OBJECTIVE: To investigate the response of subcutaneous tissue oxygen (O2) and carbon dioxide (CO2) tensions to hyperbaric oxygenation. DESIGN: Experimental study. SETTING: University hospital, Finland. SUBJECTS: 10 Wistar rats. INTERVENTION: Subcutaneous tissue PO2 and PCO2 were directly measured with an implanted Silastic tube tonometer and capillary sampling technique while breathing air and exposed to hyperbaric oxygen (HBO) at 2.5 or 2.8 ATA pressure. Hyperbaric exposures were carried out in a large multiplace chamber pressurised with air. MAIN OUTCOME MEASURES: Subcutaneous tissue PO2 and PCO2. RESULTS: The mean subcutaneous PO2 rose from the baseline of 8 kPa (60 mmHg) to 16 kPa (112 mmHg) when rats breathed room air during pressurisation to 2.8 atm. When the rats breathed oxygen at 2.5 ATA the maximal mean tissue PO2 was four times higher than the mean starting value. During the HBO treatment at 2.8 ATA the tissue PO2 rose to a value about five times above baseline. The tissue PCO2 values almost doubled during the exposure to HBO at 2.5 ATA, probably because elimination of carbon dioxide was impaired. CONCLUSION: Measurements of tissue PO2 and PCO2 with an implanted Silastic tonometer and a capillary sampling technique can successfully be adapted to hyperbaric conditions. The method yielded reproducible results and is applicable to clinical use in hyperbaric medicine.
OBJECTIVE: To investigate the response of subcutaneous tissue oxygen (O2) and carbon dioxide (CO2) tensions to hyperbaric oxygenation. DESIGN: Experimental study. SETTING: University hospital, Finland. SUBJECTS: 10 Wistar rats. INTERVENTION: Subcutaneous tissue PO2 and PCO2 were directly measured with an implanted Silastic tube tonometer and capillary sampling technique while breathing air and exposed to hyperbaric oxygen (HBO) at 2.5 or 2.8 ATA pressure. Hyperbaric exposures were carried out in a large multiplace chamber pressurised with air. MAIN OUTCOME MEASURES: Subcutaneous tissue PO2 and PCO2. RESULTS: The mean subcutaneous PO2 rose from the baseline of 8 kPa (60 mmHg) to 16 kPa (112 mmHg) when rats breathed room air during pressurisation to 2.8 atm. When the rats breathed oxygen at 2.5 ATA the maximal mean tissue PO2 was four times higher than the mean starting value. During the HBO treatment at 2.8 ATA the tissue PO2 rose to a value about five times above baseline. The tissue PCO2 values almost doubled during the exposure to HBO at 2.5 ATA, probably because elimination of carbon dioxide was impaired. CONCLUSION: Measurements of tissue PO2 and PCO2 with an implanted Silastic tonometer and a capillary sampling technique can successfully be adapted to hyperbaric conditions. The method yielded reproducible results and is applicable to clinical use in hyperbaric medicine.
Authors: Chai R Soh; Ricardo Pietrobon; John J Freiberger; Sophia T Chew; Dimple Rajgor; Mihir Gandhi; Jatin Shah; Richard E Moon Journal: Intensive Care Med Date: 2012-04-20 Impact factor: 17.440
Authors: Jonathan L Halbach; James M Prieto; Andrew W Wang; Dennis Hawisher; David M Cauvi; Tony Reyes; Jonathan Okerblom; Israel Ramirez-Sanchez; Francisco Villarreal; Hemal H Patel; Stephen W Bickler; George A Perdrizet; Antonio De Maio Journal: Am J Physiol Regul Integr Comp Physiol Date: 2019-05-15 Impact factor: 3.619