Endothelia-Targeting Protection by Escin in Decompression Sickness Rats.

Endothelial dysfunction is involved in the pathogenesis of decompression sickness (DCS) and contributes substantively to subsequent inflammatory responses. Escin, the main active compound in horse chestnut seed extract, is well known for its endothelial protection and anti-inflammatory properties. This study aimed to investigate the potential protection of escin against DCS in rats. Escin was administered orally to adult male rats for 7 d (1.8 mg/kg/day) before a simulated air dive. After decompression, signs of DCS were monitored, and blood and pulmonary tissue were sampled for the detection of endothelia related indices. The incidence and mortality of DCS were postponed and decreased significantly in rats treated with escin compared with those treated with saline (P < 0.05). Escin significantly ameliorated endothelial dysfunction (increased serum E-selectin and ICAM-1 and lung Wet/Dry ratio, decreased serum NO), and oxidative and inflammatory responses (increased serum MDA, MPO, IL-6 and TNF-α) (P < 0.05 or P < 0.01). The results suggest escin has beneficial effects on DCS related to its endothelia-protective properties and might be a drug candidate for DCS prevention and treatment.

Neuron-specific enolase and S100B protein levels in recreational scuba divers with neurological decompression sickness.

INTRODUCTION: Neuron-specific enolase (NSE) and S100B protein are brain-origin proteins commonly described to assess the presence and severity of neurological injury. To date, there are limited data examining the influence of scuba diving on these biomarkers, particularly when symptoms of decompression sickness (DCS) occur. The purpose of this controlled study was to determine whether these serum neurochemical markers could be used as 1) indicators of neurological DCS and 2) predictors of incomplete recovery. METHODS: Fifty-nine divers with neurological DCS and 37 asymptomatic divers admitted for inadequate decompression, serving as controls, were consecutively enrolled between 2010 and 2012. Blood samples were collected at initial presentation up to 6 hours after dive completion (controls) or onset of symptoms (DCS divers). Biomarkers were quantified in nonhaemolysed samples only. Clinical outcome was assessed at 6 months post-injury. RESULTS: The two groups did not differ regarding the variables examined, except for the total dive time which was slightly shorter in the control group. NSE, but not S100B protein, was higher in the DCS group than in controls (P < 0.0001). An NSE level > 15.9 µg L⁻¹ determined by ROC analysis predicted DCS development with a specificity of 100% (95% confidence interval (CI) 90 to 100) and a sensitivity of 24% (95% CI 14 to 36). There was a trend towards a higher likelihood of residual neurological deficits above this cut-off value (P = 0.08). CONCLUSIONS: Early determination of NSE was found to be useful for the diagnosis of neurological DCS with a high specificity. However, its clinical applicability in decision making for determining treatment as well as its prognostic value remains to be established. Reliability of S100B protein was not demonstrated in the present study.

[The high-pressure chemistry, barophysiological chemistry, comparative enzymology of cholinesterase the 100th anniversary from the birth of A. P. Brestkin].

There are exposed the main landmarks of the scientific biography of Professor Aleksandr Pavlovich Brestkin, connected with his investigations in the field of chemistry of high pressures, physiological chemistry of caisson disease, kinetics of esterase catalysis, and in comparative enzymology of cholinesterases.

Delayed effect of nitric oxide synthase inhibition on the survival of rats after acute decompression.

AIM: The formation of bubbles in the blood stream together with the ensuing sickness after rapid decompression is assumed to depend on the physiological condition of the vascular system. In order to gain insight into the vascular function of nitric oxide in acute decompression sickness, the effects of the nitric oxide synthase inhibition by N(omega)-nitro-L-arginine methyl ester was studied in rats. METHODS: Wistar rats under anaesthesia were exposed to hyperbaric conditions for two hours and decompressed approximately 2.5 hours after a single subcutaneous injection of N(omega)-nitro-L-arginine methyl ester. Scalar doses and different pressures were tested. RESULTS: The fraction of the rats that died after decompression was greater in rats treated with N(omega)-nitro-L-arginine methyl ester at doses greater than 8 mg Kg-1 body weight compared to untreated rats. CONCLUSION: Although we have not excluded effects of nitric oxide synthase inhibition on distribution of perfusion and therefore inert gas elimination from tissue during decompression as a factor, this result highlights a delayed benefit of nitric oxide synthase activity in preventing death in acute decompression sickness.

