Analysis of the Increase of Vascular Cell Adhesion Molecule-1 (VCAM-1) Expression and the Effect of Exposure in a Hyperbaric Chamber on VCAM-1 in Human Blood Serum: A Cross-Sectional Study

Background and Objectives: Vascular cell adhesion molecule-1 (VCAM-1) was identified as a cell adhesion molecule that helps to regulate inflammation-associated vascular adhesion and the transendothelial migration of leukocytes, such as macrophages and T cells. VCAM-1 is expressed by the vascular system and can be induced by reactive oxygen species, interleukin 1 beta (IL-1β) or tumor necrosis factor alpha (TNFα), which are produced by many cell types. The newest data suggest that VCAM-1 is associated with the progression of numerous immunological disorders, such as rheumatoid arthritis, asthma, transplant rejection and cancer. The aim of this study was to analyze the increase in VCAM-1 expression and the impact of exposure in a hyperbaric chamber to VCAM-1 levels in human blood serum. Materials and Methods: The study included 92 volunteers. Blood for the tests was taken in the morning, from the basilic vein of fasting individuals, in accordance with the applicable procedure for blood collection for morphological tests. In both groups of volunteers, blood was collected before and after exposure, in heparinized tubes to obtain plasma and hemolysate, and in clot tubes to obtain serum. The level of VCAM-1 was determined using the immunoenzymatic ELISA method. Results: The study showed that the difference between the distribution of VCAM-1 before and after exposure corresponding to diving at a depth of 30 m was at the limit of statistical significance in the divers group and that, in most people, VCAM-1 was higher after exposure. Diving to a greater depth had a much more pronounced impact on changes in VCAM-1 values, as the changes observed in the VCAM-1 level as a result of diving to a depth of 60 m were statistically highly significant (p = 0.0002). The study showed an increase in VCAM-1 in relation to the baseline value, which reached as much as 80%, i.e., VCAM-1 after diving was almost twice as high in some people. There were statistically significant differences between the results obtained after exposure to diving conditions at a depth of 60 m and the values measured for the non-divers group. The leukocyte level increased statistically after exposure to 60 m. In contrast, hemoglobin levels decreased in most divers after exposure to diving at a depth of 30 m (p = 0.0098). Conclusions: Exposure in the hyperbaric chamber had an effect on serum VCAM-1 in the divers group and non-divers group. There is a correlation between the tested morphological parameters and the VCAM-1 level before and after exposure in the divers group and the non-divers group. Exposure may result in activation of the endothelium.

Seizures Caused by Exposure to Hyperbaric Oxygen in Rats Can Be Predicted by Early Changes in Electrodermal Activity

Hyperbaric oxygen (HBO2) is breathed during undersea operations and in hyperbaric medicine. However, breathing HBO2 by divers and patients increases the risk of central nervous system oxygen toxicity (CNS-OT), which ultimately manifests as sympathetic stimulation producing tachycardia and hypertension, hyperventilation, and ultimately generalized seizures and cardiogenic pulmonary edema. In this study, we have tested the hypothesis that changes in electrodermal activity (EDA), a measure of sympathetic nervous system activation, precedes seizures in rats breathing 5 atmospheres absolute (ATA) HBO2. Radio telemetry and a rodent tether apparatus were adapted for use inside a sealed hyperbaric chamber. The tethered rat was free to move inside a ventilated animal chamber that was flushed with air or 100% O2. The animal chamber and hyperbaric chamber (air) were pressurized in parallel at ~1 atmosphere/min. EDA activity was recorded simultaneously with cortical electroencephalogram (EEG) activity, core body temperature, and ambient pressure. We have captured the dynamics of EDA using time-varying spectral analysis of raw EDA (TVSymp), previously developed as a tool for sympathetic tone assessment in humans, adjusted to detect the dynamic changes of EDA in rats that occur prior to onset of CNS-OT seizures. The results show that a significant increase in the amplitude of TVSymp values derived from EDA recordings occurs on average (±SD) 1.9 ± 1.6 min before HBO2-induced seizures. These results, if corroborated in humans, support the use of changes in TVSymp activity as an early “physio-marker” of impending and potentially fatal seizures in divers and patients.

