The Complex Role of Nitric Oxide in the Pathophysiology of Focal Cerebral Ischemia

The Complex Role of Nitric Oxide in the Pathophysiology of Focal Cerebral Ischemia Nitrogen monoxide (NO) has recently emerged as an important mediator of cellular and molecular events which impacts the pathophysiology of cerebral ischemia. Although tempting to ask whether NO is “good or bad” for cerebral ischemia, the question underestimates the complexities of NO chemistry and physiology as well as oversimplifies the pathophysiology of focal cerebral ischemia. Important vascular and neuronal actions of NO have been defined which both enhance tissue survival and mediate cellular injury and death, and these will be reviewed. Strategies which modify NO synthesis and / or metabolism may someday assume therapeutic importance, but not until the tissue compartments generating NO, the activities of the enzymes that are inducibly and constitutively expressed, and the redox state of NO during the stages of ischemic injury, are defined with greater precision. Our knowledge of these processes is rudimentary. This review will summarize the evidence from animal models which supports an emerging role for NO in ischemic pathophysiology. Important aspects of NO synthesis and inhibitors of this process will also be discussed http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Brain Pathology Wiley

The Complex Role of Nitric Oxide in the Pathophysiology of Focal Cerebral Ischemia

Loading next page...
 
/lp/wiley/the-complex-role-of-nitric-oxide-in-the-pathophysiology-of-focal-KPts0po017
Publisher site
See Article on Publisher Site

Abstract

Nitrogen monoxide (NO) has recently emerged as an important mediator of cellular and molecular events which impacts the pathophysiology of cerebral ischemia. Although tempting to ask whether NO is “good or bad” for cerebral ischemia, the question underestimates the complexities of NO chemistry and physiology as well as oversimplifies the pathophysiology of focal cerebral ischemia. Important vascular and neuronal actions of NO have been defined which both enhance tissue survival and mediate cellular injury and death, and these will be reviewed. Strategies which modify NO synthesis and / or metabolism may someday assume therapeutic importance, but not until the tissue compartments generating NO, the activities of the enzymes that are inducibly and constitutively expressed, and the redox state of NO during the stages of ischemic injury, are defined with greater precision. Our knowledge of these processes is rudimentary. This review will summarize the evidence from animal models which supports an emerging role for NO in ischemic pathophysiology. Important aspects of NO synthesis and inhibitors of this process will also be discussed

Journal

Brain PathologyWiley

Published: Jan 1, 1994

References

  • Nitric oxide as a neuronal messenger
    Snyder, Snyder; Bredt, Bredt
  • A novel neuronal messenger in brain: The free radical, nitric oxide
    Dawson, Dawson; Dawson, Dawson; Snyder, Snyder
  • Role of nitric oxide in regulation of basilar artery tone
    Faraci, Faraci
  • L‐arginine decreases infarct size caused by middle cerebral arterial occlusion in SHR
    Morikawa, Morikawa; Huang, Huang; Moskowitz, Moskowitz
  • The pharmacological and physiological role of cyclic GMP in vascular smooth muscle relaxation
    Ignarro, Ignarro; Kadowitz, Kadowitz
  • Characterization of three inhibitors of endothelial nitric oxide synthase in vitro and in vivo
    Rees, Rees; Palmer, Palmer; Schulz, Schulz; Hodson, Hodson; Moncada, Moncada
  • Inhibition of rat cerebellar nitric oxide synthase by 7‐nitro indazole and related substituted indazoles
    Babbedge, Babbedge; Bland‐Ward, Bland‐Ward; Hart, Hart; Moore, Moore
  • Identification of inhibitors of nitric oxide synthase that do not interact with endothelial cell L‐arginine transporter
    Bogle, Bogle; Moncada, Moncada; Pearson, Pearson; Mann, Mann
  • Oxygen radical mechanisms of brain injury following ischemia and reperfusion
    Traytsman, Traytsman; Kirsch, Kirsch; Koehler, Koehler

You’re reading a free preview. Subscribe to read the entire article.


DeepDyve is your
personal research library

It’s your single place to instantly
discover and read the research
that matters to you.

Enjoy affordable access to
over 18 million articles from more than
15,000 peer-reviewed journals.

All for just $49/month

Explore the DeepDyve Library

Search

Query the DeepDyve database, plus search all of PubMed and Google Scholar seamlessly

Organize

Save any article or search result from DeepDyve, PubMed, and Google Scholar... all in one place.

Access

Get unlimited, online access to over 18 million full-text articles from more than 15,000 scientific journals.

Your journals are on DeepDyve

Read from thousands of the leading scholarly journals from SpringerNature, Elsevier, Wiley-Blackwell, Oxford University Press and more.

All the latest content is available, no embargo periods.

See the journals in your area

DeepDyve

Freelancer

DeepDyve

Pro

Price

FREE

$49/month
$360/year

Save searches from
Google Scholar,
PubMed

Create folders to
organize your research

Export folders, citations

Read DeepDyve articles

Abstract access only

Unlimited access to over
18 million full-text articles

Print

20 pages / month

PDF Discount

20% off