| Sažetak | Bühlmannove dekompresijske tablice smatraju se posebno pouzdanim u prevenciji dekompresijske bolesti (DB) radi vremena dekompresije koje je duže u usporedbi s drugim tablicama. Cilj istraživanja je bio provjeriti sigurnost Bühlmannovih tablica. U istraživanju je sudjelovalo 14 zdravih, iskusnih rekreacijskih ronilaca muškog spola. Ultrazvučnim uređajem je promatrana prisutnost mjehurića inertnog plina u desnom srcu nakon izlaganja tlaku u barokomori i ronjenja u moru. U oba postupka su profili ronjenja bili granični u smislu sigurnosti po korištenim tablicama. Pri "plitkom ronjenju" (24 m tijekom 70 min), medijan stupnja mjehurića nakon izlaganja tlaku u barokomori je bio "0", a nakon ronjenja u moru je iznosio "2" (P=0,67). Kod "dubokog ronjenja" (54 m tijekom 20 min), medijan stupnja mjehurića nakon izlaganja tlaku u barokomori je bio "0", a nakon ronjenja u moru je iznosio "3" (P=0,38). Pri "plitkom ronjenju", srednji stupanj mjehurića je nakon izlaganja tlaku u barokomori iznosio 0,1 mjehurića/cm², a nakon ronjenja u moru 1,4 mjehurića/cm², što je relativno povećanje od 140%, pri čemu je razlika bila statistički visoko značajna (P=0,0001). Pri "dubokom ronjenju", srednji stupanj mjehurića nakon izlaganja tlaku u barokomori je iznosio 0,1 mjehurića/cm², a nakon ronjenja u moru 2,4 mjehurića/cm², što je relativno povećanje od 240%, a razlika je također bila statistički visoko značajna (P<0,0001). Vjerojatnost nastanka DB (P-DB) koja je iznosila 6% do 9% nakon izlaganja tlaku u barokomori, povećala se i iznosila je 19% do 28% nakon ronjenja u moru. Kako bilo, tijekom istraživanja nisu zabilježeni simptomi ni znaci DB. Ronjenje u moru na granici sigurnosti Bühlmannovih tablica povezano je s visokim stupnjem mjehurića, što može rezultirati većim rizikom od nastanka DB čak i bez manifestne bolesti. Pratili smo stvaranje venskih mjehurića nakon ronjenja u moru u osoba (n=6) s kroničnom ozljedom kralješničke moždine (SCI) i tjelesno zdravih (n=7) ronilaca (C) kako bi se procijenila P-DB. Venski mjehurići plina promatrali su se ultrazvukom 40 min nakon izranjanja. P-DB je određivana bilježenjem profila ronjenja, uz uporabu modela po Gerthu. Ronioci su ronili dva puta svakog od tri dana eksperimenta, koristeći prilagođene Bühlmannove dekompresijske tablice. Srednja P-DB za sva ronjenja je u skupini SCI iznosila 0,51±0,2%, a u skupini C 0,64±0,27%, pri čemu je P-DB kod drugih ronjenja u danu bila veća (skupina SCI: prvo ronjenje 0,52±0,26%; drugo ronjenje 0,77±0,23%, odnosno skupina C: prvo ronjenje 0,43±0,18%; drugo ronjenje 0,60±0,20%). Usporedbom vrijednosti između skupina te prvih i drugih ronjenja nisu nađene statistički značajne razlike. Broj mjehurića je u obje skupine tijekom tri dana ronjenja bio nizak i iznosio od 0,0 do 0,10 mjehurića/cm². P-DB je u ronilaca s paraplegijom bila pri vrijednostima za uobičajeno rekreacijsko ronjenje, što znači da je korišteni ronilački profil bio siguran. Akutna arterijska endotelna disfunkcija nakon ronjenja često se javlja bez vidljivih promjena u endotelnom području, što ukazuje na mogućnost biokemijskog porijekla. Budući da su granulocitni i monocitni antigeni prepoznati kao ligandi endotelnih selektina, provjeravana je njihova osjetljivost kao biljega promijenjene vazodilatacije nakon ronjenja. Protočnom citometrijom su određivani biljezi CD15 i CD15s na mononuklearnim stanicama periferne krvi u osam ronilaca i to 30 min prije i 50 min nakon samo jednog ronjenja na 54 m dubine, u trajanju od 20 min. Broj plinskih mjehurića u desnom srcu pratio se ultrazvučnim uređajem. Mjehurići su zabilježeni u svih ronilaca (1,9±1,9 mjehurića/cm²). Postotak CD15+ monocita iznosio je 38,4±19,3 prije ronjenja, dok se nakon ronjenja povećao na 67,3±34,2 (P=0,0044). Postotak "velikih" CD15s+ monocita iznosio je 3,2±1,4 prije ronjenja, a 6,7±4,0 nakon ronjenja (P=0,0195). Poslije ronjenja, ukupni broj monocita bio je povećan, premda ne i statistički značajno, dok se ukupni broj granulocita povećao za 61%. Nije zabilježena značajna korelacija između stvaranja mjehurića i CD15+ monocita (r=-0,56; P=0,17), kao ni između stvaranja mjehurića i CD15s+ monocita (r=0,43; P=0,29). Biokemijske promjene nakon scuba ronjenja primarno se očituju aktiviranjem postojećih monocita, a manje povećanjem njihova broja tijekom akutne endotelne disfunkcije. |