Increased oxygen before and during decompression reduces bubble formation in rats.

The aim of this study was to test the hypothesis that increased oxygen partial pressure shortly before and during decompression from hyperbaric pressures would decrease venous gas bubble formation. Bubbles were detected by an ultrasound Doppler technique in conscious, freely moving rats. All rats were exposed twice to 6 bar for 2 hours. In exposure A, the breathing gas mixture was 1 bar O2 and 5 bar N2. In exposure B, the breathing gas was changed to 2 bar O2 and 4 bar N2, 5 min prior to decompression. The decompression rate was 0.1 bar x s(-1) in both groups. Significantly fewer bubbles were detected after decompression in exposure B compared to A. The angiotensin converting enzyme (ACE) concentration in serum was measured as an indicator of possible damage to the pulmonary endothelium induced by bubbles. However, no correlation between ACE and bubble amount was found. In conclusion, this study in conscious rats indicates that safer decompression may be obtained by increasing the oxygen partial pressure before and during decompression.

Diver with decompression injury, elevation of serum transaminase levels, and rhabdomyolysis.

A 43-year-old female recreational scuba diver presented to the emergency department 1 hour after a rapid, uncontrolled ascent. Her presentation included progressing confusion, slow and slurred speech, and complaints of headache and hypesthesia over her forearms and anterior thighs bilaterally. Differential diagnosis included arterial gas embolism and decompression sickness. She underwent recompression therapy with US Navy Table 6 within 120 minutes of her ascent. After recompression therapy, the patient had signs and symptoms consistent with severe rhabdomyolysis, including creatine kinase levels of 36,000 U/L and myoglobinuria.

Survival following accidental decompression to an altitude greater than 74,000 feet (22,555 m).

A man was accidentally decompressed to an altitude greater than 22,555 m (74,000 ft) in an industrial vacuum chamber. He experienced burst lung, massive decompression sickness, and sustained ebulism. He remained at altitude for a period of 3-5 min. By 5.5 h following the accident, he was still profoundly unconscious. He was subsequently treated in a hyperbaric chamber with recompression on a modified U.S. Navy Table 6A and had eventual clinical recovery. The CPK peaked at 8000 units 2 d after the accident, demonstrating substantial barotrauma to the tissues.

Interdependence of decompression sickness and plasma enzymes on dive profile and vitamin B-6 status.

The mortality rate due to decompression injury was found to be significantly greater in a rat population with a mild vitamin B-6 deficiency, compared to an adequately fed control group, when subjected to a bends-producing N2-O2 dive. Relative post-dive changes in lactate dehydrogenase, creatine phosphokinase, and transaminase levels in plasma do not appear to be sufficiently different to allow a ready distinction in the degree of susceptibility of one nutritionally defined population from the other.

Changes in blood enzyme activity and hematology of rats with decompression sickness.

Plasma activities of lactic dehydrogenase (LDH), creatine phosphokinase (CPK), glutamic pyruvic transaminase (GPT), and alkaline phosphatase (ALP) were studied, along with hematological changes, in rats suffering from various degrees of experimental decompression sickness (DS). By 1 h after decompression, LDH and CPK activities were elevated in moderate and severe DS whereas GOT and GPT were elevated only in severe DS. ALP was reduced in all decompressed rats. Hematological changes indicated hemoconcentration, the degree of which paralleled the severity of DS. By 24 h after decompression, all enzyme activities were approaching control levels with the exception of GOT, which was further elevated from the 1-h value. The observed lung damage in rats with severe DS in conjunction with the hematologic and enzyme data suggested that hypoxemic-hypoxia, incident to bubble embolization of pulmonary vasculature, was a major factor in altering the blood enzyme pattern in DS. Serum enzyme data from two inadequately decompressed divers are also reported.