Immersion before dry simulated dive reduces cardiomyocyte function and increases mortality after decompression.
Diving and decompression performed under immersed conditions have been shown to reduce cardiac function. The mechanisms for these changes are not known. The effect of immersion before a simulated hyperbaric dive on cardiomyocyte function was studied. Twenty-three rats were assigned to four groups: control, 1 h thermoneutral immersion, dry dive, and 1 h thermoneutral immersion before a dive (preimmersion dive). Rats exposed to a dive were compressed to 700 kPa, maintained for 45 min breathing air, and decompressed linearly to the surface at a rate of 50 kPa/min. Postdive, the animals were anesthetized and the right ventricle insonated for bubble detection using ultrasound. Isolation of cardiomyocytes from the left ventricle was performed and studied using an inverted fluorescence microscope with video-based sarcomere spacing. Compared with a dry dive, preimmersion dive significantly increased bubble production and decreased the survival time (bubble grade 1 vs. 5, and survival time 60 vs. 17 min, respectively). Preimmersion dive lead to 18% decreased cardiomyocyte shortening, 20% slower diastolic relengthening, and 22% higher calcium amplitudes compared with controls. The protein levels of the sarco-endoplasmic reticulum calcium ATPase (SERCA2a), Na+/Ca2+ exchanger (NCX), and phospholamban phosphorylation in the left ventricular tissue were significantly reduced after both dry and preimmersion dive compared with control and immersed animals. The data suggest that immersion before a dive results in impaired cardiomyocyte and Ca2+ handling and may be a cellular explanation to reduced cardiac function observed in humans after a dive.
Gaustad
Svein Erik
SE
Department of Circulation and Medical Imaging, Medical Technology Center, Norwegian University of Science and Technology, Olav Kyrres gt. 9, N-7489 Trondheim, Norway. svein.e.gaustad@ntnu.no
Brubakk
Alf O
AO
Høydal
Morten
M
Catalucci
Daniele
D
Condorelli
Gianluigi
G
Dujic
Zeljko
Z
Marinovic
Jasna
J
Ljubkovic
Marko
M
Møllerløkken
Andreas
A
Wisløff
Ulrik
U
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002135:Calcium-Binding Proteins / Q000378:metabolism; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000378:metabolism; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism; D003664:Decompression / Q000009:adverse effects*; D003665:Decompression Sickness / Q000000981:diagnostic imaging / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D004242:Diving / Q000009:adverse effects*; D004558:Electric Stimulation; D005260:Female; D007101:Immersion / Q000009:adverse effects*; D007700:Kinetics; D009200:Myocardial Contraction; D032383:Myocytes, Cardiac / Q000378:metabolism*; D010766:Phosphorylation; D051381:Rats; D017207:Rats, Sprague-Dawley; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000378:metabolism; D019831:Sodium-Calcium Exchanger / Q000378:metabolism; D014463:Ultrasonography; D016277:Ventricular Function, Left; D000099211:Phospholamban
D002118:Calcium; D002135:Calcium-Binding Proteins; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D017868:Cyclic AMP-Dependent Protein Kinases; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D019831:Sodium-Calcium Exchanger; D000099211:Phospholamban