Simulated breath-hold diving to 20 meters: cardiac performance in humans

Cardiac performance was assessed in six subjects breath-hold diving to 20 m in a hyperbaric chamber, while nonsubmersed or submersed in a thermoneutral environment. Cardiac index and systolic time intervals were obtained with impedance cardiography and intrathoracic pressure with an esophageal balloon. Breath holding at large lung volume (80% vital capacity) decreased cardiac index, probably by increasing intrathoracic pressure and thereby impeding venous return. During diving, cardiac index increased (compared with breath holding at the surface) by 35.1% in the nonsubmersed and by 29.5% in the submersed condition. This increase was attributed to a fall in intrathoracic pressure. Combination of the opposite effects of breath holding and diving to 20 m left cardiac performance unchanged during the dives (relative to the surface control). A larger intrathoracic blood redistribution probably explains a smaller reduction in intrathoracic pressure observed during submersed compared with nonsubmersed diving. Submersed breath-hold diving may entail a smaller risk of thoracic squeeze (lesser intrathoracic pressure drop) but a greater risk of overloading the central circulation (larger intrathoracic blood pooling) than simulated nonsubmersed diving.     

Scuba diving enhances endogenous antioxidant defenses in lymphocytes and neutrophils

The aim was to study the effects of a scuba diving session on the lymphocyte antioxidant system, NO synthesis, the capability to produce reactive oxygen species and the antioxidant response in neutrophils. For that purpose seven male divers performed an immersion at a depth of 40 m for 25 min. The same parameters were measured after an hyperbaric oxygen (HBO) treatment at resting conditions in a hyperbaric chamber. Lymphocyte H₂O₂ production rose after diving and after HBO treatment. Glutathione peroxidase (GPx) and catalase activities increased after diving in lymphocytes, while after HBO exposure only increased GPx activity. Lymphocyte HO-1 mRNA expression increased after diving and after HBO exposure, while iNOS levels and nitrite levels significantly increased after diving. The hyperoxia associated to scuba diving leads to a condition of oxidative stress with increased lymphocyte H₂O₂ production, HO-1 expression, NO synthesis and antioxidant enzyme adaptations in order to avoid oxidative damage.     

Scuba diving enhances endogenous antioxidant defenses in lymphocytes and neutrophils

The aim was to study the effects of a scuba diving session on the lymphocyte antioxidant system, NO synthesis, the capability to produce reactive oxygen species and the antioxidant response in neutrophils. For that purpose seven male divers performed an immersion at a depth of 40 m for 25 min. The same parameters were measured after an hyperbaric oxygen (HBO) treatment at resting conditions in a hyperbaric chamber. Lymphocyte H₂O₂ production rose after diving and after HBO treatment. Glutathione peroxidase (GPx) and catalase activities increased after diving in lymphocytes, while after HBO exposure only increased GPx activity. Lymphocyte HO-1 mRNA expression increased after diving and after HBO exposure, while iNOS levels and nitrite levels significantly increased after diving. The hyperoxia associated to scuba diving leads to a condition of oxidative stress with increased lymphocyte H₂O₂ production, HO-1 expression, NO synthesis and antioxidant enzyme adaptations in order to avoid oxidative damage.     

高气压对脑循环的影响

对32名男性潜水员和25头家兔进行了下列3项内容的观察:1)不同压力下脑阻抗图(REG)的改变;2)模拟潜水时REG的变化与颅内压(ICP)的关系;3)职业潜水员的工令对脑循环的影响。结果表明,在高气压下,REG的波幅、dz/dt和上升时间/心动周期比值均有不同程度的变化。这些指标的变化可以说明博动性脑血容量减少和血管阻力增加,提示脑血流量减少。这些变化主要是由于高分压氧的作用。     

Cerebral gas embolism absorption during hyperbaric therapy: theory.

