Journal article
Effects of activation of sympathetic nerves on cerebral blood flow during hypercapnia in cats and rabbits
The Journal of physiology, Vol.347(1), pp.35-45
1984
DOI: 10.1113/jphysiol.1984.sp015051
PMCID: PMC1199432
PMID: 6423816
Abstract
Effects of unilateral and bilateral activation of sympathetic nerves on cerebral blood flow (c.b.f.) and cerebrovascular resistance (c.v.r.) during hypercapnia were compared in anaesthetized cats and awake rabbits. Sympathetic nerves supplying cerebral vessels were sectioned on one or both sides in anaesthetized cats and unanaesthetized rabbits. Cerebral blood flow was measured with 15 micron radioactive microspheres. In cats, c.b.f. was greater than 110 ml/min per 100 g during hypercapnia (PCO2 greater than 65 mmHg). Unilateral section of sympathetic nerves did not change c.b.f. or c.v.r. but unilateral electrical stimulation decreased c.b.f. by 12 +/- 3% and increased c.v.r. by 15 +/- 4%. Bilateral section of sympathetic nerves decreased c.v.r. by 21 +/- 7% (P less than 0.005, compared with unilateral section) and electrical stimulation increased c.v.r. by 66 +/- 16% (P less than 0.005, compared with unilateral stimulation). In awake rabbits, c.b.f. was greater than 110 ml/min per 100 g during hypercapnia (PCO2 greater than 50 mmHg). Unilateral sympathetic denervation did not change c.v.r. but bilateral denervation decreased it by 18 +/- 8% (P less than 0.08, compared with unilateral section; P less than 0.03, compared with intact nerves). Thus, reflex activation of sympathetic nerves, as well as electrical stimulation, increases c.v.r. during hypercapnia. In addition, effects of bilateral stimulation or denervation of sympathetic nerves are greater than unilateral effects.
Details
- Title: Subtitle
- Effects of activation of sympathetic nerves on cerebral blood flow during hypercapnia in cats and rabbits
- Creators
- D. W BUSIJA - Univ. Iowa, coll. medicineD. D HEISTAD - Univ. Iowa, coll. medicine
- Resource Type
- Journal article
- Publication Details
- The Journal of physiology, Vol.347(1), pp.35-45
- DOI
- 10.1113/jphysiol.1984.sp015051
- PMID
- 6423816
- PMCID
- PMC1199432
- NLM abbreviation
- J Physiol
- ISSN
- 0022-3751
- eISSN
- 1469-7793
- Publisher
- Blackwell; Oxford
- Language
- English
- Date published
- 1984
- Academic Unit
- Cardiovascular Medicine; Neuroscience and Pharmacology; Internal Medicine
- Record Identifier
- 9984040576602771
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