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Dual response of cerebrocortical blood flow and arterial blood pressure to transient CO2 stimulus after inhibition of nitric oxide synthesis in rats

100%
Wolk R., Sieminska J., Trzebski A.
Acta Neurobiologiae Experimentalis
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1995
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vol. 55
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issue 2
73-83
EN
Inhibition of nitric oxide synthase (NOS) by Nitro-L-arginine-methyl-ester in 16 male Wistar rats anaesthetized with urethane, paralysed and artificially ventilated, increased siginficantly local peripheral vascular resistance in the parietal cortex (CVR) along with augmentatoin of the mean arterial blood presure (MP) and no change of the local cerebrocortical blood flow (CBF) recorded with a Laser-Doppler-Flowmeter.In 11 rats L-NAME reversed a pressor effect of brief hypercapnia induced by 10% Co2/air mixture into depressor esponse,reduced CBF esponse proportionally to the reduction of MAP and did notinfluence CVR response to CO2. In 5 rats L-NAME did not abolish the central pressor effect of CO2-stimulus and significantly augmented CO2-induced vasodilatory response in the cortex by a larger reduction of CVR.It is concluded that NO does not mediate the vasodilatory effect of brief hypercapnia in the cortex.NO apears critical for the central pressor effect of CO2.In those rats in which the central pressor effect of a CO2-stimulus was not abolished by an NOS blocker, an increased CBF and augmented decrease in CVR was observed during brief hypercapnia.Possible mechanisms of this dual responsiveness of cortical blood flow and arterial blood pressure to CO2, induceds bu inhibition of NOS, are discussed.
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Role of hypercapnia in brain oxygenation in sleep-disordered breathing

75%
Brzecka A.
Acta Neurobiologiae Experimentalis
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2007
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vol. 67
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issue 2
197-206
EN
Adaptive mechanisms may diminish the detrimental effects of recurrent nocturnal hypoxia in obstructive sleep apnea (OSA). The potential role of elevated carbon dioxide (CO2) in improving brain oxygenation in the patients with severe OSA syndrome is discussed. CO2 increases oxygen uptake by its influence on the regulation of alveolar ventilation and ventilation-perfusion matching, facilitates oxygen delivery to the tissues by changing the affinity of oxygen to hemoglobin, and increases cerebral blood flow by effects on arterial blood pressure and on cerebral vessels. Recent clinical studies show improved brain oxygenation when hypoxia is combined with hypercapnia. Anti-inflammatory and protective against organ injury properties of CO2 may also have therapeutic importance. These biological effects of hypercapnia may improve brain oxygenation under hypoxic conditions. This may be especially important in patients with severe OSA syndrome.
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