Cerebral gas embolism is a serious consequence of diving. It is associated with decompression sickness and is assumed to cause severe neurological dysfunction. A mathematical model previously developed to calculate embolism absorption time based on in vivo bubble geometry is used in which various conditions of hyperbaric therapy are considered. Effects of varying external pressure and inert gas concentrations in the breathing mixtures, according to US Navy and Royal Navy diving treatment tables, are predicted. Recompression alone is calculated to reduce absorption times of a 50-nl bubble by up to 98% over the untreated case. Lowering the inhaled inert gas concentration from 67.5% to 50% reduces absorption time by 37% at a given pressure. Bubbles formed after diving and decompression with He are calculated to absorb up to 73% faster than bubbles created after diving and decompression with air, regardless of the recompression gas breathed. This model is a useful alternative to impractical clinical trials in assessing which initial step in hyperbaric therapy is most effective in eliminating cerebral gas embolisms should they occur.     

Effect of increased pressure and changed gaseous media on biological properties of microorganisms

Bacterial contamination of diving outfit and inner surfaces of pressure complex increases at the expense of expansion of gram-negative microflora during long exploitation of undersea complexes. Gram-negative bacteria were hypothesized to effectively adapt to hyperbaric conditions. We investigated the effect of hyperbaric conditions and changed gaseous environment on the cultural and morphological characteristics of colonies, growth rate and time of generation of test cultures (P. aeruginosa ATCC 10145, E. coli Tg1, and Bac. subtilis GB2036). Phenotypically modified clones were selected for subsequent analysis of changes at a genetic level. Experiments revealed no essential changes in the studied properties under the effect of extreme conditions.     

Acclimatization to neurological decompression sickness in rabbits

Diving acclimatization refers to a reduced susceptibility to acute decompression sickness (DCS) in individuals undergoing repeated compression-decompression cycles. We demonstrated in a previous study that the mechanism responsible for this acclimatization is similar to that of stress preconditioning. In this study, we investigated the protective effect of prior DCS preconditioning on the severity of neurological DCS in subsequent exposure to high pressure in rabbits. We exposed the rabbits (n = 10) to a pressure cycle of 6 absolute atmospheres (ATA) for 90 min, which induced signs of neurological DCS in 60% of the animals. Twenty-four hours after the pressure cycle, rabbits with DCS expressed more heat-shock protein 70 (HSP70) in the lungs, liver, and heart than rabbits without signs of disease or those in the control group (n = 6). In another group of rabbits (n = 24), 50% of animals presented signs of neurological DCS after exposure to high pressure, with a neurological score of 46.5 (SD 19.5). A course of hyperbaric oxygen therapy alleviated the signs of neurological DCS and ensured the animals' survival for 24 h. Experiencing another pressure cycle of 6 ATA for 90 min, 50% of 12 rabbits with prior DCS preconditioning developed signs of DCS, with a neurological score of 16.3 (SD 28.3), significantly lower than that before hyperbaric oxygen therapy (P = 0.002). In summary, our results show that the occurrence of DCS in rabbits after rapid decompression is associated with increased expression of a stress protein, indicating that the stress response is induced by DCS. This phenomenon was defined as "DCS preconditioning." DCS preconditioning attenuated the severity of neurological DCS caused by subsequent exposure to high pressure. These results suggest that bubble formation in tissues activates the stress response and stress preconditioning attenuates tissue injury on subsequent DCS stress, which may be the mechanism responsible for diving acclimatization.     

Effects of various hyperbaric gas mixtures on metabolic parameters of human blood

