Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Inhibition of nitric oxide synthase (NOS) by Nitro-L-arginine-methyl-ester (L-NAME 15 mg and 70 mg/kg i.v.) in 16 male Wistar rats anaesthetized with urethane, paralysed and artificially ventilated, increased significantly local peripheral vascular resistance in the parietal cortex (CVR) along with augmentation of the mean arterial blood pressure (MAP) 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 (PaCO2 84.1 +/- 5 mm Hg) into a depressor response, reduced CBF response proportionally to the reduction of MAP and did not influence CVR response to CO2. In 5 rats L-NAME did not abolish the central pressor effect of a CO2-stimulus and significantly augmented CO2-induced vasodilatatory response in the cortex (43.4 +/- 24% before L-NAME and 137.8 +/- 38.8% after L-NAME) by a larger reduction of CVR (-11 +/- 8% before L-NAME and -47.1 +/- 7.6% after L-NAME). It is concluded that NO does not mediate the vasodilatatory effect of brief hypercapnia in the cortex. NO appears 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, induced by inhibition of NOS, are discussed.
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PMID:Dual response of cerebrocortical blood flow and arterial blood pressure to transient CO2 stimulus after inhibition of nitric oxide synthesis in rats. 754 47

The study was designed to check the role of endogenous NO in maintaining the vasodilatory tone and in mediation of local cerebral blood flow (CBF) responses to CO2 in rostral ventrolateral medulla (RVLM) in the rat. The ventral surface of the medulla was exposed and CBF in the RVLM continuously recorded with a laser-Doppler flowmeter. Local vascular resistance (CVR) was estimated as the ratio of mean arterial pressure (MAP) to CBF. During 1 min exposure to 10% CO2 in oxygen PaCO2 rose from 39.9 +/- 2 mm Hg to 89.7 +/- 4.6 mm Hg and pH fell from 7.4 +/- 0.04 to 7.1 +/- 0.03. After intravenous administration of 15 mg/kg L-NAME (Nitro-L-arginine-methyl ester) MAP increased by 43 +/- 2.9 mm Hg (p < 0.001), local CBF increased by 33 +/- 6% (p < 0.001) and CVR increased by 17 +/- 6% (p < 0.01). L-NAME significantly reduced CBF flow response to 60 s hypercapnia from 47 +/- 9% (p < 0.001) before administration of L-NAME to 14 +/- 5% (p < 0.001). This effect was due to reversal by L-NAME of a pressor response to hypercapnia to a depressor response. The attenuation of CVR response to CO2 by L-NAME was too small to account alone for the significant reduction of local CBF responsiveness to hypercapnia. We conclude that endogenous NO plays a role in maintaining a local vasodilatory tone in RVLM, but it is less significant than in the cortical microcirculation. NO is not a major mediator in the increase in local CBF in RVLM during brief hypercapnia. Endogenous NO is critical for the neurogenic pressor response to brief hypercapnia.
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PMID:Role of the endogenous nitric oxide in the vasodilatory tone and CO2 responsiveness of the rostral ventrolateral medulla microcirculation in the rat. 767 Jan 22