Jean-Michel Pontier

Haemodynamic changes induced by submaximal exercise before a dive and its consequences on bubble formation

Objectives: To evaluate the effects of a submaximal exercise performed 2 h before a simulated dive on bubble formation and to observe the haemodynamic changes and their influence on bubble formation. Participants and methods: 16 trained divers were compressed in a hyperbaric chamber to 400 kPa for 30 min and decompressed at a rate of 100 kPa/min with a 9 min stop at 130 kPa (French Navy MN90 procedure). Each diver performed two dives 3 days apart, one without exercise and one with exercise before the dive. All participants performed a 40 min constant-load submaximal and calibrated exercise, which consisted of outdoor running 2 h before the dive. Circulating bubbles were detected with a precordial Doppler at 30, 60 and 90 min after surfacing. Haemodynamic changes were evaluated with Doppler echocardiography. Results: A single bout of strenuous exercise 2 h before a simulated dive significantly reduced circulating bubbles. Post-exercise hypotension (PEH) was observed after exercise with reductions in diastolic and mean blood pressure (DBP and MBP), but total peripheral resistance was unchanged. Stroke volume was reduced, whereas cardiac output was unchanged. Simulated diving caused a similar reduction in cardiac output independent of pre-dive exercise, suggesting that pre-dive exercise only changed DBP and MBP caused by reduced stroke volume. Conclusion: A single bout of strenuous exercise 2 h before a dive significantly reduced the number of bubbles in the right heart of divers and protected them from decompression sickness. Declining stroke volume and moderate dehydration induced by a pre-dive exercise might influence inert gas load and bubble formation.

Bubble-induced platelet aggregation in a rat model of decompression sickness

Previous studies have highlighted that bubble-induced platelet aggregation is a predictor index of decompression sickness (DCS) severity in animals and bubble formation after a single air dive in humans. The present study attempted to investigate plasmatic indexes of the coagulation system and platelet activation in our rat model of DCS. Male Sprague-Dawley rats were assigned to one experimental group with a hyperbaric exposure and one control group maintained at atmospheric pressure. Rats were compressed to 1,000 kPa (90 m saltwater) for 45 min while breathing air. The onset of death time and DCS symptoms were recorded during a 30-min observed period after rats had surfaced. Plasmatic indexes were platelet factor 4 (PF4) for platelet activation, soluble glycoprotein V (sGPV) for thrombin generation, and thrombin-antithrombin complexes for the coagulation system. Blood samples for a platelet count and markers were taken 3 wk before the experimental protocol and within the 30 min after rats had surfaced. We confirmed a correlation between the percent fall in platelet count and DCS severity. Plasmatic levels of sGPV and PF4 were significantly increased after the hyperbaric exposure, with no change in the control group. The present study confirms platelet consumption as a potential index for evaluating decompression stress and DCS severity. The results point to the participation of thrombin generation in the coagulation cascade and platelet activation in bubble-induced platelet aggregation. In our animal model of DCS, the results cannot prejudge the mechanisms of platelet activation between bubble-induced vessel wall injury and bubble-blood component interactions.

Blood platelet count and severity of decompression sickness in rats after a provocative dive.

INTRODUCTION Previous animal studies reported that platelet count (PC) is decreased following decompression. Adherence and aggregation of platelets to the bubble surface has been demonstrated in severe decompression sickness (DCS). The present study was designed to clarify the relationship between post-dive platelet levels and the severity of DCS in a rat model. METHODS A total of 57 male Sprague-Dawley rats were assigned to either one experimental group with a hyperbaric exposure (N = 22) or one control group (N = 27). Rats were compressed to 1000 kPa (90 msw) for 45 min while breathing air and decompressed to surface in 38 min with stops at 200, 160, and 130 kPa. Onset of neurological DCS and death time were recorded during a 120-min observation period after surfacing. In the control group, rats were maintained at atmospheric pressure in the same chamber for an equivalent period of time. Blood samples for PC were taken 30 min before and immediately after exposure in two groups. RESULTS Blood PC after hyperbaric exposure had significantly decreased, whereas PC had increased in the control group. We found a correlation between % fall in PC and latency to death time. The platelet loss tended to decrease when fatal DCS was delayed. Rats suffering from severe DCS with a short latency to death presented a pronounced decline in platelets. DISCUSSION The present study highlighted a relationship between the post-dive decrease in PC and DCS severity in rats. Platelet consumption could offer a new index for evaluating decompression stress.