Changes in metabolic parameters of healthy subjects were studied during experimental 4-to 21-day courses of simulated diving in hyperbaric normoxic (oxygen-helium), hyperoxic (oxygen-nitrogen-helium), and argon-containing gas mixtures with different oxygen contents. The blood concentrations of primary substrates and activity of enzymes were measured spectrophotometrically. In most cases, the clinical and biochemical parameters of the blood remained within normal clinical ranges and exhibited significant individual variations. Long-term simulated deep dives (>200 m) resulted in changes in lipid metabolism expressed as an increase in the plasma concentrations of triglycerides, low-density lipoproteins, and polyunsaturated fatty acids. No significant changes were found during experimental 70-m dives performed according to recompression treatment table with the use of a hyperoxic helium-containing gas mixture. In contrast, long-term exposure to a normoxic argon-containing mixture at a pressure of 5 msw caused a significant increase in the blood contents of triglycerides, total cholesterol, and glucose, as well as a smaller increase in the activities of several tissue enzymes. At the same pressure, hypoxic oxygen-nitrogen-argon and oxygen-nitrogen mixtures did not affect the majority of clinical and biochemical parameters examined. However, in some subjects, they increased the atherogenicity index, concentrations of triglycerides, and activities of lactate dehydrogenase and alkaline phosphatase. The absence of any pathological changes in clinical and biochemical parameters of the blood indicates that both gas mixtures are safe and can be used in barochambers. Episodic changes in lipid metabolism and enzyme activities observed in healthy subjects exposed to helium-and argon-containing gas mixtures can be interpreted as a reversible hepatic dysfunction due to the high pressure. The extent of the changes in the parameters of lipid metabolism in the blood is determined by the magnitude of the overpressure and the duration of the exposure.     

Modeling pulmonary and CNS O(2) toxicity and estimation of parameters for humans.

The power expression for cumulative oxygen toxicity and the exponential recovery were successfully applied to various features of oxygen toxicity. From the basic equation, we derived expressions for a protocol in which PO(2) changes with time. The parameters of the power equation were solved by using nonlinear regression for the reduction in vital capacity (DeltaVC) in humans: %DeltaVC = 0.0082 x t(2)(PO(2)/101.3)(4.57), where t is the time in hours and PO(2) is expressed in kPa. The recovery of lung volume is DeltaVC(t) = DeltaVC(e) x e(-(-0.42 + 0.00379PO(2))t), where DeltaVC(t) is the value at time t of the recovery, DeltaVC(e) is the value at the end of the hyperoxic exposure, and PO(2) is the prerecovery oxygen pressure. Data from different experiments on central nervous system (CNS) oxygen toxicity in humans in the hyperbaric chamber (n = 661) were analyzed along with data from actual closed-circuit oxygen diving (n = 2,039) by using a maximum likelihood method. The parameters of the model were solved for the combined data, yielding the power equation for active diving: K = t(2) (PO(2)/101.3)(6.8), where t is in minutes. It is suggested that the risk of CNS oxygen toxicity in diving can be derived from the calculated parameter of the normal distribution: Z = [ln(t) - 9.63 +3.38 x ln(PO(2)/101.3)]/2.02. The recovery time constant for CNS oxygen toxicity was calculated from the value obtained for the rat, taking into account the effect of body mass, and yielded the recovery equation: K(t) = K(e) x e(-0.079t), where K(t) and K(e) are the values of K at time t of the recovery process and at the end of the hyperbaric oxygen exposure, respectively, and t is in minutes.     

Tufted ducks Aythya fuligula do not control buoyancy during diving

Work against buoyancy during submergence is a large component of the energy costs for shallow diving ducks. For penguins, buoyancy is less of a problem, however they still seem to trade‐off levels of oxygen stores against the costs and benefits of buoyant force during descent and ascent. This trade‐off is presumably achieved by increasing air sac volume and hence pre‐dive buoyancy (B_pre) when diving deeper. Tufted ducks, Aythya fuligula, almost always dive with nearly full oxygen stores so these cannot be increased. However, the high natural buoyancy of tufted ducks guarantees a passive ascent, so they might be expected to decrease B_pre before particularly deep, long dives to reduce the energy costs of diving. Body heat lost to the water can also be a cause of substantial energy expenditure during a dive, both through dissipation to the ambient environment and through the heating of ingested food and water. Thus dive depth (d_d), duration and food type can influence how much heat energy is lost during a dive. The present study investigated the relationship between certain physiological and behavioural adjustments by tufted ducks to d_d and food type. Changes in B_pre, deep body temperature (T_b) and dive time budgeting of four ducks were measured when diving to two different depths (1.5 and 5.7 m), and for two types of food (mussels and mealworms). The hypothesis was that in tufted ducks, B_pre decreases as d_d increases. The ducks did not change B_pre in response to different diving depths, and thus the hypothesis was rejected. T_b was largely unaffected by dives to either depth. However, diving behaviour changed at the greater d_d, including an increase in dive duration and vertical descent speed. Behaviour also changed depending on the food type, including an increase in foraging duration and vertical descent speed when mussels were present. Behavioural changes seem to represent the major adjustment made by tufted ducks in response to changes in their diving environment.     