| Sažetak (engleski) | Bühlmann's diving tables are usually considered to be very safe in sense of prevention of decompression sickness (DCS) due to longer decompression time in comparison with other tables. The objective of this study was to evaluate safety of Bühlmann's diving tables. In this study, 14 healthy experienced recreational male divers participated. Ultrasound scanner was used to detect the presence of vascular gas bubbles in the right heart after chamber pressure exposures ("dry" dives) and in-water scuba dives. Both diving profiles were at the limits of safety in Bühlmann's tables. When "shallow dive profile" (24 m/70 min) was used, mean number of bubbles increased from "0" after "dry" dives to "2" after in-water dives (P=0.67). When "deep dive profile" (54 m/20 min) was used, mean number of bubbles increased from "0" after "dry" dives to "3" after in-water dives (P=0.38). In "shallow dive profile" (24 m/70 min), mean number of bubbles/cm² increased from 0.1 after "dry" dives to 1.4 after "wet" dives, representing an increase of 140% (P=0.0001). In "deep dive profile" (54 m/20 min), mean number of bubbles/cm² increased from 0.1 after "dry" dives to 2.4 after "wet" dives, representing an increase of 240% (P<0.0001). Probability of DCS (P-DCS), ranging from 6 to 9% after the "dry" dives, increased after the in-water dives and ranged from 19 to 28%. However, no clinical signs of DCS were noticed in any of the divers in this series. In-water dives performed at the safety limits of Bühlmann's tables were associated with unexpectedly high bubble grade resulting in a considerable DCS risk, expressed as increased P-DCS values. The objective of this study was to evaluate the formation of venous gas bubbles and assess P-DCS after in-water scuba dives in divers with chronic spinal cord injury (SCI) (n=6) and able-bodied controls (C) (n=7). Gas bubbles were monitored with an ultrasound scanner 40 min after surfacing. P-DCS was estimated from diving profiles using Gerth's decompression model. Divers were diving for three consecutive days and completed two dives a day using modified Bühlmann's decompression tables. Mean P-DCS was similar in both groups (SCI: 0.51±0.2%; and C: 0.64±0.27%, respectively) but was higher after repetitive dives (SCI: first dive 0.52±0.26%; second dive 0.77±0.23%, and C: first dive 0.43±0.18%; second dive 0.60±0.20%, respectively). Comparison of P-DCS values between the groups and between the dives revealed no statistically significant differences. Number of bubbles was low in both groups on all three days of the experiment, ranging from 0.0 to 0.1 bubbles/cm². In SCI subjects, P-DCS was within the range expected for average low risk recreational dives, suggesting that the used diving profile was very safe. Acute arterial endothelial dysfunction after scuba diving often occurs without visible changes in the endothelial layer, suggesting its biochemical origin. Since granulocyte and monocyte antigens were recognized as ligands of endothelial selectins, we tested their sensitivity as markers of acute arterial endothelial dysfunction. Flow cytometry was used to determine CD15+ and CD15s+ on peripheral blood mononuclear cells in eight divers, 30 min before and 50 min after a single dive to 54 m for 20 min bottom time. The number of gas bubbles in the right heart was monitored by ultrasound scanner. Gas bubbles were observed in all divers, with the average number of bubbles/cm² 1.9±1.9. The proportion of CD15+ monocytes measuring 38.4±19.3 before the dive, increased to 67.3±34.2 after the dive (P=0.0044). The proportion of CD15s+ monocytes measuring 3.2±1.4 before the dive, increased to 6.7±4.0 after the dive (P=0.0195). The absolute number of monocytes was slightly increased after the dive, whereas the absolute number of granulocytes was significantly higher (61%). No significant correlations were observed neither between bubble formation and CD15+ monocyte expression (r=-0.56; P=0.17), nor between bubble formation and CD15s monocyte expression (r=0.43; P=0.29). This study suggests that biochemical changes induced by scuba diving primarily activate the existing monocytes rather than cause an increase of the number of monocytes at the time of acute arterial endothelial dysfunction. |