Agreement of rebound and applanation tonometry intraocular pressure measurements during atmospheric pressure change

This study investigated the agreement of intraocular pressure measurements using rebound tonometry and applanation tonometry in response to atmospheric changes in a hyperbaric chamber. Twelve eyes of 12 healthy subjects were included in this prospective, comparative, single-masked study. Intraocular pressure measurements were performed by rebound tonometry followed by applanation tonometry in a multiplace hyperbaric chamber at 1 Bar, followed by 2, 3 and 4 Bar during compression and again at 3 and 2 Bar during decompression. Mean differences between rebound and applanation intraocular pressure measurements were 1.6, 1.7, and 2.1 mmHg at 2, 3, and 4 Bar respectively during compression and 2.6 and 2.2 mmHg at 3 and 2 Bar during decompression. Lower limits of agreement ranged from -3.7 to -5.9 mmHg and upper limits ranged from -0.3 to 1.9 mmHg. Multivariate analysis showed that the differences between rebound and applanation intraocular pressure measurements were independent of atmospheric pressure changes (p = 0.79). Intraocular pressure measured by rebound tonometry shows a systematic difference compared to intraocular measured by applanation tonometry, but this difference is not influenced by changes of atmospheric pressure up to 4 Bar in a hyperbaric chamber. Agreement in magnitude of change between devices suggests rebound tonometry is viable for assessing intraocular pressure during atmospheric changes. Future studies should be designed in consideration of expected differences in IOP values provided by the two devices.

Evaluation and Characteristic of Modified Ventilator Under Hyperbaric Conditions During Volume-controlled Ventilation

Purpose：The stability of the modified ventilator (Shangrila590, Beijing Aeonmed Company, Beijing, China) was evaluated under hyperbaric conditions during volume-controlled ventilation in this study by Michigan test lung (5601i, Grand Rapids, MI, US).Methods：Experiments were performed inside the multiplace hyperbaric chamber at 1.0, 1.5 and 2.0 atmospheres absolute (ATA). The modified ventilator placed inside the hyperbaric chamber was connected to the test lung. During volume-controlled ventilation (VCV), data for the test lung were collected by a personal computer outside the hyperbaric chamber. The preset tide volume (VTset) of the ventilator (400-1000 ml) and the resistance and compliance of the testing lung were adjusted before the experiments at every ambient pressure. With every test setting, the tide volume (VT), inspiratory airway peak pressure (Ppeak) and minute volume (MV) displayed by the ventilator and the test lung were recorded by the computer. We compared the ventilator and test lung data under 1.0, 1.5 and 2.0 ATA to evaluate the stability of the modified ventilator.Results：The variation in VT in the test lung and the ventilator at different ambient pressures changed within a narrow range, and the differences were statistically significant. In every test setting, changes in the MV of the ventilator were limited and acceptable, with significant differences at different ambient pressures. However, Ppeak increased obviously, as detected by the ventilator and test lung at higher ambient pressure during VCV.Conclusions：The modified Shangrila590 ventilator can work well in a hyperbaric chamber. It can provide relatively stable VT and MV during VCV with VTset from 400 ml to 1000 ml when the ambient pressure increases from 1.0 ATA to 2.0 ATA. The raised ambient pressure will lead to increased gas density, which may result in more airway resistance and higher Ppeak during VCV.

Carotid body chemosensitivity is not attenuated during cold water diving

Introduction: Tonic carotid body (CB) activity is reduced during exposure to cold and hyperoxia. We tested the hypotheses that cold water diving lowers CB chemosensitivity and augments CO2 retention more than thermoneutral diving. Methods: Thirteen subjects (age: 26±4 y; BMI: 26±2 kg/m2) completed two, four-hour head out water immersion protocols in a hyperbaric chamber (1.6 ATA) in cold (15°C) and thermoneutral (25°C) water. CB chemosensitivity was assessed using brief hypercapnic ventilatory response (CBCO2) and hypoxic ventilatory response (CBO2) tests pre-dive, 80 and 160 min into the dives (D80 and D160, respectively), immediately following and 60 min post-dive. Data are reported as an absolute mean (SD) change from pre-dive. Results: End-tidal CO2 pressure increased during both the thermoneutral water dive (D160: +2(3) mmHg; p=0.02) and cold water dive (D160: +1(2) mmHg; p=0.03). Ventilationincreased during the cold water dive (D80: 4.13(4.38) and D160: 7.75(5.23) L·min-1; both p<0.01) and was greater than the thermoneutral water dive at both time points (both p<0.01). CBCO2 was unchanged during the dive (p=0.24) and was not different between conditions (p=0.23). CBO2 decreased during the thermonutral water dive (D80: -3.45(3.61) and D160: -2.76(4.04) L·min·mmHg-1; p<0.01 and p=0.03, respectively), but not the cold water dive. However, CBO2 was not different between conditions (p=0.17). Conclusion: CB chemosensitivity was not attenuated during the cold stress diving condition and does not appear to contribute to changes in ventilation or CO2 retention.