Decompression sickness in the rat following a dive on trimix: recompression therapy with oxygen vs. heliox and oxygen.

Trimix (a mixture of helium, nitrogen, and oxygen) has been used in deep diving to reduce the risk of high-pressure nervous syndrome during compression and the time required for decompression at the end of the dive. There is no specific recompression treatment for decompression sickness (DCS) resulting from trimix diving. Our purpose was to validate a rat model of DCS on decompression from a trimix dive and to compare recompression treatment with oxygen and heliox (helium-oxygen). Rats were exposed to trimix in a hyperbaric chamber and tested for DCS while walking in a rotating wheel. We first established the experimental model, and then studied the effect of hyperbaric treatment on DCS: either hyperbaric oxygen (HBO) (1 h, 280 kPa oxygen) or heliox-HBO (0.5 h, 405 kPa heliox 50%-50% followed by 0.5 h, 280 kPa oxygen). Exposure to trimix was conducted at 1,110 kPa for 30 min, with a decompression rate of 100 kPa/min. Death and most DCS symptoms occurred during the 30-min period of walking. In contrast to humans, no permanent disability was found in the rats. Rats with a body mass of 100-150 g suffered no DCS. The risk of DCS in rats weighing 200-350 g increased linearly with body mass. Twenty-four hours after decompression, death rate was 40% in the control animals and zero in those treated immediately with HBO. When treatment was delayed by 5 min, death rate was 25 and 20% with HBO and heliox, respectively.     

Evaluation of risk profiles by subcutaneous adipose tissue topography in obese juveniles

Objective: To compare subcutaneous adipose tissue topography (SAT‐top) in obese juveniles with age‐matched normal‐weight controls. Research Methods and Procedures: The optical device LIPOMETER (European Patent EP 0516251) enables the non‐invasive, rapid, safe, and precise measurement of the thickness of subcutaneous adipose tissue. Fifteen defined body sites (1 = neck to 15 = calf) characterize the individual SAT‐top like an individual fingerprint. SAT‐top of 1351 juveniles (obese: 42 boys, 59 girls, normal weight: 680 boys, 570 girls) from 7 to 19 years of age were measured. For visual comparison, the 15‐dimensional SAT‐top information was condensed by factor analysis into a two‐dimensional factor plot. Results: Both female and male obese juveniles had markedly increased adipose tissue layers at 7 = upper abdomen, 8 = lower abdomen, 5 = front chest, and 6 = lateral chest. The pubertal changes of body shape and fat distribution of the normal‐weight boys and girls (boys show thinner adipose tissue layers on their legs, whereas girls had thicker adipose tissue layers at the extremities) were not seen in the obese group. Independently of age and sex, all of the obese juveniles showed a similar, more android body fat distribution with increased trunk fat. Discussion: SAT‐top of the obese juveniles is similar to that of patients with type 2 diabetes, polycystic ovary syndrome, and coronary heart disease. Patients with these metabolic disorders and obese juveniles are located in the factor plot in the same area. This body shape may indicate a risk profile for developing polycystic ovary syndrome (women), type 2 diabetes, and early atherosclerosis (both sexes).     

Is Cancer in Israeli Professional Divers Exposed to Polluted Waters an Occupational Disease?

