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Research Article Free access | 10.1172/JCI105858

Effect of norepinephrine, epinephrine, and angiotensin on blood flow in the internal carotid artery of man

Joseph C. Greenfield Jr. and George T. Tindall

Department of Medicine (Division of Cardiology), Duke University Medical Center and the Durham Veterans Administration Hospital, Durham, North Carolina 27705

Department of Surgery (Division of Neurosurgery), Duke University Medical Center and the Durham Veterans Administration Hospital, Durham, North Carolina 27705

Find articles by Greenfield, J. in: PubMed | Google Scholar

Department of Medicine (Division of Cardiology), Duke University Medical Center and the Durham Veterans Administration Hospital, Durham, North Carolina 27705

Department of Surgery (Division of Neurosurgery), Duke University Medical Center and the Durham Veterans Administration Hospital, Durham, North Carolina 27705

Find articles by Tindall, G. in: PubMed | Google Scholar

Published July 1, 1968 - More info

Published in Volume 47, Issue 7 on July 1, 1968
J Clin Invest. 1968;47(7):1672–1684. https://doi.org/10.1172/JCI105858.
© 1968 The American Society for Clinical Investigation
Published July 1, 1968 - Version history
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Abstract

Internal carotid artery blood flow and arterial pressure were measured with a sine-wave electromagnetic flowmeter and a pressure transducer in 22 patients during control period and after the intravenous and intracarotid administration of norepinephrine, epinephrine, and angiotensin. Intravenous infusion of both norepinephrine and angiotensin was accompanied by an increase in cerebral vascular resistance. Administration of norepinephrine, epinephrine, and angiotensin into the internal carotid artery failed to alter blood flow immediately. However, when the systemic blood pressure increased, a concomitant passive rise in blood flow did not occur. Thus, at this time cerebral vascular resistance was significantly increased. It is concluded that these drugs do not have a direct action on the cerebral vessels, but that the increased cerebral vascular resistance after their administration is due to autoregulation or to a combination of autoregulation and reduced arterial carbon dioxide pressure (PCO2) secondary to hyperventilation.

Similar studies were carried out in the external carotid artery of six patients. Within 10 sec after injection blood flow was markedly reduced, indicating a direct vasoconstricting action on this vascular bed.

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