MRI FINDINGS AND CLINICAL OUTCOME IN 45 DIVERS WITH SPINAL CORD DECOMPRESSION SICKNESS

BACKGROUND Decompression sickness (DCS) affecting the spinal cord is the most dangerous form of diving-related injury with potential sequelae. This study was conducted to evaluate the relationship between spinal cord lesions on MRI and clinical findings in divers with spinal DCS. METHODS We studied 45 cases of DCS that were referred to our hyperbaric facility with clinical evidence of spinal involvement during the period 2002-2007. The study included only patients who underwent MRI within 10 d of injury. The severity of spinal DCS for each patient was rated numerically for both the acute event and 1 mo later. The presence or absence of back pain was also noted. RESULTS Spinal cord lesions were significantly more frequent in divers with severe DCS, and did not occur in any diver who experienced a favorable outcome (sensitivity = 67%, specificity = 100%, negative predictive value = 77%, positive predictive value = 100%). The presence of vertebral degenerative changes that impinged on the spinal cord was strongly associated with MRI abnormalities, but not with a negative outcome. Acute back pain was associated with hyperintense lesions and persistence of neurological sequelae [OR = 14 (95% CI, 3.1 to 63.5)]. CONCLUSION The results show that MRI could be helpful in predicting clinical outcome in divers with spinal cord DCS. The presence of medullary compressive factors and vertebral back pain after surfacing indicate increased likelihood of severe myelopathy with incomplete recovery.

Blood Platelet Count and Bubble Formation After a Dive to 30 msw for 30 min

INTRODUCTION Previous human studies reported that platelet count (PC) is decreased following decompression. Platelet aggregation and adherence to the bubble surface has been demonstrated in severe decompression sickness (DCS). The present study was designed to clarify the relationship between post-dive changes in blood PC and the level of bubble formation in divers. METHODS There were 40 healthy experienced divers who were assigned to 1 experimental group (N = 30) with an open-sea air dive to 30 msw for 30 min in field conditions and 1 control group (N = 10) without hyperbaric exposure. Bubble grades were monitored with a pulsed Doppler according to the Spencer scale and Kissman integrated severity score (KISS). Blood samples for red blood cell counts (RBC), hematocrit (Hct), and PC were taken 1 h before and after exposure in two groups. RESULTS None of the divers developed any signs of DCS. In two groups, the results showed significant increase in RBC count and Hct related with hemoconcentration and no change in PC. Divers with a high KISS score (39 +/- 5.8; mean +/- SD) presented a significantly more pronounced percent fall in PC than divers with a lower KISS score. We found a significant correlation between the percent fall in PC after a dive and the bubble KISS score. DISCUSSION The present study highlighted a relationship between the post-dive decrease in PC and the magnitude of bubble level after decompression. Our primary result is that the post-dive decrease in PC could be a predictor of decompression severity after diving.