Because there is some contamination of practically every body of water, risk analysis is important to determine diving exposure standards to pollutants, including requirements for protective equipment. In the following study we attempt to determine the increased risk of cancer in Israeli Naval divers exposed to pollutants in the Kishon River system. We calculated two risks, one using maximally recorded levels of pollutants outside the diving areas (worst-case scenario), and the other using maximally recorded levels in the actual diving areas. For both calculations we used conservative assumptions for exposure (2500 exposure hours with 50% of body covered with sediment), and a synergistic risk model. We considered all chemicals that were carcinogenic by inhalation also to be carcinogenic by oral and dermal absorption. The relative risk was 1.13 for the worst-case scenario, and 1.004 for exposures in actual diving areas. We conclude that it is unlikely that exposure to the polluted Kishon River waters can cause a detectable increase in cancer risk in Israeli Navy divers. This study has implications for professional divers exposed to polluted waters.     

Ponderal somatograms assess changes in anthropometric measurements over an academic year in Division III collegiate football players

Ponderal somatograms evaluate body size and shape by converting muscular (shoulders, chest, biceps, forearm, thigh, calf) and nonmuscular (abdomen, hips, knee, ankle, wrist) girths into ponderal equivalent (PE) values. Anthropometric measurements, including stature, body mass, girths, and percent body fat by densitometry were collected in 54 Division III football players in preseason camp (fall) and at the beginning (winter) and end (spring) of the team strength and conditioning program. PE values were calculated for each girth as PE, kg = (girth, cm / k)(2) x stature, dm, where k = k constant from Behnke's reference man. PE values were compared to body mass to indicate overdevelopment (PE > body mass) and underdevelopment (PE < body mass) at specific girth sites. From fall to winter, body mass (+1.6 kg), percent fat (+1.3%), fat mass (+1.6 kg), nonmuscular abdominal and hip girths (+2.1 cm, +1.5 cm), and PE values (+5.3 kg, +2.6 kg) increased significantly (p < 0.05). From winter to spring, percent fat (-1.5%), fat mass (-1.4 kg), nonmuscular abdominal girth (-1.0 cm), and PE value (-2.5 kg) decreased significantly (p < 0.05). Fat-free mass (+1.5 kg), muscular biceps girth (+0.4 cm), and PE value (+2.6 kg) increased significantly (p < 0.05) from winter to spring. Ponderal somatogram muscular components were generally overdeveloped, with the greatest overdevelopment at the biceps in fall (+14.7 kg), winter (+14.9 kg), and spring (+17.4 kg). Nonmuscular components generally were underdeveloped, except abdomen and hips that were overdeveloped. The abdomen remained the greatest nonmuscular overdevelopment in fall (+6.8 kg), winter (+10.5 kg), and spring (+7.9 kg). Ponderal somatograms provide a relatively simple, practical method to track specific changes in body size and shape over time.     

Chemical control of tracheal vascular resistance in dogs

With anesthetized dogs we have measured upper tracheal vascular resistance on both sides of the trachea simultaneously by perfusing the cranial tracheal arteries and measuring inflow pressures at constant flows. The ratio of pressure to flow gave vascular resistance (Rtv). Lung airflow, blood pressure (BP), heart rate, and pressure in a cervical tracheal balloon (Ptr) were also measured. In paralyzed dogs, systemic hypoxia due to artificial ventilation with 10% O2-90% N2 increased Rtv by +8.1 +/- 1.0% (SE), Ptr by +76 +/- 22.8%, and BP by +18.9 +/- 24%. After bilateral cervical vagosympathectomy the increases in Rtv and BP were present (+8.8 +/- 0.9 and +22.3 +/- 0.3%, respectively). After carotid body denervation Rtv, Ptr, and BP increased (+6.4 +/- 1.3, +58.6 +/- 31.6, and +14.6 +/- 3.3%, respectively). After vagotomy Rtv and BP increased (+14.1 +/- 1.7 and +22.4 +/- 10.1%, respectively). Tracheal perfusion with hypoxic blood caused a small vasodilation (-2.2 +/- 1.1%). Systemic hypercapnia due to artificial ventilation with 8% CO2-92% air increased Rtv by +16.7 +/- 3.8%, Ptr by +67 +/- 2.0%, and BP by +12.9 +/- 9.9%. Tracheal perfusion with hypercapnic blood caused a small vasodilation (-2.5 +/- 1.2%). Stimulation of the carotid body chemoreceptors with KCN caused a small increase in Rtv (+1.2 +/- 0.5%) and increases in Ptr (+49.8 +/- 13.6%) and BP (+11.1 +/- 2.1%). Systemic hypoxia and hypercapnia caused tracheal vasoconstriction mainly by an action on the central nervous system.     

