Browsing by Author "Camporesi, Enrico M"
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Item Open Access Arterial Blood Gas Analysis in Breath-Hold Divers at Depth.(Frontiers in physiology, 2018-01) Bosco, Gerardo; Rizzato, Alex; Martani, Luca; Schiavo, Simone; Talamonti, Ennio; Garetto, Giacomo; Paganini, Matteo; Camporesi, Enrico M; Moon, Richard EThe present study aimed to evaluate the partial pressure of arterial blood gases in breath-hold divers performing a submersion at 40 m. Eight breath-hold divers were enrolled for the trials held at "Y-40 THE DEEP JOY" pool (Montegrotto Terme, Padova, Italy). Prior to submersion, an arterial cannula in the radial artery of the non-dominant limb was positioned. All divers performed a sled-assisted breath-hold dive to 40 m. Three blood samplings occurred: at 10 min prior to submersion, at 40 m depth, and within 2 min after diver's surfacing and after resuming normal ventilation. Blood samples were analyzed immediately on site. Six subjects completed the experiment, without diving-related problems. The theoretically predicted hyperoxia at the bottom was observed in 4 divers out of 6, while the other 2 experienced a reduction in the partial pressure of oxygen (paO2) at the bottom. There were no significant increases in arterial partial pressure of carbon dioxide (paCO2) at the end of descent in 4 of 6 divers, while in 2 divers paCO2 decreased. Arterial mean pH and mean bicarbonate ( HCO3- ) levels exhibited minor changes. There was a statistically significant increase in mean arterial lactate level after the exercise. Ours was the first attempt to verify real changes in blood gases at a depth of 40 m during a breath-hold descent in free-divers. We demonstrated that, at depth, relative hypoxemia can occur, presumably caused by lung compression. Also, hypercapnia exists at depth, to a lesser degree than would be expected from calculations, presumably because of pre-dive hyperventilation and carbon dioxide distribution in blood and tissues.Item Open Access Arterial blood gases in divers at surface after prolonged breath-hold.(European journal of applied physiology, 2020-02) Bosco, Gerardo; Paganini, Matteo; Rizzato, Alex; Martani, Luca; Garetto, Giacomo; Lion, Jacopo; Camporesi, Enrico M; Moon, Richard EPURPOSE:Adaptations during voluntary breath-hold diving have been increasingly investigated since these athletes are exposed to critical hypoxia during the ascent. However, only a limited amount of literature explored the pathophysiological mechanisms underlying this phenomenon. This is the first study to measure arterial blood gases immediately before the end of a breath-hold in real conditions. METHODS:Six well-trained breath-hold divers were enrolled for the experiment held at the "Y-40 THE DEEP JOY" pool (Montegrotto Terme, Padova, Italy). Before the experiment, an arterial cannula was inserted in the radial artery of the non-dominant limb. All divers performed: a breath-hold while moving at the surface using a sea-bob; a sled-assisted breath-hold dive to 42 m; and a breath-hold dive to 42 m with fins. Arterial blood samples were obtained in four conditions: one at rest before submersion and one at the end of each breath-hold. RESULTS:No diving-related complications were observed. The arterial partial pressure of oxygen (96.2 ± 7.0 mmHg at rest, mean ± SD) decreased, particularly after the sled-assisted dive (39.8 ± 8.7 mmHg), and especially after the dive with fins (31.6 ± 17.0 mmHg). The arterial partial pressure of CO2 varied somewhat but after each study was close to normal (38.2 ± 3.0 mmHg at rest; 31.4 ± 3.7 mmHg after the sled-assisted dive; 36.1 ± 5.3 after the dive with fins). CONCLUSION:We confirmed that the arterial partial pressure of oxygen reaches hazardously low values at the end of breath-hold, especially after the dive performed with voluntary effort. Critical hypoxia can occur in breath-hold divers even without symptoms.Item Open Access Environmental Physiology and Diving Medicine.(Frontiers in psychology, 2018-01) Bosco, Gerardo; Rizzato, Alex; Moon, Richard E; Camporesi, Enrico MMan's experience and exploration of the underwater environment has been recorded from ancient times and today encompasses large sections of the population for sport enjoyment, recreational and commercial purpose, as well as military strategic goals. Knowledge, respect and maintenance of the underwater world is an essential development for our future and the knowledge acquired over the last few dozen years will change rapidly in the near future with plans to establish secure habitats with specific long-term goals of exploration, maintenance and survival. This summary will illustrate briefly the physiological changes induced by immersion, swimming, breath-hold diving and exploring while using special equipment in the water. Cardiac, circulatory and pulmonary vascular adaptation and the pathophysiology of novel syndromes have been demonstrated, which will allow selection of individual characteristics in order to succeed in various environments. Training and treatment for these new microenvironments will be suggested with description of successful pioneers in this field. This is a summary of the physiology and the present status of pathology and therapy for the field.Item Open Access Hippocampal cellular loss after brief hypotension.(SpringerPlus, 2013-12) Chaparro, Rafael E; Quiroga, Carolina; Bosco, Gerardo; Erasso, Diana; Rubini, Alessandro; Mangar, Devanand; Parmagnani, Andrea; Camporesi, Enrico MBrief episodes of hypotension have been shown to cause acute brain damage in animal models. We used a rat hemorrhagic shock model to assess functional outcome and to measure the relative neuronal damage at 1, 4 and 14 days post-injury (3 min of hypotension). All rats underwent a neurological assessment including motor abilities, sensory system evaluation and retrograde memory at post-hypotensive insult. Brains were harvested and stained for Fluorojade C and Nissl. Stereology was used to analyze Fluorojade C and Nissl stained brain sections to quantitatively detect neuronal damage after the hypotensive insult. Statistical analysis was performed using Graphpad Prism 5 with the Bonferroni test at a 95% confidence interval after ANOVA. A Mixed Effect Model was used for the passive avoidance evaluation. Stereologically counted fluorojade positive cells in the hippocampus revealed significant differences in neuronal cell injury between control rats and rats that received 3 min of hypotension one day after insult. Quantification of Nissl positive neuronal cells showed a significant decrease in the number hippocampal cells at day 14. No changes in frontal cortical cells were evident at any time, no significative changes in neurological assessments as well. Our observations show that brief periods of hemorrhage-induced hypotension actually result in neuronal cell damage in Sprague-Dawley rats even if the extent of neuronal damage that was incurred was not significant enough to cause changes in motor or sensory behavior.