PURPOSE: Carbogen has long been under investigation as an adjuvant to radiotherapy of tumors. A major factor confounding its evaluation is its inconsistency in raising blood partial pressure of CO(2) (pCO(2)). We investigated whether a new partial rebreathing method would provide better control of pCO(2) than carbogen. METHODS AND MATERIALS: We compared the efficacy of each method in 10 healthy volunteers. Volunteers breathed 1.5, 3 and 5% carbogen in 5-min stages via the usual non-rebreathing circuit. All the volunteers then breathed 100% O(2) through a commercial sequential gas delivery (SGD) circuit modified by attaching a reservoir to its exhalation port. Hypercarbia was induced by step reductions in oxygen flow to the SGD circuit. We monitored minute ventilation and end-tidal pCO(2) (ETpCO(2)) as a surrogate for its arterial value. RESULTS: Inhalation of 1.5 and 3% carbogen did not increase ETpCO(2) from baseline (40 +/- 1.5 mmHg); 5% carbogen increased ETpCO(2) to 45 +/- 1.6 mmHg (p < 0.001). With the SGD circuit, reducing O(2) flow to 4.3 +/- 0.7 l/min increased ETpCO(2) in all subjects from 41 +/- 2.0 mmHg (baseline) to 46 +/- 2.1 mmHg (p < 0.001). Voluntary hyperventilation reduced ETpCO(2) with 5% carbogen but not with SGD (p = 0.379). CONCLUSIONS: We confirm previous observations that carbogen inhalation does not result in a predictable rise in ETpCO(2) and suggest that a precise and stable target ETpCO(2) can instead be induced by simply controlling O(2) flow into a modified SGD circuit. We hoped that the reliable control of pCO(2) will enable studies that address first, the efficacy of raising ETpCO(2) on specific tumor blood flow, and eventually, its benefit as an adjuvant to radiotherapy.
PURPOSE:Carbogen has long been under investigation as an adjuvant to radiotherapy of tumors. A major factor confounding its evaluation is its inconsistency in raising blood partial pressure of CO(2) (pCO(2)). We investigated whether a new partial rebreathing method would provide better control of pCO(2) than carbogen. METHODS AND MATERIALS: We compared the efficacy of each method in 10 healthy volunteers. Volunteers breathed 1.5, 3 and 5% carbogen in 5-min stages via the usual non-rebreathing circuit. All the volunteers then breathed 100% O(2) through a commercial sequential gas delivery (SGD) circuit modified by attaching a reservoir to its exhalation port. Hypercarbia was induced by step reductions in oxygen flow to the SGD circuit. We monitored minute ventilation and end-tidal pCO(2) (ETpCO(2)) as a surrogate for its arterial value. RESULTS: Inhalation of 1.5 and 3% carbogen did not increase ETpCO(2) from baseline (40 +/- 1.5 mmHg); 5% carbogen increased ETpCO(2) to 45 +/- 1.6 mmHg (p < 0.001). With the SGD circuit, reducing O(2) flow to 4.3 +/- 0.7 l/min increased ETpCO(2) in all subjects from 41 +/- 2.0 mmHg (baseline) to 46 +/- 2.1 mmHg (p < 0.001). Voluntary hyperventilation reduced ETpCO(2) with 5% carbogen but not with SGD (p = 0.379). CONCLUSIONS: We confirm previous observations that carbogen inhalation does not result in a predictable rise in ETpCO(2) and suggest that a precise and stable target ETpCO(2) can instead be induced by simply controlling O(2) flow into a modified SGD circuit. We hoped that the reliable control of pCO(2) will enable studies that address first, the efficacy of raising ETpCO(2) on specific tumor blood flow, and eventually, its benefit as an adjuvant to radiotherapy.
Authors: Rami R Hallac; Yao Ding; Qing Yuan; Roderick W McColl; Jayanthi Lea; Robert D Sims; Paul T Weatherall; Ralph P Mason Journal: NMR Biomed Date: 2012-05-23 Impact factor: 4.044
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Authors: Olivia Sobczyk; Jorn Fierstra; Lakshmikumar Venkatraghavan; Julien Poublanc; James Duffin; Joseph A Fisher; David J Mikulis Journal: Front Physiol Date: 2021-07-07 Impact factor: 4.566