Ventilatory behavior after hypoxia in C57BL/6J and A/J mice.

Given the environmental forcing by extremes in hypoxia-reoxygenation, there might be no genetic effect on posthypoxic short-term potentiation of ventilation. Minute ventilation (VE), respiratory frequency (f), tidal volume (VT), and the airway resistance during chemical loading were assessed in unanesthetized unrestrained C57BL/6J (B6) and A/J mice using whole body plethysmography. Static pressure-volume curves were also performed. In 12 males for each strain, after 5 min of 8% O2 exposure, B6 mice had a prominent decrease in VE on reoxygenation with either air (-11%) or 100% O2 (-20%), due to the decline of f. In contrast, A/J animals had no ventilatory undershoot or f decline. After 5 min of 3% CO2-10% O2 exposure, B6 exhibited significant decrease in VE (-28.4 vs. -38.7%, air vs. 100% O2) and f (-13.8 vs. -22.3%, air vs. 100% O2) during reoxygenation with both air and 100% O2; however, A/J mice showed significant increase in VE (+116%) and f (+62.2%) during air reoxygenation and significant increase in VE (+68.2%) during 100% O2 reoxygenation. There were no strain differences in dynamic airway resistance during gas challenges or in steady-state total respiratory compliance measured postmortem. Strain differences in ventilatory responses to reoxygenation indicate that genetic mechanisms strongly influence posthypoxic ventilatory behavior.     

Increased axonal excitability during exposure to hyperbaric oxygen

The effect of high oxygen pressure on neural function was studied in the isolated nervous system of the cockroach. Intracellular and extracellular action potentials were recorded from single giant axons during exposure to 7 ATA (atmosphere absolute) (1 ATA = 0.1 MPa) of oxygen. Axonal excitability was measured as changes in stimulus strength-duration relationship. Initially, a transient increase in the rheobase current was observed followed by a significant decline to 75% of air control values. This decrease was accompanied by a parallel increase in the membrane time constant. The results demonstrate that hyperbaric oxygen increases axonal excitability. Such changes are consistent with the epileptogenic properties of high oxygen pressure.     

Thermoregulatory consequences of long-term microwave exposure at controlled ambient temperatures

This study was designed to identify and measure changes in thermoregulatory responses, both behavioral and physiological, that may occur when squirrel monkeys are exposed to 2450-MHz continuous wave microwaves 40 hr/week for 15 weeks. Power densities of 1 or 5 mW/cm2 (specific absorption rate = 0.16 W/kg per mW/cm2) were presented at controlled environmental temperatures of 25, 30, or 35 degrees C. Standardized tests, conducted periodically, before, during, and after treatment, assessed changes in thermoregulatory responses. Dependent variables that were measured included body mass, certain blood properties, metabolic heat production, sweating, skin temperatures, deep body temperature, and behavioral responses by which the monkeys selected a preferred environmental temperature. Results showed no reliable alteration of metabolic rate, internal body temperature, blood indices, or thermoregulatory behavior by microwave exposure, although the ambient temperature prevailing during chronic exposure could exert an effect. An increase in sweating rate occurred in the 35 degrees C environment, but sweating was not reliably enhanced by microwave exposure. Skin temperature, reflecting vasomotor state, was reliably influenced by both ambient temperature and microwaves. The most robust consequence of microwave exposure was a reduction in body mass, which appeared to be a function of microwave power density.