Hyperoxic Ventilation in Critical Dilutional Anemia: Intestinal O2Transport and Tissue Oxygenation

Autor: Jörg Hutter, Kristian B Packert, Oliver Habler, F. Meisner, Christoph J. Wojtczyk, Gregor Kemming, J.M. Meier, J. Tillmanns, Martin Kleen, D. Bottino
Rok vydání: 2004
Předmět:
Zdroj: Transfusion Alternatives in Transfusion Medicine. 5:523-532
ISSN: 1778-428X
1295-9022
Popis: Summary Objective: The onset of hyperoxic ventilation after hemodilution to the critical hematocrit (Hctcrit) improves myocardial and peripheral tissue oxygenation. However, it is unknown whether at Hctcrit hyperoxemia is also beneficial to intestinal oxygenation, since intestinal tissue hypoxia might even worsen as a result of hyperoxic vasoconstriction. To study this, we investigated whether hyperoxic ventilation started at Hctcrit is beneficial in terms of intestinal oxygenation. Method: 18 anesthetized pigs were hemodiluted to their individual Hctcrit (onset of myocardial ischemia; ECG) by 1:1 exchange of blood with 6% pentastarch (200,000/0.5). At Hctcrit hyperoxic ventilation was initiated. Nine complete datasets were obtained and analyzed at baseline, at Hctcrit and during hyperoxic ventilation. Analysis included intestinal O2 transport parameters (portal blood gases), intestinal mucosal O2 partial pressure (MDO-Electrode) and regional intestinal blood flow (microsphere method). Results: At Hctcrit (7.2 ±1.2%), intestinal O2 delivery was reduced. Despite increased O2 extraction, local tissue hypoxia was documented by markedly reduced portal venous (26 ± 2 Torr) and jejunal O2 (9 ± 3 Torr) partial pressures. Portal venous base excess (-10 ± 3 mmol/L) and lactate concentration (4.3 ± 1.4 mmol/L) evidenced anaerobic intestinal metabolism (all p < 0.05). During hyperoxic ventilation, intestinal O2 delivery increased (p < 0.05) requiring a less intensive O2 extraction; physically dissolved O2 extracted from plasma was predominantly responsible for the restoration of portal and intestinal mucosal O2 partial pressure (49 ± 2 Torr and 17 ± 4 Torr; p < 0.05 vs. Hctcrit). Portal base excess (-12 ± 6 mmol/L) and lactate concentration (4.3 ± 1.9 mmol/L) did not recover. Conclusion: Hyperoxic ventilation at Hctcrit did improve intestinal O2 transport and mucosal oxygenation after 15 min. However, intestinal O2 debt persisted during the observation time. Summary Hyperoxic ventilation reverses manifest intestinal mucosal tissue hypoxia at Hctcrit due to the efficacious utilization of physically dissolved O2. There is no evidence that at Hctcrit hyperoxia-induced vasoconstriction further does impair microvascular intestinal blood flow and O2 transport. It remains unclear, to which extent hyperoxic ventilation may induce relevant O2 shunts. Hence, the true value of this technique for a possible use in humans remains to be elucidated.
Databáze: OpenAIRE
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