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Article: Mechanism of action of prostaglandin E2 in the dog skeletal muscle circulation

TitleMechanism of action of prostaglandin E2 in the dog skeletal muscle circulation
Authors
Issue Date1998
PublisherChinese Medical Association. The Journal's web site is located at http://www.cmj.org/
Citation
Chinese Medical Journal, 1998, v. 111 n. 10, p. 945-950 How to Cite?
AbstractObjective. To determine whether prostaglandin E2 (PGE2) influences the dog skeletal muscle circulation by a direction on the vascular smooth muscle or via pre- or post-synaptic modulation of sympathetic neurotransmission. Methods. In 18 anaesthetised dogs, a gracilis muscle was vascularly isolated and perfused at constant flow. Sympathetic vasoconstrictor tone on the muscles was reflexly controlled by alterations to the pressure at which the isolated carotid sinuses were perfused. The effects of PGE2 injection into the muscle were compared at low carotid sinus pressure, high carotid sinus pressure, and following denervation of the muscle, with or without noradrenaline infusion. Results. At all levels of sympathetic tone, PGE2 produced significantly more vasodilation than the saline vehicle. However, at a carotid sinus pressure of 46.0 ± 2.3 mmHg (1 mmHg = 0.133 kPa), PGE2 caused a decrease in femoral arterial perfusion pressure of 52.6 ± 7.1 mmHg, which was significantly greater than the response at a carotid sinus pressure of 208.5 ± 3.7 (33.6 ± 4.2 mmHg decrease) or following denervation (25.6 ± 3.7 mmHg decrease). In a separate group of denervated muscles, PGE2 caused a similar decrease in perfusion pressure in the presence or absence of a noradrenaline infusion. Conclusions. PGE2 appears to cause vasodilation through two separate mechanisms: one mechanism involves presynaptic inhibition of sympathetic vasoconstrictor tone, while the other is independent of the sympathetic nervous system, and is therefore presumably a direct action on the vascular smooth muscle or endothelium. Under our experimental conditions, both mechanisms contributed equally to the vasodilation.
Persistent Identifierhttp://hdl.handle.net/10722/171647
ISSN
2015 Impact Factor: 0.957
2015 SCImago Journal Rankings: 0.428
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorBallard, HJen_US
dc.contributor.authorAchike, FIen_US
dc.date.accessioned2012-10-30T06:16:08Z-
dc.date.available2012-10-30T06:16:08Z-
dc.date.issued1998en_US
dc.identifier.citationChinese Medical Journal, 1998, v. 111 n. 10, p. 945-950en_US
dc.identifier.issn0366-6999en_US
dc.identifier.urihttp://hdl.handle.net/10722/171647-
dc.description.abstractObjective. To determine whether prostaglandin E2 (PGE2) influences the dog skeletal muscle circulation by a direction on the vascular smooth muscle or via pre- or post-synaptic modulation of sympathetic neurotransmission. Methods. In 18 anaesthetised dogs, a gracilis muscle was vascularly isolated and perfused at constant flow. Sympathetic vasoconstrictor tone on the muscles was reflexly controlled by alterations to the pressure at which the isolated carotid sinuses were perfused. The effects of PGE2 injection into the muscle were compared at low carotid sinus pressure, high carotid sinus pressure, and following denervation of the muscle, with or without noradrenaline infusion. Results. At all levels of sympathetic tone, PGE2 produced significantly more vasodilation than the saline vehicle. However, at a carotid sinus pressure of 46.0 ± 2.3 mmHg (1 mmHg = 0.133 kPa), PGE2 caused a decrease in femoral arterial perfusion pressure of 52.6 ± 7.1 mmHg, which was significantly greater than the response at a carotid sinus pressure of 208.5 ± 3.7 (33.6 ± 4.2 mmHg decrease) or following denervation (25.6 ± 3.7 mmHg decrease). In a separate group of denervated muscles, PGE2 caused a similar decrease in perfusion pressure in the presence or absence of a noradrenaline infusion. Conclusions. PGE2 appears to cause vasodilation through two separate mechanisms: one mechanism involves presynaptic inhibition of sympathetic vasoconstrictor tone, while the other is independent of the sympathetic nervous system, and is therefore presumably a direct action on the vascular smooth muscle or endothelium. Under our experimental conditions, both mechanisms contributed equally to the vasodilation.en_US
dc.languageengen_US
dc.publisherChinese Medical Association. The Journal's web site is located at http://www.cmj.org/en_US
dc.relation.ispartofChinese Medical Journalen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCarotid Sinus - Drug Effectsen_US
dc.subject.meshDinoprostone - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshFemaleen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle, Skeletal - Blood Supplyen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshRegional Blood Flow - Drug Effectsen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleMechanism of action of prostaglandin E2 in the dog skeletal muscle circulationen_US
dc.typeArticleen_US
dc.identifier.emailBallard, HJ:ballard@hkucc.hku.hken_US
dc.identifier.authorityBallard, HJ=rp00367en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.pmid11189246-
dc.identifier.scopuseid_2-s2.0-0031796263en_US
dc.identifier.hkuros44333-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031796263&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume111en_US
dc.identifier.issue10en_US
dc.identifier.spage945en_US
dc.identifier.epage950en_US
dc.identifier.isiWOS:000076622300026-
dc.publisher.placeChinaen_US
dc.identifier.scopusauthoridBallard, HJ=7005286310en_US
dc.identifier.scopusauthoridAchike, FI=6701844593en_US

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