The Influence of Expiratory Time on the Arterial to End-tidal Carbon dioxide Tension Differences.

Sha, Muneyasu; Koishi, Keiko; Ohmura, Akito; Miyaji, T; Shimazu, Toshihiro

doi:10.2199/jjsca.13.54

Cited by 2 publications

(2 citation statements)

References 10 publications

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“…Decreases in carbonic anhydrase activity have been shown to induce a greater increase in arterial blood PCOOE (PaCO2) than in pulmonary capillary PCO2, which has been equated with PCO2 in the end-tidal expiratory gas (PETCO2) [1][2][3]. The difference in PCO2 between the tissues and mixed venous blood is thought to involve the same mechanism that operates in the presence of a carbonic anhydrase inhibitor.…”

Section: Introductionmentioning

confidence: 99%

Acetazolamide-induced increase in blood flow to rabbit organs is confirmed using colored microspheres

Taki¹,

Hirahara²,

Tomita³

et al. 1998

Heart Vessels

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Inhibitors of carbonic anhydrase activity have been found to increase blood and organ PCO2 and to increase blood flow (BF) in individual organs. To determine whether carbonic anhydrase inhibition coordinately induces an increase in BF in several organs, we assayed the effect of the carbonic anhydrase inhibitor, acetazolamide (AZ), on BF in rabbit organs using the colored microsphere (CM) assay. Eight female white rabbits were anesthetized with ketamine and urethane, and administered three sequential doses of 4 mg/kg AZ. After each dose, the rabbits were injected with 9 x 10(5) CMs of different colors, and arterial blood was collected. We found that AZ had no effect on blood pressure, body temperature, hemoglobin concentration, or PaCO2. In contrast, 12 mg/kg AZ significantly increased PaO2 and significantly decreased base excess. When we measured organ BF, we observed, in response to 12 mg/kg AZ, an 82% increase in brain BF and a 55% increase in kidney BF, but no change in BF of the liver, stomach wall, or abdominal muscle. These findings suggest that the inhibition of carbonic anhydrase activity by AZ, which decreases the rate of CO2 conversion to HCO3-, causes the retention of CO2 in tissues and organs, and thus increases BF in specific organs. Administration of carbonic anhydrase inhibitors, such as AZ, may increase BF to the brain and kidney without reducing PaO2, thereby increasing the supply of oxygen in conditions involving hypoxia such as ischemia and shock.

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Section: Introductionmentioning

confidence: 99%

Acetazolamide-induced increase in blood flow to rabbit organs is confirmed using colored microspheres

Taki¹,

Hirahara²,

Tomita³

et al. 1998

Heart Vessels

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show abstract

“…This difference between PaCO2 and PETCO2, [(a-ET)PCO2], changes the ventilation/perfusion (V/Q) relation [1][2][3], stimulating respiration. When CA activity is decreased by such inhibitors as acetazolamide (AZ), the conversion velocity to CO2 from HCO3-is slowed, resulting in an imbalance between CO2 and HCO3 in the pulmonary venous system.…”

Section: Introductionmentioning

confidence: 99%

Detection of acetazolamide-induced increase in organ blood flow in rabbits by laser flowmetry

Taki¹,

Nagasawa²,

Hirahara

et al. 1997

J Anesth

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The Influence of Expiratory Time on the Arterial to End-tidal Carbon dioxide Tension Differences.

Abstract: The influence of expiratory time on the arterial to end-tidal carbon dioxide tension

Cited by 2 publications

References 10 publications

Acetazolamide-induced increase in blood flow to rabbit organs is confirmed using colored microspheres

Acetazolamide-induced increase in blood flow to rabbit organs is confirmed using colored microspheres

Detection of acetazolamide-induced increase in organ blood flow in rabbits by laser flowmetry

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