Blood platelet-derived microparticles release and bubble formation after an open-sea air dive

Bubble-induced platelet aggregation offers an index for evaluating decompression severity in humans and in a rat model of decompression sickness. Endothelial cells, blood platelets, or leukocytes shed microparticles (MP) upon activation and during cell apoptosis. The aim was to study blood platelet MP (PMP) release and bubble formation after a scuba-air dive in field conditions. Healthy, experienced divers were assigned to 1 experimental group (n = 10) with an open-sea air dive to 30 msw for 30 min and 1 control group (n = 5) during head-out water immersion for the same period. Bubble grades were monitored with a pulsed doppler according to Kissman Integrated Severity Score (KISS). Blood samples for platelet count (PC) and PMP (annexin V and CD41) were taken 1 h before and after exposure in both groups. The result showed a decrease in post-dive PC compared with pre-dive values in experimental group with no significant change in the control group. We observed a significant increase in PMP values after the dive while no change was revealed in the control group. There was a significant positive correlation between the PMP values after the dive and the KISS bubble score. The present study highlighted a relationship between the post-dive decrease in PC, platelet MP release, and bubble formation. Release of platelet MPs could reflect bubble-induced platelet aggregation and could play a key role in alteration of the coagulation. Further studies must investigate endothelial and leukocyte MP release in the same field conditions.

Bubble Formation and Endothelial Function Before and After 3 Months of Dive Training

INTRODUCTION It has been suggested that repeated compression-decompression cycles reduce diver susceptibility to decompression sickness (DCS). This study examined whether intensive scuba dive training would reduce bubble formation and modulate endothelial function as shown by skin circulation. METHODS There were 22 military divers who were studied before and after a 90-d program of physical training and open-sea air diving (mean 67 dives total). Skin blood flow in the forearm was measured at rest (baseline), during post-occlusive hyperemia (endothelium-dependent vasodilatation), and with local heating to 42 degrees C (maximal vasodilatation). Subjects were also examined by pulsed Doppler for venous bubbles 30, 60, and 90 min after surfacing from a hyperbaric exposure to 400 kPa (30 msw) for 30 min in a dry chamber. RESULTS None of the divers experienced DCS during the training period. There was no change in weight, body mass index, maximal oxygen uptake, or endothelial function. Bubble grades by the Kisman Integrated Severity Score were significantly decreased immediately after the diving training period (3.6 +/- 9.2 vs. 16.4 +/- 14.3) and increased 3 mo after this period (10.3 +/- 13.9 vs. 3.6 +/- 9.2). DISCUSSION The results highlight that repeated scuba dives and regular physical exercise activity reduce bubble formation and probably have a protective effect against DCS risk. Although this phenomenon has been observed for decades, the mechanism remains complex and the results cannot elucidate the effects of physical exercise and NO production. Bubble formation could activate the stress response which could be the basis for diving acclimatization.

Pharmacological intervention against bubble-induced platelet aggregation in a rat model of decompression sickness.

Decompression sickness (DCS) with alterations in coagulation system and formation of platelet thrombi occurs when a subject is subjected to a reduction in environmental pressure. Blood platelet consumption after decompression is clearly linked to bubble formation in humans and offers an index for evaluating DCS severity in animal models. Previous studies highlighted a predominant involvement of platelet activation and thrombin generation in bubble-induced platelet aggregation (BIPA). To study the mechanism of the BIPA in DCS, we examined the effect of acetylsalicylic acid (ASA), heparin (Hep), and clopidogrel (Clo), with anti-thrombotic dose pretreatment in a rat model of DCS. Male Sprague-Dawley rats (n = 208) were randomly assigned to one experimental group treated before the hyperbaric exposure and decompression protocol either with ASA (3×100 mg·kg(-1)·day(-1), n = 30), Clo (50 mg·kg(-1)·day(-1), n = 60), Hep (500 IU/kg, n = 30), or to untreated group (n = 49). Rats were first compressed to 1,000 kPa (90 msw) for 45 min and then decompressed to surface in 38 min. In a control experiment, rats were treated with ASA (n = 13), Clo (n = 13), or Hep (n = 13) and maintained at atmospheric pressure for an equivalent period of time. Onset of DCS symptoms and death were recorded during a 60-min observation period after surfacing. DCS evaluation included pulmonary and neurological signs. Blood samples for platelet count (PC) were taken 30 min before hyperbaric exposure and 30 min after surfacing. Clo reduces the DCS mortality risk (mortality rate: 3/60 with Clo, 15/30 with ASA, 21/30 with Hep, and 35/49 in the untreated group) and DCS severity (neurological DCS incidence: 9/60 with Clo, 6/30 with ASA, 5/30 with Hep, and 12/49 in the untreated group). Clo reduced fall in platelet count and BIPA (-4,5% with Clo, -19.5% with ASA, -19,9% with Hep, and -29,6% in the untreated group). ASA, which inhibits the thromboxane A2 pathway, and Hep, which inhibits thrombin generation, have no protective effect on DCS incidence. Clo, a specific ADP-receptor antagonist, reduces post-decompression platelet consumption. These results point to the predominant involvement of the ADP release in BIPA but cannot differentiate definitively between bubble-induced vessel wall injury and bubble-blood component interactions in DCS.

