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. 2008 Jul;193(3):303-8.
doi: 10.1111/j.1748-1716.2008.01846.x. Epub 2008 Feb 12.

Heart and brain circulation and CO2 in healthy men

Affiliations

Heart and brain circulation and CO2 in healthy men

I Yokoyama et al. Acta Physiol (Oxf). 2008 Jul.

Abstract

Aim: To compare blood flow response to arterial carbon dioxide tension change in the heart and brain of normal elderly men.

Methods: Thirteen healthy elderly male volunteers were studied. Hypercapnea was induced by carbon dioxide inhalation and hypocapnea was induced by hyperventilation. Myocardial blood flow [mL min(-1) x (100 g of perfusable tissue)(-1)] and cerebral blood flow [mL min(-1) x (100 g of perfusable tissue)(-1)] were measured simultaneously at rest, under carbon dioxide gas inhalation and hyperventilation using the combination of two positron emission tomography scanners.

Results: Arterial carbon dioxide tension increased significantly during carbon dioxide inhalation (43.1 +/- 2.7 mmHg, P < 0.05) and decreased significantly during hyperventilation (29.2 +/- 3.4 mmHg, P < 0.01) from baseline (40.2 +/- 2.4 mmHg). Myocardial blood flow increased significantly during hypercapnea (88.7 +/- 22.4, P < 0.01) from baseline (78.2 +/- 12.6), as did the cerebral blood flow (baseline: 39.8 +/- 5.3 vs. hypercapnea: 48.4 +/- 10.4, P < 0.05). During hypocapnea cerebral blood flow decreased significantly (27.0 +/- 6.3, P < 0.01) from baseline as did the myocardial blood flow (55.1 +/- 14.6, P < 0.01). However, normalized myocardial blood flow by cardiac workload [100 mL mmHg(-1) x (heart beat)(-1) x (gram of perfusable tissue)(-1)] was not changed from baseline (93.4 +/- 16.6) during hypercapnea (90.5 +/- 14.3) but decreased significantly from baseline during hypocapnea (64.5 +/- 18.3, P < 0.01).

Conclusion: In normal elderly men, hypocapnea produces similar vasoconstriction both in the heart and brain. Mild hypercapnea increased cerebral blood flow but did not have an additional effect to dilate coronary arteries beyond the expected range in response to an increase in cardiac workload.

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