Emergency Medicine Cases in Underwater and Hyperbaric Environments: The Use of in situ Simulation as a Learning Technique

IntroductionHyperbaric chambers and underwater environments are challenging and at risk of serious accidents. Personnel aiming to assist patients and subjects should be appropriately trained, and several courses have been established all over the world. In healthcare, simulation is an effective learning technique. However, there have been few peer-reviewed articles published in the medical literature describing its use in diving and hyperbaric medicine.MethodsWe implemented the curriculum of the Master’s degree in hyperbaric and diving medicine held at the University of Padova with emergency medicine seminars created by the faculty and validated by external experts. These seminars integrated traditional lectures and eight in situ simulation scenarios.ResultsFor the hyperbaric medicine seminar, simulations were carried out inside a real hyperbaric chamber at the ATIP Hyperbaric Treatment Centre, only using air and reproducing compression noise without pressurization to avoid damages to the manikins. The four scenarios consisted of hyperoxic seizures, pneumothorax, hypoglycemia, and sudden cardiac arrest. Furthermore, we added a hands-on session to instruct participants to prepare an intubated patient undergoing hyperbaric oxygen treatment with a checklist and simulating the patient transfer inside and outside the hyperbaric chamber. The diving medicine seminar was held at the Y-40 The Deep Joy pool in Montegrotto Terme (Italy), also involving SCUBA/breath-hold diving (BHD) instructors to rescue subjects from the water. These diving medicine scenarios consisted of neurologic syndrome (“taravana/samba”) in BHD, drowning of a breath-hold diver, pulmonary barotrauma in BHD, and decompression illness in a SCUBA diver.ConclusionWith this experience, we report the integration of simulation in the curriculum of a teaching course in diving and hyperbaric medicine. Future studies should be performed to investigate learning advantages, concept retention, and satisfaction of participants.

Lung function changes of divers after single deep heliox diving

ObjectivesThis study detects the changes in pulmonary function of divers after 80m, 100 m, and 120 m helium-oxygen (heliox) dive. Methods: A total of 26 divers participated in the experiment, of which 15 divers performed the 80m dive, 5 divers performed the 100m dive, and 6 divers performed the 120m dive. The exposure phases included breathing heliox or air in water and O2 in the hyperbaric chamber. Pulmonary function (forced flow-volume) was measured twice before diving, within 30 minutes after diving, and 24 hours after diving. The parameters examined were forced vital capacity (FVC), forced expired volume in 1 second (FEV1), forced expired flow from 25% to 75% volume expired (FEF25-75%), 25-75 percent maximum expiratory flow as compared with vital capacity (MEF 25-75%) and peak expiratory flow (PEF). Results: FEV1/FVC and MEF25% markedly decreased (p = 0.0395, p = 0.0496) within 30min after the 80m dive, but returned to base values at 24h after the dive. Other indicators showed a downward trend within 30min after 80m heliox diving (no statistical difference). Interestingly, FEV1, FEV1/FVC, PEF, MEF decreased after 100m heliox dives, but there was no statistical difference. However, in the 120m heliox dive, FEV1/FVC and MEF75% significantly decreased again after diving (p = 0.0098, p = 0.0073). The relatively small number and more proficient diving skills of divers in 100m and 120m diving may be responsible for the inconsistent results. But when the diving depth reached 120m, results again showed a significant statistical change. Conclusion: Single deep heliox diving can cause temporary expiratory and small airway dysfunction, which can be recovered at 24h after diving.

Variability in venous gas emboli following the same dive at 3,658 meters

Exposure to a reduction in ambient pressure such as in high-altitude climbing, flying in aircrafts, and decompression from underwater diving results in circulating vascular gas bubbles (i.e., venous gas emboli [VGE]). Incidence and severity of VGE, in part, can objectively quantify decompression stress and risk of decompression sickness (DCS) which is typically mitigated by adherence to decompression schedules. However, dives conducted at altitude challenge recommendations for decompression schedules which are limited to exposures of 10,000 feet in the U.S. Navy Diving Manual (Rev. 7). Therefore, in an ancillary analysis within a larger study, we assessed the evolution of VGE for two hours post-dive using echocardiography following simulated altitude dives at 12,000 feet. Ten divers completed two dives to 66 fsw (equivalent to 110 fsw at sea level by the Cross correction method) for 30 minutes in a hyperbaric chamber. All dives were completed following a 60-minute exposure at 12,000 feet. Following the dive, the chamber was decompressed back to altitude for two hours. Echocardiograph measurements were performed every 20 minutes post-dive. Bubbles were counted and graded using the Germonpré and Eftedal and Brubakk method, respectively. No diver presented with symptoms of DCS following the dive or two hours post-dive at altitude. Despite inter- and intra-diver variability of VGE grade following the dives, the majority (11/20 dives) presented a peak VGE Grade 0, three VGE Grade 1, one VGE Grade 2, four VGE Grade 3, and one VGE Grade 4. Using the Cross correction method for a 66-fsw dive at 12,000 feet of altitude resulted in a relatively low decompression stress and no cases of DCS.