Abstract |
In the canine basilar artery during chronic vasospasm following subarachnoid hemorrhage, endothelium-dependent relaxations were diminished. Release of endothelium-derived relaxing factor (EDRF), as measured by a bioassay method, was unchanged. Relaxation to nitric oxide (NO) in preparations without endothelium was smaller in the spastic arteries. Production of cyclic GMP, measured by radioimmunoassay, was reduced in the spastic arteries; the impaired production was accompanied by decrease in GTP, the substrate for the production of cyclic nucleotide. The contents of other high-energy phosphates, such as creatine phosphate and ATP were also markedly reduced. Close temporal correlation between the metabolic failure and development of vasospasm was observed. Sarcolemmal regulation of intracellular calcium concentration was impaired in the pathological condition, suggesting a link between the metabolic failure and the pathological protracted contractions. Metabolic changes, and resultant affected viability of smooth muscle cells are likely to be an important factor in the pathogenesis of chronic vasospasm.
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Authors | P Kim |
Journal | Journal of the autonomic nervous system
(J Auton Nerv Syst)
Vol. 49 Suppl
Pg. S157-62
(Sep 1994)
ISSN: 0165-1838 [Print] Netherlands |
PMID | 7836674
(Publication Type: Journal Article)
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Chemical References |
- Calcium Channels
- Nitric Oxide
- Guanosine Triphosphate
- Adenosine Triphosphate
- Cyclic GMP
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Topics |
- Adenosine Triphosphate
(metabolism)
- Animals
- Basilar Artery
(drug effects, physiopathology)
- Calcium Channels
(metabolism)
- Cell Membrane Permeability
(physiology)
- Chronic Disease
- Cyclic GMP
(biosynthesis)
- Dogs
- Guanosine Triphosphate
(metabolism)
- Ischemic Attack, Transient
(metabolism, physiopathology)
- Muscle Relaxation
(drug effects, physiology)
- Muscle, Smooth, Vascular
(drug effects, metabolism, physiopathology)
- Nitric Oxide
(metabolism, pharmacology, physiology)
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