Influence of repetitive open sea dives and physical exercises on right-to-left shunting in healthy divers

Objective: Paradoxical gas embolism through right-to-left (R/L) shunts is considered as a potential cause of certain types of decompression sickness. Aim: To assess whether 4 months of repetitive diving and strenuous exercises would lead to an increased prevalence of R/L shunting in a group of military divers. Methods: Using a standardised contrast-enhanced transcranial Doppler technique, 17 divers were re-examined for the presence of a R/L shunt 4 months after their initial examinations. R/L shunts were classified as type I if observed only after a straining manoeuvre, and type II if present at rest. Results: Initial prevalence of R/L shunt was 41%: six type I shunts and one type II. At the second examination, prevalence was 47%, with the appearance of one type I shunt that was not previously present. We found no significant increase in the prevalence and size of R/L shunts. Conclusion: It is speculated that diving-related phenomena, such as variations in right atrial pressures during the end stages of or events immediately after a dive could generate an R/L shunt. However, extreme conditions of repetitive diving and strenuous exercises do not cause permanent modification in R/L permeability over a period of 4 months.

Effect of decompression-induced bubble formation on highly trained divers microvascular function

We previously showed microvascular alteration of both endothelium‐dependent and ‐independent reactivity after a single SCUBA dive. We aimed to study mechanisms involved in this postdive vascular dysfunction. Ten divers each completed three protocols: (1) a SCUBA dive at 400 kPa for 30 min; (2) a 41‐min duration of seawater surface head immersed finning exercise to determine the effect of immersion and moderate physical activity; and (3) a simulated 41‐min dive breathing 100% oxygen (hyperbaric oxygen [HBO]) at 170 kPa in order to analyze the effect of diving‐induced hyperoxia. Bubble grades were monitored with Doppler. Cutaneous microvascular function was assessed by laser Doppler. Endothelium‐dependent (acetylcholine, ACh) and ‐independent (sodium nitroprusside, SNP) reactivity was tested by iontophoresis. Endothelial cell activation was quantified by plasma Von Willebrand factor and nitric oxide (NO). Inactivation of NO by oxidative stress was assessed by plasma nitrotyrosine. Platelet factor 4 (PF4) was assessed in order to determine platelet aggregation. Blood was also analyzed for measurement of platelet count. Cutaneous vascular conductance (CVC) response to ACh delivery was not significantly decreased by the SCUBA protocol (23 ± 9% before vs. 17 ± 7% after; P = 0.122), whereas CVC response to SNP stimulation decreased significantly (23 ± 6% before vs. 10 ± 1% after; P = 0.039). The HBO and immersion protocols did not affect either endothelial‐dependent or ‐independent function. The immersion protocol induced a significant increase in NO (0.07 ± 0.01 vs. 0.12 ± 0.02 μg/mL; P = 0.035). This study highlighted change in microvascular endothelial‐independent but not ‐dependent function in highly trained divers after a single air dive. The results suggest that the effects of decompression on microvascular function may be modified by diving acclimatization.