| ||||||||||||||
|
|
|||||||||||||
Department of Anesthesiology and Critical Care Medicine, and *Second Department of Internal Medicine, Gifu University School of Medicine, Gifu City, Gifu, Japan
Address correspondence and reprint requests to Hiroki Iida, MD, Department of Anesthesiology and Critical Care Medicine, Gifu University School of Medicine, 40 Tsukasamachi, Gifu-City, Gifu 500-8705, Japan. Address e-mail to iida{at}cc.gifu-u.ac.jp
The effects of
-human atrial natriuretic peptide (HANP) and milrinone on cerebral pial vessels, especially during blood-brain barrier (BBB) disruption, are not clear. We studied topical HANP (10-14, 10-12, and 10-10 M) or milrinone (10-7, 10-5, and 10-3 M), and IV HANP (0.1, 0.2, and 1.0 µg · kg-1 · min-1) or milrinone (0.5, 5.0, and 20.0 µg · kg-1 · min-1) with or without hyperosmolar BBB disruption, using a rabbit cranial window preparation. At 10-12 and 10-10 M topical HANP produced significant arteriolar (16%, 20%, respectively), but no venular dilation. Topical milrinone (10-3 M) produced significant arteriolar and venular dilation (21%, 8%, respectively). IV HANP produced no arteriolar or venular changes at any dose except during BBB disruption, when it caused a significant arteriolar (16%, 16%, and 17%, respectively), but no venular dilation. In contrast, IV milrinone caused small but significant arteriolar and venular dilation without BBB disruption (arterioles, 6%, 7% and 8%, respectively; venules, 6% at 20.0 µg · kg-1 · min-1). During BBB disruption, these responses to milrinone were similar. Although HANP and milrinone each have a direct vasodilator effect on arterioles, their systemic administration at clinical doses could induce different effects. BBB disruptive conditions could increase the response of pial vessels to systemically administered HANP.
Implications: Although
-human atrial natriuretic peptide (HANP) and milrinone each havea direct vasodilator effect on cerebral pial arterioles, their systemicadministration at clinical doses could have different effects andblood-brain-barrier disruptive conditions could alter the response of pialvessels to HANP, but not to milrinone.
This article has been cited by other articles:
![]() |
M. Uchida, H. Iida, M. Iida, M. Kumazawa, K. Sumi, M. Takenaka, and S. Dohi Both Milrinone and Colforsin Daropate Attenuate the Sustained Pial Arteriolar Constriction Seen After Unclamping of an Abdominal Aortic Cross-Clamp in Rabbits Anesth. Analg., July 1, 2005; 101(1): 9 - 16. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y. J. Oh, S. H. Kim, H. K. Shinn, C. S. Lee, Y. W. Hong, and Y. L. Kwak Effects of milrinone on jugular bulb oxygen saturation and cerebrovascular carbon dioxide reactivity in patients undergoing coronary artery bypass graft surgery Br. J. Anaesth., November 1, 2004; 93(5): 634 - 638. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Takenaka, H. Iida, M. Iida, M. Uchida, and S. Dohi The Comparative Effects of Prostaglandin E1 and Nicardipine on Cerebral Microcirculation in Rabbits Anesth. Analg., April 1, 2003; 96(4): 1139 - 1144. [Abstract] [Full Text] [PDF] |
||||
|