ROLE OF NITRIC OXIDE AND ATP-SENSITIVE K+CHANNELS IN REGULATION OF BASAL BLOOD FLOW AND HYPERCAPNIC VASODILATATION
OF CEREBRAL BLOOD VESSELS IN RABBIT

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NAJAFIPOUR H.; VAKILI A.; YEGANEH HADJ AHMADI M.; ESMAIELI F.

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Journal Paper

Paper Information

Journal: IRANIAN JOURNAL OF MEDICAL SCIENCES Year:2002 | Volume:27 | Issue:1 Page(s): 22-29

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Title

ROLE OF NITRIC OXIDE AND ATP-SENSITIVE K+CHANNELS IN REGULATION OF BASAL BLOOD FLOW AND HYPERCAPNIC VASODILATATION OF CEREBRAL BLOOD VESSELS IN RABBIT

Author(s)

NAJAFIPOUR H. | VAKILI A. | YEGANEH HADJ AHMADI M. | ESMAIELI F. | Issue Writer Certificate

Keywords

CEREBRAL BLOOD FLOW • HYPERCAPNIA • ATP-SENSITIVE POTASSIUM CHANNELS • NITRIC OXIDE

Abstract

Background: The mechanisms underlying cerebral hypercapnic vasodilatation are not fully understood.Objective: To investigate the role of nitric oxide (NO) and ATPsensitive potassium (KATP) channels in basal blood flow regulation and hypercapnia-induced vasodilatation in rabbit cerebral blood vessels. Methods: The change in cerebral blood flow was measured by a laser Doppler flowmeter in 18 New Zealand white rabbits, in two groups, under general anesthesia with sodium pentobarbital. Nomega- nitro-L-arginine methyl ester (L-NAME) and glibenclamide were administered locally and systemically before and during induction of hypercapnia.Results: The change in cerebral blood flow was not significant following local and systemic L-NAME administration, showing a nonsignificant role of local and systemic NO in regulation of rabbit basal cerebral blood flow. Hypercapnia increased cerebral blood flow by 17.3±4.4% before and 17.3±5.8% after local, and 5.8±3.2% (p<0.05) after systemic L-NAME administration. The change in cerebral blood flow was not significant after local and systemic administration of glibenclamide indicating a lack of KATP channel role in basal blood flow regulation. Hypercapnia increased cerebral blood flow by 27.2±8.7% before and 24.7±6.4% after local, and 49.3±9.7% after systemic administration of glibenclamide (p: NS in both cases).Conclusion: Regional NO production had no role in basal cortical blood flow regulation and systemic NO contributed to 66% increment in cerebral blood flow during hypercapnia. Also, the KATP channels did not mediate the effect of NO or other vasodilators responsible for increasing cerebral blood flow during hypercapnia.

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APA: Copy

NAJAFIPOUR, H., VAKILI, A., YEGANEH HADJ AHMADI, M., & ESMAIELI, F.. (2002). ROLE OF NITRIC OXIDE AND ATP-SENSITIVE K+CHANNELS IN REGULATION OF BASAL BLOOD FLOW AND HYPERCAPNIC VASODILATATION OF CEREBRAL BLOOD VESSELS IN RABBIT. IRANIAN JOURNAL OF MEDICAL SCIENCES (IJMS), 27(1), 22-29. SID. https://sid.ir/paper/275919/en

Vancouver: Copy

NAJAFIPOUR H., VAKILI A., YEGANEH HADJ AHMADI M., ESMAIELI F.. ROLE OF NITRIC OXIDE AND ATP-SENSITIVE K+CHANNELS IN REGULATION OF BASAL BLOOD FLOW AND HYPERCAPNIC VASODILATATION OF CEREBRAL BLOOD VESSELS IN RABBIT. IRANIAN JOURNAL OF MEDICAL SCIENCES (IJMS)[Internet]. 2002;27(1):22-29. Available from: https://sid.ir/paper/275919/en

IEEE: Copy

H. NAJAFIPOUR, A. VAKILI, M. YEGANEH HADJ AHMADI, and F. ESMAIELI, “ROLE OF NITRIC OXIDE AND ATP-SENSITIVE K+CHANNELS IN REGULATION OF BASAL BLOOD FLOW AND HYPERCAPNIC VASODILATATION OF CEREBRAL BLOOD VESSELS IN RABBIT,” IRANIAN JOURNAL OF MEDICAL SCIENCES (IJMS), vol. 27, no. 1, pp. 22–29, 2002, [Online]. Available: https://sid.ir/paper/275919/en

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