Nitric Oxide in Cerebrovascular Regulation and Ischemia

1997 ◽  
pp. 28-45
Author(s):  
T. Dalkara ◽  
M.A. Moskowitz
Keyword(s):  
Nitric Oxide ◽  
Cerebrovascular Regulation

Arginine-nitric oxide pathway and cerebrovascular regulation in cortical spreading depression

1995 ◽  
Vol 269 (1) ◽  
pp. H23-H29 ◽  
Author(s):  
M. Fabricius ◽  
N. Akgoren ◽  
M. Lauritzen
Keyword(s):  
Nitric Oxide ◽  
Cortical Spreading Depression ◽  
Vascular Reactivity ◽  
Spreading Depression ◽  
Clinical Importance ◽  
Receptor Activation ◽  
Marked Rise ◽  
Doppler Flowmetry ◽  
Pial Arterioles ◽  
Cerebrovascular Regulation

Nerve cells release nitric oxide (NO) in response to activation of glutamate receptors of the N-methyl-D-aspartate (NMDA) subtype. We explored the hypothesis that NO influences the changes of cerebral blood flow (CBF) during cortical spreading depression (CSD), which is known to be associated with NMDA receptor activation. CBF was monitored in parietal cortex by laser-Doppler flowmetry in halothane-anesthetized rats. Under control conditions, CSD induced regular changes of CBF, which consisted of four phases: a brief hypoperfusion before the direct current (DC) shift; a marked CBF rise during the DC shift; followed by a smaller, but protracted increase of CBF; and a prolonged CBF reduction (the oligemia). NO synthase inhibition by intravenous and/or topical application of NG-nitro-L-arginine enhanced the brief initial hypoperfusion, but the CBF increases and the oligemia were unchanged. L-Arginine prevented the development of the prolonged oligemia after CSD but had no influence on the marked rise of CBF during CSD. Animals treated with L-arginine recovered the reduced vascular reactivity to hypercapnia after CSD much faster than control rats. Functional denervation of cortical and pial arterioles by tetrodotoxin accentuated the pre-CSD hypoperfusion and the oligemia but did not affect the CBF increases. The results suggest that NO is important for the changes of cerebrovascular regulation following CSD. The observations may have clinical importance, since CBF changes during migraine may be triggered by CSD.

scholarly journals Nitric Oxide Synthase Inhibition and Cerebrovascular Regulation

1994 ◽  
Vol 14 (2) ◽  
pp. 175-192 ◽  
Author(s):  
Costantino Iadecola ◽  
Dale A. Pelligrino ◽  
Michael A. Moskowitz ◽  
Niels A. Lassen
Keyword(s):  
Nitric Oxide ◽  
Cerebral Circulation ◽  
Ischemic Damage ◽  
Considerable Controversy ◽  
The Subject ◽  
Cerebral Ischemic ◽  
Cerebral Ischemic Damage ◽  
Oxide Synthase ◽  
Cerebrovascular Regulation

There is increasing evidence that nitric oxide (NO) is an important molecular messenger involved in a wide variety of biological processes. Recent data suggest that NO is also involved in the regulation of the cerebral circulation. Thus, NO participants in the maintenance of resting cerebrovascular tone and may play an important role in selected vasodilator responses of the cerebral circulation. Furthermore, evidence has been presented suggesting that NO participates in the mechanisms of cerebral ischemic damage. Despite the widespread attention that NO has captured in recent years and the large number of studies that have been published on the subject, there is considerable controversy regarding the role of this agent in cerebrovascular regulation and in ischemic damage. In this paper the results of investigations on NO and the cerebral circulation are reviewed and the evidence for and against a role of NO is critically examined.

scholarly journals Cerebrovascular Regulation During an Insulin‐Glucose Challenge: Contribution of Nitric Oxide

2018 ◽  
Vol 32 (S1) ◽  
Author(s):  
Aaron T. Ward ◽  
Katrina J. Carter ◽  
Christina J. Sauder ◽  
J. Mikhail Kellawan ◽  
Oliver Weiben ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Glucose Challenge ◽  
Cerebrovascular Regulation

Nitric Oxide and Cerebrovascular Regulation

2014 ◽  
pp. 347-385 ◽  
Author(s):  
Seyed Nasrollah Tabatabaei ◽  
Hélène Girouard
Keyword(s):  
Nitric Oxide ◽  
Cerebrovascular Regulation

Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

1996 ◽  
Vol 54 ◽  
pp. 786-787
Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Cardiac Tissues ◽  
Mammalian Tissues ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

Nitric Oxide Reduces Pressor Responsiveness During Ovine Hypoadrenocorticism

2001 ◽  
Vol 28 (5-6) ◽  
pp. 459-462
Author(s):  
Pini Orbach ◽  
Charles E Wood ◽  
Maureen Keller-Wood
Keyword(s):  
Nitric Oxide
Sign in / Sign up

Export Citation Format

Share Document