasis on required methodological accuracy and its achievement in view of certain properties of mass spectrometer performance. A method for the breath-by-breath analysis of errors in measured N2 elimination profiles is also described.

Adaptation, Physiological

A likelihood analysis of experiments to test altitude decompression protocols for shuttle operations.

The principle of maximum likelihood and the method of linear regression both are used to fit mathematical models to experimental data, but likelihood can be applied to binary data such as the outcome of a decompression, whereas linear regression cannot. Maximum likelihood was applied to 548 individual altitude exposures from 30 experimental pressure profiles tested by NASA and the Air Force. Twelve decompression models were studied including modified Haldane models and models which assume that stationary bubbles cause Type I decompression sickness. The data was best represented by a model in which a bubble in tissue is surrounded by a diffusion barrier, but this representation was statistically indistinguishable from a single tissue Haldane model with a halftime of 508 min. By providing a quantitative measure of the agreement between theory and data, the principle of maximum likelihood offers an opportunity for improving the understanding of decompression mechanisms and for developing safer and faster decompression procedures.

Altitude

Air and nitrox saturation decompression: a report of 4 schedules and 77 subjects.

Seventy-seven subjects were decompressed from air or nitrogen-oxygen (nitrox) saturation exposures at 18.3 to 40.2 meters sea water (msw) [60 to 132 feet sea water (fsw)] using four different decompression schedules. A h schedule for decompression from an air saturation-excursion profile at 18.3 msw (60 fsw) resulted in pain-only decompression sickness (DCS) symptoms in 2 of 23 subjects. A 32 and 35 h schedule from a different air saturation profile at 19.8 and 22.9 msw (65 and 75 fsw), respectively, resulted in DCS symptoms in 1 of 24 subjects. A third and fourth schedule for air or nitrox saturation at 40.2 msw (132 fsw) resulted in DCS symptoms in 3 of 12 and 1 of 18, respectively. No serious (type II) symptoms were observed as a result of any of the decompressions. All DCS cases consisted of knee pain occurring either in the last 3 msw of the decompression or shortly after surfacing. Doppler ultrasound monitoring revealed venous gas emboli (VGE) in several subjects, but generally only shallow to 6.1 msw (20 fsw). Results demonstrate an overall DCS incidence of 9%, and all cases were pain-only and localized to the knee. The third schedule (U.S. Navy heliox saturation decompression schedule) seems to produce a higher incidence of DCS than the other schedules when used in air or nitrox exposures. Differentiation between the schedules designed for nitrox was impossible due to the limited number of subjects in each and the variable nature of the exposures.

Adult

A theoretical method for selecting space craft and space suit atmospheres.

A theoretical method for selecting space craft and space suit atmospheres assumes that gas bubbles cause decompression sickness and that the risk increases when a critical bubble volume is exceeded. The method is consistent with empirical decompression exposures for humans under conditions of nitrogen equilibrium between the lungs and tissues. Space station atmospheres are selected so that flight crews may decompress immediately from sea level to station pressure without preoxygenation. Bubbles form as a result of this decompression but are less than the critical volume. The bubbles are absorbed during an equilibration period after which immediate transition to suit pressure is possible. Exercise after decompression and incomplete nitrogen equilibrium are shown to increase bubble size, and limit the usefulness of one previously tested stage decompression procedure for the Shuttle. The method might be helpful for evaluating decompression procedures before testing.

Decompression Sickness

Decompression induced nitrogen elimination.

A method for measuring nitrogen elimination after air diving has been developed in which a subject breathes air instead of oxygen or helium-oxygen. Accuracy is improved with this method because only nitrogen absorbed during the dive is eliminated. Nitrogen stored in the lungs and tissues at sea level is unaffected. Measurements were made with a closed-circuit breathing apparatus using a spirometer as a counterlung. The oxygen partial pressure in the apparatus was controlled at 0.209 +/- 0.003 atm. The spirometer volume was recorded periodically with the subject holding his breath at functional residual capacity. Increases in spirometer volume were used to define a nitrogen elimination curve. Elimination measurements were made after resting and exercising dives to 60, 100, and 130 fsw (2.8, 4.0, and 4.9 atm) at the U.S. Navy no-decompression exposure limits. Exercise during a dive increased the volume of nitrogen eliminated after the dive, but results for both resting and exercising divers were variable. Possible causes of this variability include bubble formation and changes in blood flow.

Adult

Decompression from a deep nitrogen/oxygen saturation dive--a case report.

Ten divers participated in a 4.5 d nitrogen/oxygen saturation dive to 165 fsw. There were daily 2 h excursions to 61 msw (200 fsw). The divers breathed air during the excursions and 0.51 bar (0.5 atm) oxygen in nitrogen at 50.3 msw (165 fsw). The final decompression began 6 h after the last excursion. The oxygen partial pressure was 0.51 bar (0.5 atm) from 50.3 to 13.7 msw (165 to 45 fsw), and air was used from 13.7 msw (45 fsw) to the surface. By 6.1 msw (20 fsw), four divers had developed decompression sickness. A fifth diver developed decompression sickness during a commercial air flight 68 h after surfacing. Comparison of ascent rates for this dive and for air or nitrogen/oxygen saturation dives reported in the literature suggests that deeper dives require slower rates of ascent. Dives shallower than 30.5 msw (100 fsw) had a mean ascent rate of 1 msw/h (3.2 fsw/h) and 14 decompression incidents in 107 man-exposures. Dives deeper than 30.5 msw (100 fsw) had a mean rate of 0.76 msw/h (2.5 fsw/h) and 14 incidents in 45 man-exposures.

Adaptation, Physiological

Evidence for gas nuclei in decompressed rats.

In vitro and in vivo studies have shown that pressure treatment before decompression reduces bubble formation. This has been interpreted as evidence that bubbles originate from pre-existing gas nuclei. The present experiments were conducted to determine if pressure treatment during air or liquid breathing before a 2-h air dive would reduce the decompression sickness (DCS) indicence for rats. Control dives, preceded by liquid breathing with 17 and 24 rats to 135- and 150-fsw had DCS incidences of 35% and 29%. Liquid-breathing pressure treatment at 1347 fsw before 135 fsw dive (11 rats) or at 1796 fsw before the 150-fsw dive (24 rats) reduced the incidences to 0% and 8%. In the air-breathing experiments, a 240-fsw control dive with 200 rats gave an 83% incidence. Pressure treatment at 600 fsw (195 rats) or 100 fsw (153 rats) reduced the DCS incidence to 74% and 64%. These experiments suggest that the bubbles responsible for DCS in the rat originate from gas nuclei.

Air